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1.
Medicine (Baltimore) ; 100(32): e26931, 2021 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-34397939

RESUMO

ABSTRACT: Peripheral arterial disease (PAD) is one of major vascular diseases which frequently coexists with coronary arterial disease and cerebrovascular disease. The patients with PAD have a poor prognosis when it progresses. A new blood pressure testing device enables to simultaneously measure brachial blood pressure (BP), central BP, and several vascular parameters, with easy and non-invasive, in a short time. Here, we aimed to evaluate these arterial stiffness parameters in patients with PAD.In this study, 243 consecutive patients who were suspected of having PAD and referred to our hospital from September 2016 to June 2019, were registered. Several parameters, such as brachial BP, central BP, aortic pulse wave velocity (aPWV), total vascular resistance (TVR), augmentation index (AI) and augmentation pressure (AP), were determined by Mobil-O-Graph. Ankle-brachial pressure index (ABI) was used to define PAD (ABI ≤ 0.9 as PAD). The relationship between PAD and central BP, aPWV, TVR, AI, or AP were investigated.One hundred sixty-two patients (67%) were categorized as the PAD group and 81 patients (33%) as the non-PAD group. In the PAD group, the systolic brachial BP and central systolic BP were significantly higher than those in the non-PAD group (138 ±â€Š24 mmHg vs 131 ±â€Š19 mmHg, P < .05, 125 ±â€Š22 mmHg vs 119 ±â€Š18 mmHg, P < .05, respectively). TVR, AI, and AP were significantly higher in the PAD group (1785 ±â€Š379 dyn s/cm5 vs 1661 ±â€Š317 dyn s/cm5, P < .05, 26.2 ±â€Š13.0% vs 22.2 ±â€Š13.3%, P < .05, 13.5 ±â€Š9.4 mmHg vs 10.7 ±â€Š7.2 mmHg, P < .05, respectively). No significant differences in diastolic BP, central diastolic BP, and aPWV were found between the groups. Multivariate logistic regression analysis revealed that PAD was significantly associated with TVR, AI, and AP (P < .05, respectively).TVR/AP/AI were significantly higher in the PAD group than in the non-PAD group.


Assuntos
Velocidade do Fluxo Sanguíneo/fisiologia , Pressão Sanguínea/fisiologia , Doença Arterial Periférica/fisiopatologia , Resistência Vascular/fisiologia , Rigidez Vascular/fisiologia , Idoso , Índice Tornozelo-Braço , Estudos Transversais , Feminino , Humanos , Masculino , Análise de Onda de Pulso , Estudos Retrospectivos
2.
J Interv Cardiol ; 2021: 9971874, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34149324

RESUMO

Background: To validate a simplified invasive method for the calculation of the index of microvascular resistance (IMR). Methods: This is a prospective, single-center study of patients with chronic coronary syndromes presenting with nonobstructive coronary artery disease. IMR was obtained using both intravenous (IV) adenosine and intracoronary (IC) papaverine. Each IMR measurement was obtained in duplicate. The primary objective was the agreement between IMR acquired using adenosine and papaverine. Secondary objectives include reproducibility of IMR and time required for the IMR measurement. Results: One hundred and sixteen IMR measurements were performed in 29 patients. The mean age was 68.8 ± 7.24 years, and 27.6% was diabetics. IMR values were similar between papaverine and adenosine (17.7 ± 7.26 and 20.1 ± 8.6, p=0.25; Passing-Bablok coefficient A 0.58, 95% CI -2.42 to 3.53; coefficient B 0.90, 95% CI -0.74 to 1.07). The reproducibility of IMR was excellent with both adenosine and papaverine (ICC 0.78, 95% CI 0.63 to 0.88 and ICC 0.93, 95% CI 0.87 to 0.97). The time needed for microvascular assessment was significantly shortened by the use of IC papaverine (3.23 (2.84, 3.78) mins vs. 5.48 (4.94, 7.09) mins, p < 0.0001). Conclusion: IMR can be reliably measured using IC papaverine with similar results compared to intravenous infusion of adenosine with increased reproducibility and reduced procedural time. This approach simplifies the invasive assessment of the coronary microcirculation in the catheterization laboratory.


Assuntos
Cateterismo Cardíaco , Doença da Artéria Coronariana , Microcirculação/fisiologia , Duração da Cirurgia , Resistência Vascular/fisiologia , Idoso , Cateterismo Cardíaco/métodos , Cateterismo Cardíaco/normas , Doença da Artéria Coronariana/diagnóstico , Doença da Artéria Coronariana/fisiopatologia , Circulação Coronária/fisiologia , Vasos Coronários/fisiopatologia , Feminino , Humanos , Masculino , Estudos Prospectivos , Reprodutibilidade dos Testes , Índice de Gravidade de Doença , Simplificação do Trabalho
3.
Heart Fail Clin ; 17(3): 415-422, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-34051973

RESUMO

Heart failure (HF) is an ongoing crisis reaching epidemic proportions worldwide. About 50% of HF patients have a preserved ejection fraction. Invasive hemodynamics have shown varied results in patients who have HF with preserved ejection fraction (HFpEF). This article attempts to summarize the importance of detecting pulmonary vascular remodeling in HFpEF using invasive hemodynamics. Incorporating newer invasive hemodynamic parameters such as diastolic pulmonary gradient, pulmonary arterial compliance, pulmonary vascular resistance, and pulmonary arterial pulsatility index may improve patient selection for studies used in defining advanced therapies and clinical outcomes. Profiling of patients using invasive hemodynamic parameters may lead to better patient selection for clinical research.


Assuntos
Insuficiência Cardíaca/fisiopatologia , Artéria Pulmonar/fisiopatologia , Volume Sistólico/fisiologia , Remodelação Vascular/fisiologia , Resistência Vascular/fisiologia , Insuficiência Cardíaca/diagnóstico , Hemodinâmica , Humanos
5.
Am J Physiol Heart Circ Physiol ; 320(5): H2058-H2065, 2021 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-33769914

RESUMO

African American (AA) individuals are at a greater risk for the development of cardiovascular complications, such as hypertension, compared with European Americans (EAs). Higher vagally mediated heart rate variability (HRV) is typically associated with lower blood pressure (BP) and total peripheral resistance (TPR). However, research has yet to examine the differential impact of HRV on longitudinal hemodynamic activity between AAs and EAs. We sought to rectify this in a sample of 385 normotensive youths (207 AAs, 178 EAs; mean age 23.16 ± 2.9 yr). Individuals participated in two laboratory evaluations spanning approximately 6 yr. Bioimpedance was used to assess HRV at time 1 and cardiac output at both time 1 and time 2. Mean arterial pressure (MAP) was measured at both time points via an automated BP machine. TPR was calculated as MAP divided by cardiac output. Results showed AAs to have higher BP and higher TPR at time 2 compared with EAs, independent of several important covariates. Also, higher HRV at time 1 significantly predicted both lower TPR and BP at time 2 among EAs only; these associations were attenuated and not significant in AAs. HRV did not significantly predict cardiac output at time 2 in the full sample or split by ethnicity. Our findings highlight that AAs show TPR mediated long-term increases in BP irrespective of resting HRV, providing a physiological pathway linking AAs with a greater risk for mortality and morbidity from hypertension and potentially other cardiovascular disease.NEW & NEWSWORTHY African Americans and European Americans differ in hemodynamics underlying long-term blood pressure regulation. Over 6 yr, African Americans show total peripheral resistance-mediated increases in blood pressure compared with European Americans. Higher heart rate variability predicts lower blood pressure and total peripheral resistance 6 yr later in European Americans but not African Americans.


Assuntos
Pressão Sanguínea/fisiologia , Coração/fisiologia , Nervo Vago/fisiologia , Resistência Vascular/fisiologia , Adolescente , Adulto , Afro-Americanos , Grupo com Ancestrais do Continente Europeu , Feminino , Frequência Cardíaca/fisiologia , Hemodinâmica/fisiologia , Humanos , Masculino , Adulto Jovem
6.
J Intensive Care Med ; 36(6): 655-663, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33678052

RESUMO

BACKGROUND: It has been suggested that COVID-19-associated severe respiratory failure (CARDS) might differ from usual acute respiratory distress syndrome (ARDS) due to failing autoregulation of pulmonary vessels and higher shunt. We sought to investigate pulmonary hemodynamics and ventilation properties in patients with CARDS compared to patients with ARDS of pulmonary origin. METHODS: This was a retrospective analysis of prospectively collected data from consecutive adults with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 patients treated in our ICU in 04/2020 and a comparison of the data to matched controls with ARDS due to respiratory infections treated in our ICU from 01/2014 to 08/2019 for whom pulmonary artery catheter data were available. RESULTS: CARDS patients (n = 10) had ventilation characteristics similar to those of ARDS (n = 10) patients. Nevertheless, mechanical power applied by ventilation was significantly higher in CARDS patients (23.4 ± 8.9 J/min) than in ARDS (15.9 ± 4.3 J/min; P < 0.05). COVID-19 patients had similar pulmonary artery pressure but significantly lower pulmonary vascular resistance, as cardiac output was higher in CARDS vs. ARDS patients (P < 0.05). Shunt fraction and dead space were similar in CARDS compared to ARDS (P > 0.05) and were correlated with hypoxemia in both groups. The arteriovenous pCO2 difference (▵pCO2) was elevated (CARDS 5.5 ± 2.8 mmHg vs. ARDS 4.7 ± 1.1 mmHg; P > 0.05), as was the P(v-a)CO2/C(a-v)O2 ratio (CARDS mean 2.2 ± 1.5 vs. ARDS 1.7 ± 0.8; P > 0.05). CONCLUSIONS: Respiratory failure in COVID-19 patients seems to differ only slightly from ARDS regarding ventilation characteristics and pulmonary hemodynamics. Our data indicate microcirculatory dysfunction. More data need to be collected to assure these findings and gain more pathophysiological insights into COVID-19 and respiratory failure.


Assuntos
COVID-19/complicações , COVID-19/fisiopatologia , Débito Cardíaco/fisiologia , Respiração Artificial , Insuficiência Respiratória/fisiopatologia , Resistência Vascular/fisiologia , Idoso , Idoso de 80 Anos ou mais , COVID-19/terapia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Artéria Pulmonar , Insuficiência Respiratória/terapia , Insuficiência Respiratória/virologia , Estudos Retrospectivos
7.
Am J Physiol Heart Circ Physiol ; 320(5): H1923-H1934, 2021 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-33739156

RESUMO

Stimulation of soluble guanylate cyclase (sGC) improves fetal growth at gestational day 20 in the reduced uterine perfusion pressure (RUPP) rat model of placental ischemia suggesting a role for sGC in the etiology of intrauterine growth restriction (IUGR). This study tested the hypothesis that stimulation of sGC until birth attenuates asymmetric IUGR mitigating increased cardiovascular risk in offspring. Sham or RUPP surgery was performed at gestational day 14 (G14); vehicle or the sGC stimulator Riociguat (10 mg/kg/day sc) was administered G14 until birth. Birth weight was reduced in offspring from RUPP [intrauterine growth restricted (IUGR)], sGC RUPP (sGC IUGR), and sGC Sham (sGC Control) compared with Sham (Control). Crown circumference was maintained, but abdominal circumference was reduced in IUGR and sGC IUGR compared with Control indicative of asymmetrical growth. Gestational length was prolonged in sGC RUPP, and survival at birth was reduced in sGC IUGR. Probability of survival to postnatal day 2 was also significantly reduced in IUGR and sGC IUGR versus Control and in sGC IUGR versus IUGR. At 4 mo of age, blood pressure was increased in male IUGR and sGC IUGR but not male sGC Control born with symmetrical IUGR. Global longitudinal strain was increased and stroke volume was decreased in male IUGR and sGC IUGR compared with Control. Thus late gestational stimulation of sGC does not mitigate asymmetric IUGR or increased cardiovascular risk in male sGC IUGR. Furthermore, late gestational stimulation of sGC is associated with symmetrical growth restriction in sGC Control implicating contraindications in normal pregnancy.NEW & NOTEWORTHY The importance of the soluble guanylate cyclase-cGMP pathway in a rat model of placental ischemia differs during critical windows of development, implicating other factors may be critical mediators of impaired fetal growth in the final stages of gestation. Moreover, increased blood pressure at 4 mo of age in male intrauterine growth restriction offspring is associated with impaired cardiac function including an increase in global longitudinal strain in conjunction with a decrease in stroke volume, ejection fraction, and cardiac output.


Assuntos
Retardo do Crescimento Fetal/metabolismo , Placenta/irrigação sanguínea , Insuficiência Placentária/metabolismo , Guanilil Ciclase Solúvel/metabolismo , Animais , Pressão Sanguínea/fisiologia , Ativadores de Enzimas/farmacologia , Feminino , Retardo do Crescimento Fetal/etiologia , Gravidez , Pirazóis/farmacologia , Pirimidinas/farmacologia , Ratos , Ratos Sprague-Dawley , Resistência Vascular/fisiologia
8.
Am Heart J ; 236: 69-79, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33640333

RESUMO

OBJECTIVE: While the surgical stages of single ventricle (SV) palliation serve to separate pulmonary venous and systemic venous return, and to volume-unload the SV, staged palliation also results in transition from parallel to series circulation, increasing total vascular resistance. How this transition affects pressure loading of the SV is as yet unreported. METHODS: We performed a retrospective chart review of Stage I, II, and III cardiac catheterization (CC) and echocardiographic data from 2001-2017 in all SV pts, with focus on systemic, pulmonary, and total vascular resistance (SVR, PVR, TVR respectively). Longitudinal analyses were performed with log-transformed variables. Effects of SVR-lowering medications were analyzed using Wilcoxon rank-sum testing. RESULTS: There were 372 total patients who underwent CC at a Stage I (median age of 4.4 months, n=310), Stage II (median age 2.7 years, n = 244), and Stage III (median age 7.3 years, n = 113). Total volume loading decreases with progression to Stage III (P< 0.001). While PVR gradually increases from Stage II to Stage III, and SVR increases from Stage I to Stage III, TVR dramatically increases with progress towards series circulation. TVR was not affected by use of systemic vasodilator therapy. TVR, PVR, SVR, and CI did not correlate with indices of SV function at Stage III. CONCLUSIONS: TVR steadily increases with an increasing contribution from SVR over progressive stages. TVR was not affected by systemic vasodilator agents. TVR did not correlate with echo-based indices of SV function. Further studies are needed to see if modulating TVR can improve exercise tolerance and outcomes.


Assuntos
Doenças Assintomáticas/terapia , Procedimentos Cirúrgicos Cardíacos , Coração Univentricular , Resistência Vascular/fisiologia , Circulação Sanguínea , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Procedimentos Cirúrgicos Cardíacos/métodos , Procedimentos Cirúrgicos Cardíacos/estatística & dados numéricos , Criança , Pré-Escolar , Progressão da Doença , Ecocardiografia/métodos , Feminino , Humanos , Lactente , Estudos Longitudinais , Masculino , Avaliação de Processos e Resultados em Cuidados de Saúde , Cuidados Paliativos/métodos , Estudos Retrospectivos , Tempo , Coração Univentricular/diagnóstico por imagem , Coração Univentricular/fisiopatologia , Coração Univentricular/cirurgia , Vasodilatadores/uso terapêutico , Função Ventricular
9.
Am J Physiol Regul Integr Comp Physiol ; 320(6): R851-R870, 2021 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-33596744

RESUMO

Although Guyton's graphical analysis of cardiac output-venous return has become a ubiquitous tool for explaining how circulatory equilibrium emerges from heart-vascular interactions, this classical model relies on a formula for venous return that contains unphysiological assumptions. Furthermore, Guyton's graphical analysis does not predict pulmonary venous pressure, which is a critical variable for evaluating heart failure patients' risk of pulmonary edema. Therefore, the purpose of the present work was to use a minimal closed-loop mathematical model to develop an alternative to Guyton's analysis. Limitations inherent in Guyton's model were addressed by 1) partitioning the cardiovascular system differently to isolate left ventricular function and lump all blood volumes together, 2) linearizing end-diastolic pressure-volume relationships to obtain algebraic solutions, and 3) treating arterial pressures as constants. This approach yielded three advances. First, variables related to morbidities associated with left ventricular failure were predicted. Second, an algebraic formula predicting left ventricular function was derived in terms of ventricular properties. Third, an algebraic formula predicting flow through the portion of the system isolated from the left ventricle was derived in terms of mechanical properties without neglecting redistribution of blood between systemic and pulmonary circulations. Although complexities were neglected, approximations necessary to obtain algebraic formulas resulted in minimal error, and predicted variables were consistent with reported values.


Assuntos
Débito Cardíaco/fisiologia , Insuficiência Cardíaca/fisiopatologia , Hemodinâmica/fisiologia , Função Ventricular Esquerda/fisiologia , Pressão Sanguínea/fisiologia , Volume Sanguíneo/fisiologia , Humanos , Modelos Cardiovasculares , Resistência Vascular/fisiologia , Pressão Venosa/fisiologia
10.
Transplant Proc ; 53(2): 565-568, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33549349

RESUMO

PURPOSE: Hemodynamic management in brain-dead donors (BDDs) is challenging due to hemodynamic instabilities. We compared functional parameters with traditional parameters for hemodynamic monitoring in BDDs. MATERIALS AND METHODS: Seventeen BDDs with a positive balance of >500 mL for 8 hours were included. Functional hemodynamic monitoring, including pulse pressure variation (PPV), stroke volume variation (SVV), cardiac output, and systemic vascular resistance index (SVRI) was performed in the setting of tidal volume of 6 mL/kg to 8 mL/kg and minimal positive end-expiratory pressure of 5 cm to 8 cm H2O. Responders were defined by a cardiac output increase of >15% after fluid therapy. RESULTS: Among the 17 BDDs (mean age, 46.80±13.91 years), 15 were male. Seven responders out of 17 (41.1%) had a significantly higher PPV (22.8±8.4 vs 13.4±5.9%, P = .038) and serum albumin level (3.2±0.6 vs 2.6±0.5 g/L, P = .040) at baseline than nonresponders. However, other hemodynamic markers such as SVV and SVRI were similar between groups. Traditional markers of volume status, such as heart rate, central venous pressure, hemoglobin, and serum uric acid level were also similar between the 2 groups. Hemodynamic markers including PPV, SVV, and SVRI were significantly reduced in responders. CONCLUSIONS: PPV was the most valuable hemodynamic marker for predicting volume responsiveness in BDDs.


Assuntos
Pressão Sanguínea/fisiologia , Morte Encefálica/diagnóstico , Hidratação/métodos , Adulto , Biomarcadores/análise , Morte Encefálica/fisiopatologia , Débito Cardíaco/fisiologia , Pressão Venosa Central , Feminino , Frequência Cardíaca/fisiologia , Hemodinâmica/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Respiração com Pressão Positiva , Valor Preditivo dos Testes , Reprodutibilidade dos Testes , Albumina Sérica/metabolismo , Volume Sistólico/fisiologia , Volume de Ventilação Pulmonar/fisiologia , Ácido Úrico/sangue , Resistência Vascular/fisiologia
12.
Am J Respir Cell Mol Biol ; 64(1): 100-114, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33052714

RESUMO

In pulmonary arterial hypertension (PAH), progressive structural remodeling accounts for the pulmonary vasculopathy including the obliteration of the lung vasculature that causes an increase in vascular resistance and mean blood pressure in the pulmonary arteries ultimately leading to right heart failure-mediated death. Deciphering the molecular details of aberrant signaling of pulmonary vascular cells in PAH is fundamental for the development of new therapeutic strategies. We aimed to identify kinases as new potential drug targets that are dysregulated in PAH by means of a peptide-based kinase activity assay. We performed a tyrosine kinase-dependent phosphorylation assay using 144 selected microarrayed substrate peptides. The differential signature of phosphopeptides was used to predict alterations in tyrosine kinase activities in human pulmonary arterial smooth muscle cells (HPASMCs) from patients with idiopathic PAH (IPAH) compared with healthy control cells. Thereby, we observed an overactivation and an increased expression of Jak2 (Janus kinase 2) in HPASMCs from patients with IPAH as compared with controls. In vitro, IL-6-induced proliferation and migration of HPASMCs from healthy individuals as well as from patients with IPAH were reduced in a dose-dependent manner by the U.S. Food and Drug Administration-approved Jak1 and Jak2 inhibitor ruxolitinib. In vivo, ruxolitinib therapy in two experimental models of pulmonary arterial hypertension dose-dependently attenuated the elevation in pulmonary arterial pressure, partially reduced right ventricular hypertrophy, and almost completely restored cardiac index without signs of adverse events on cardiac function. Therefore, we propose that ruxolitinib may present a novel therapeutic option for patients with PAH by reducing pulmonary vascular remodeling through effectively blocking Jak2-Stat3 (signal transducer of activators of transcription)-mediated signaling pathways.


Assuntos
Hipertensão Pulmonar/metabolismo , Janus Quinases/metabolismo , Fatores de Transcrição STAT/metabolismo , Transdução de Sinais/fisiologia , Animais , Células Cultivadas , Humanos , Hipertensão Pulmonar/tratamento farmacológico , Hipertrofia Ventricular Direita/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Músculo Liso Vascular/efeitos dos fármacos , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Artéria Pulmonar/efeitos dos fármacos , Artéria Pulmonar/metabolismo , Pirazóis/farmacologia , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos , Remodelação Vascular/efeitos dos fármacos , Remodelação Vascular/fisiologia , Resistência Vascular/efeitos dos fármacos , Resistência Vascular/fisiologia
13.
BJOG ; 128(2): 167-175, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-32314535

RESUMO

OBJECTIVE: To describe maternal haemodynamic differences in gestational hypertension with small-for-gestational-age babies (HDP + SGA), gestational hypertension with appropriate-for-gestational-age babies (HDP-only) and control pregnancies. DESIGN: Prospective cohort study. SETTING: Tertiary Hospital, UK. POPULATION: Women with gestational hypertension and healthy pregnant women. METHODS: Maternal haemodynamic indices were measured using a non-invasive Ultrasound Cardiac Output Monitor (USCOM-1A® ) and corrected for gestational age and maternal characteristics using device-specific reference ranges. MAIN OUTCOME MEASURES: Maternal cardiac output, stroke volume, systemic vascular resistance. RESULTS: We included 114 HDP + SGA, 202 HDP-only and 401 control pregnancies at 26-41 weeks of gestation. There was no significant difference in the mean arterial blood pressure (110 versus 107 mmHg, P = 0.445) between the two HDP groups at presentation. Pregnancies complicated by HDP + SGA had significantly lower median heart rate (76 versus 85 bpm versus 83 bpm), lower cardiac output (0.85 versus 0.98 versus 0.97 MoM) and higher systemic vascular resistance (1.4 versus 1.0 versus 1.2 MoM) compared with control and HDP-only pregnancies, respectively (all P < 0.05). CONCLUSION: Women with HDP + SGA present with more severe haemodynamic dysfunction than HDP-only. Even HDP-only pregnancies exhibit impaired haemodynamic indices compared with normal pregnancies, supporting a role of the maternal cardiovascular system in gestational hypertension irrespective of fetal size. Central haemodynamic changes may play a role in the pathogenesis of pre-eclampsia and should be considered alongside placental aetiology. TWEETABLE ABSTRACT: Hypertensive disorders of pregnancy are associated with worse maternal haemodynamic function when associated with small-for-gestational-age birth.


Assuntos
Débito Cardíaco/fisiologia , Frequência Cardíaca/fisiologia , Pré-Eclâmpsia/fisiopatologia , Resistência Vascular/fisiologia , Adulto , Estudos de Casos e Controles , Feminino , Humanos , Recém-Nascido , Recém-Nascido Pequeno para a Idade Gestacional , Gravidez , Estudos Prospectivos , Fatores de Risco , Reino Unido
14.
Scand J Med Sci Sports ; 31(4): 790-798, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33280195

RESUMO

Preload to the heart may be limited during rowing because both blood pressure and central venous pressure increase when force is applied to the oar. Considering that only the recovery phase of the rowing stroke allows for unhindered venous return, rowing may induce large fluctuations in stroke volume (SV). Thus, the purpose of this study was to evaluate SV continuously during the rowing stroke. Eight nationally competitive oarsmen (mean ± standard deviation: age 21 ± 2 years, height 190 ± 9 cm, and weight 90 ± 10 kg) rowed on an ergometer at a targeted heart rate of 130 and 160 beats per minute. SV was derived from arterial pressure waveform by pulse contour analysis, while ventilation and force on the handle were measured. Mean arterial pressure was elevated during the stroke at both work rates (to 133 ± 10 [P < .001] and 145 ± 11 mm Hg [P = .024], respectively). Also, SV fluctuated markedly during the stroke with deviations being largest at the higher work rate. Thus, SV decreased by 27 ± 10% (31 ± 11 mL) at the beginning of the stroke and increased by 25 ± 9% (28 ± 10 mL) in the recovery (P = .013), while breathing was entrained with one breath during the drive of the stroke and one prior to the next stroke. These observations indicate that during rowing cardiac output depends critically on SV surges during the recovery phase of the stroke.


Assuntos
Volume Sistólico/fisiologia , Esportes Aquáticos/fisiologia , Pressão Sanguínea/fisiologia , Voluntários Saudáveis , Humanos , Masculino , Resistência Vascular/fisiologia , Adulto Jovem
15.
Scand J Med Sci Sports ; 31(5): 956-966, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33382462

RESUMO

Blood pressure is a function of cardiac output and peripheral vascular resistance. During graded exercise testing (GXT), systolic blood pressure (SBP) is expected to increase gradually along with work rate, oxygen consumption, heart rate, and cardiac output. Individuals exposed to chronic endurance training attain a greater exercise SBP than in their untrained state and sedentary counterparts, but it is currently unknown what is considered a safe upper limit. This review discusses key studies examining blood pressure response in sedentary individuals and athletes. We highlight the physiological characteristics of highly fit individuals in terms of cardiovascular physiology and exercise blood pressure and review the state of the current literature regarding the safety of high SBP during exercise in this particular subgroup. Findings from this review indicate that a consensus on what is a normal SBP response to exercise in highly fit subjects and direct causation linking high GXT SBP to pathology is lacking. Consequently, applying GXT SBP guidelines developed for a "normal" population to endurance-trained individuals appears unsupported at this time. Lack of evidence for poor outcomes leads us to infer that elevated peak SBP in this subgroup could more likely reflect an adaptive response to training, rather than a pathological outcome. Future studies should track clinical outcomes of those achieving elevated SBP and develop athlete-specific guidelines.


Assuntos
Pressão Sanguínea/fisiologia , Treino Aeróbico , Adaptação Fisiológica , Débito Cardíaco/fisiologia , Teste de Esforço , Frequência Cardíaca/fisiologia , Humanos , Consumo de Oxigênio/fisiologia , Esforço Físico/fisiologia , Comportamento Sedentário , Esportes/fisiologia , Resistência Vascular/fisiologia
16.
J Am Coll Cardiol ; 76(23): 2755-2763, 2020 12 08.
Artigo em Inglês | MEDLINE | ID: mdl-33272370

RESUMO

BACKGROUND: Pulmonary vascular disease, pulmonary endothelial dysfunction, liver fibrosis, renal disease, and exercise intolerance are common in adults with Fontan physiology. Although the pathophysiologic mechanisms linking these phenomena have been studied, certain aspects are not well understood. OBJECTIVES: This study hypothesized that impaired pulmonary vascular reserve (VR) plays a central role linking these abnormalities, and that patients with abnormal pulmonary VR with exercise, compared with patients with normal VR, would display poorer pulmonary endothelial function, greater liver stiffness, more renal dysfunction, and poorer exercise capacity. METHODS: Symptomatic adults with the Fontan palliation (n = 29) underwent invasive cardiopulmonary exercise testing, echocardiography, and assessment of microvascular function. Abnormal pulmonary VR was defined by the slope of increase in pulmonary pressure relative to cardiac output with exercise >3 mm Hg/l/min. Pulmonary endothelial function was assessed using reactive hyperemia index. End-organ function was assessed using magnetic resonance elastography-derived liver stiffness, glomerular filtration rate, N-terminal pro-B-type natriuretic peptide, and peak oxygen consumption (Vo2). RESULTS: Compared with individuals with normal VR (n = 8), those with abnormal VR (n = 21) displayed higher central and pulmonary venous pressures, and more severely impaired cardiac output and stroke volume responses to exertion, but similar pulmonary vascular resistance at rest. Patients with abnormal VR displayed more severely impaired reactive hyperemia index, increased liver stiffness, lower glomerular filtration rate, higher N-terminal pro-B-type natriuretic peptide, and lower peak Vo2. As compared to pulmonary vascular resistance at rest, slope of increase in pulmonary pressure relative to cardiac output displayed stronger correlations with reactive hyperemia index (r = -0.63 vs. r = -0.31; Meng test p = 0.009), magnetic resonance elastography-derived liver stiffness (r = 0.47 vs. r = 0.29; Meng test p = 0.07), glomerular filtration rate (r = -0.52 vs. r = -0.24; Meng test p = 0.03), N-terminal pro-B-type natriuretic peptide (r = 0.56 vs. r = 0.17; Meng test p = 0.02), and peak Vo2 (r = -0.63 vs. r = -0.26; Meng test p = 0.02). CONCLUSIONS: Pulmonary vascular limitations in Fontan physiology are related to pulmonary endothelial and end-organ dysfunction, suggesting a mechanistic link between these commonly observed findings, and these abnormalities are more apparent during exercise testing, with little relationship at rest.


Assuntos
Débito Cardíaco/fisiologia , Técnica de Fontan , Cardiopatias Congênitas/fisiopatologia , Doenças Vasculares Periféricas/diagnóstico , Circulação Pulmonar/fisiologia , Resistência Vascular/fisiologia , Adulto , Endotélio Vascular/fisiopatologia , Exercício Físico/fisiologia , Teste de Esforço , Feminino , Cardiopatias Congênitas/complicações , Cardiopatias Congênitas/cirurgia , Humanos , Masculino , Doenças Vasculares Periféricas/etiologia , Doenças Vasculares Periféricas/fisiopatologia , Estudos Prospectivos , Descanso/fisiologia , Adulto Jovem
18.
BMC Pregnancy Childbirth ; 20(1): 680, 2020 Nov 11.
Artigo em Inglês | MEDLINE | ID: mdl-33176723

RESUMO

BACKGROUND: Downstream remodeling of the spiral arteries (SpA) decreases utero-placental resistance drastically, allowing sustained and increased blood flow to the placenta under all circumstances. We systematically evaluated available reports to visualize adaptation of spiral arteries throughout pregnancy by ultra-sonographic measurements and evaluated when this process is completed. METHODS: A systematic review and meta-analysis of spiral artery flow (pulsatility index (PI), resistance index (RI) and peak systolic velocity (PSV)) was performed. English written articles were obtained from Pubmed, EMBASE and Cochrane Library and included articles were assessed on quality and risk of bias. Weighted means of Doppler indices were calculated using a random-effects model. RESULTS: In healthy pregnancies, PI and RI decreased from 0.80 (95% CI: 0.70-0.89) and 0.50 (95% CI: 0.47-0.54) in the first trimester to 0.50 (95% CI: 0.45-0.55, p < 0.001) and 0.39 (95% CI: 0.37-0.42, p < 0.001) in the second trimester and to 0.49 (95% CI: 0.44-0.53, p = 0.752) and 0.36 (95% CI: 0.35-0.38, p = 0.037) in the third trimester, respectively. In parallel, PSV altered from 0.22 m/s (95% CI: 0.13-0.30 m/s) to 0.28 m/s (95% CI: 0.17-0.40 m/s, p = 0.377) and to 0.25 m/s (95% CI: 0.20-0.30 m/s, p = 0.560) in the three trimesters. In absence of second and third trimester Doppler data in complicated gestation, only a difference in PI was observed between complicated and healthy pregnancies during the first trimester (1.49 vs 0.80, p < 0.001). Although individual studies have identified differences in PI between SpA located in the central part of the placental bed versus those located at its periphery, this meta-analysis could not confirm this (p = 0.349). CONCLUSIONS: This review and meta-analysis concludes that an observed decrease of SpA PI and RI from the first towards the second trimester parallels the physiological trophoblast invasion converting SpA during early gestation, a process completed in the midst of the second trimester. Higher PI was found in SpA of complicated pregnancies compared to healthy pregnancies, possibly reflecting suboptimal utero-placental circulation. Longitudinal studies examining comprehensively the predictive value of spiral artery Doppler for complicated pregnancies are yet to be carried out.


Assuntos
Placenta/irrigação sanguínea , Circulação Placentária/fisiologia , Ultrassonografia Doppler , Útero/irrigação sanguínea , Artérias/diagnóstico por imagem , Velocidade do Fluxo Sanguíneo , Feminino , Hemodinâmica , Humanos , Gravidez , Primeiro Trimestre da Gravidez , Segundo Trimestre da Gravidez , Resistência Vascular/fisiologia
19.
BMC Pregnancy Childbirth ; 20(1): 706, 2020 Nov 19.
Artigo em Inglês | MEDLINE | ID: mdl-33213415

RESUMO

The reactivity of the pulmonary vascular bed to the administration of oxygen is well established in the post-natal circulation. The vasoreactivity demonstrated by the fetal pulmonary artery Doppler waveform in response to maternal hyperoxia has been investigated. We sought to investigate the relationship between the reactivity of the fetal pulmonary arteries to hyperoxia and subsequent neonatal cardiac function in the early newborn period. METHODS: This explorative study with convenience sampling measured pulsatility index (PI), resistance index (RI), acceleration time (AT), and ejection time (ET) from the fetal distal branch pulmonary artery (PA) at baseline and following maternal hyperoxygenation (MH). Oxygen was administered for 10 min at a rate of 12 L/min via a partial non-rebreather mask. A neonatal functional echocardiogram was performed within the first 24 h of life to assess ejection fraction (EF), left ventricular output (LVO), and neonatal pulmonary artery AT (nPAAT). This study was conducted in the Rotunda Hospital, Dublin, Ireland. RESULTS: Forty-six women with a singleton pregnancy greater than or equal to 31 weeks' gestational age were prospectively recruited to the study. The median gestational age was 35 weeks. There was a decrease in fetal PAPI and PARI following MH and an increase in fetal PAAT, leading to an increase in PA AT:ET. Fetuses that responded to hyperoxygenation were more likely to have a higher LVO (135 ± 25 mL/kg/min vs 111 ± 21 mL/kg/min, p < 0.01) and EF (54 ± 9% vs 47 ± 7%,p = 0.03) in the early newborn period than those that did not respond to MH prenatally. These findings were not dependent on left ventricular size or mitral valve (MV) annular diameter but were related to an increased MV inflow. There was no difference in nPAAT. CONCLUSION: These findings indicate a reduction in fetal pulmonary vascular resistance (PVR) and an increase in pulmonary blood flow and left atrial return following MH. The fetal response to hyperoxia reflected an optimal adaptation to postnatal life with rapid reduction in PVR increasing measured cardiac output.


Assuntos
Hiperóxia/fisiopatologia , Recém-Nascido/fisiologia , Artéria Pulmonar/fisiologia , Volume Sistólico/fisiologia , Resistência Vascular/fisiologia , Administração por Inalação , Adulto , Ecocardiografia Doppler em Cores , Feminino , Feto/irrigação sanguínea , Feto/fisiologia , Coração/diagnóstico por imagem , Coração/fisiologia , Humanos , Hiperóxia/etiologia , Troca Materno-Fetal/fisiologia , Oxigênio/administração & dosagem , Projetos Piloto , Gravidez , Terceiro Trimestre da Gravidez , Estudos Prospectivos , Artéria Pulmonar/diagnóstico por imagem , Circulação Pulmonar/fisiologia , Ultrassonografia Doppler de Pulso , Ultrassonografia Pré-Natal
20.
PLoS One ; 15(11): e0242026, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33201925

RESUMO

Angiopoietin (Angpt)-2, a permeability-increasing growth factor, is involved in vascular leakage of sepsis and acute lung injury, and could be released from endothelium in response to anaphylaxis-related secretagogues such as histamine and leukotrienes, or cytokines. However, roles of Angpt-2 in the hyperpermeability during systemic anaphylaxis are not known. Thus, we determined plasma levels of Angpt-2 and cytokines and vascular permeability during anaphylactic hypotension in unanesthetized rats. Anaphylaxis was induced by an intravenous injection of ovalbumin antigen. Mean arterial blood pressure (MBP) was measured, and hematocrit (Hct) and plasma levels of Angpt-2 and cytokines were assessed for 24 h after antigen injection. Separately, vascular permeability was measured in various organs using the Evans blue dye method, and Angpt-2 mRNA expression in liver was measured. After antigen injection, MBP decreased to the nadir at 6 min, and returned to baseline at 45 min, and Hct peaked at 20 min and thereafter progressively declined, suggesting that vascular leak and hypotension occurred within 20 min. Plasma Angpt-2 levels began to increase significantly at 1 h after antigen, reaching the peak 2.7-fold baseline at 6 h with a return to baseline at 24 h. Detected cytokines of IL-1α, IL-1ß, IL-6, IL-10, and TNF-α peaked 1 or 2 h after antigen. Angpt-2 mRNA increased at 2 h and showed an increasing tendency at 6 h. Vascular permeability in bronchus, trachea, intestines, mesentery and skeletal muscle was increased at 10 min but not at 6 h after antigen. In addition, we confirmed using anesthetized rat anaphylaxis models that plasma Angpt-2 levels increased at 1 h after antigen. In conclusion, plasma Angpt-2 is elevated presumably due to increased cytokines and enhanced gene transcription during anaphylaxis in anesthetized and unanesthetized rats.


Assuntos
Anafilaxia/metabolismo , Angiopoietina-2/metabolismo , Hipotensão/metabolismo , Anestesia/métodos , Animais , Permeabilidade Capilar/fisiologia , Citocinas/metabolismo , Masculino , Pressão na Veia Porta/fisiologia , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Transcrição Genética/fisiologia , Resistência Vascular/fisiologia
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