Reduced Morbidity and Mortality Associated With Minimally Invasive Single-vessel Coronary Artery Bypass Compared With Conventional Sternotomy.

OBJECTIVE: We aimed to describe the safety and clinical benefits of minimally invasive, nonsternotomy coronary artery bypass grafting (MICABG) using data from The Society of Thoracic Surgeons (STS) National Database. BACKGROUND: MICABG has gained popularity, owing to expected lower perioperative morbidity and shorter recovery. Despite this, concerns remain regarding anastomotic quality and the validity of proposed perioperative benefits. METHODS: We queried the STS National Database for all patients who underwent single-vessel coronary artery bypass grafting (CABG) from January 2014 to December 2016 to compare outcomes of MICABG with conventional CABG. Patients who underwent concomitant or emergent procedures were excluded. Propensity-weighted cohorts were compared by operative approach with adjustment for variability across institutions. RESULTS: Of 12,406 eligible patients, 2688 (21.7%) underwent MICABG, and 9818 (78.3%) underwent conventional CABG. Propensity weighting produced excellent balance in patient characteristics, including completeness of revascularization, body mass index, and STS predictive risk scores. MICABG was associated with significant reduction of in-hospital mortality [odds ratio (OR)=0.32, absolute reduction (AR)=0.91%, P <0.0001]; 30-day mortality (OR=0.51, AR=0.88%, P =0.001), duration of ventilation (8.62 vs 12.6 hours, P <0.0001), prolonged hospitalization (OR=0.77, AR=1.6, P =0.043), deep wound infection (OR=0.33, AR=0.68, P <0.004), postoperative transfusions (OR=0.52, AR=7.7%, P <0.0001), and STS composite morbidity (OR=0.72, AR=1.19%, P =0.008). Subgroup analysis of only off-pump left internal mammary artery-left anterior descending CABG showed similar findings. Major adverse cardiac events and graft occlusion did not differ between groups. CONCLUSIONS: MICABG is associated with lower mortality and perioperative morbidity compared with conventional sternotomy CABG. MICABG may have a role in treating single-vessel disease.

Venovenous Extracorporeal Membrane Oxygenation to Facilitate Removal of Endobronchial Tumors.

Short-term extracorporeal membrane oxygenation is a useful adjunct to thoracic procedures. We report the cases of 2 middle-aged men who were supported with venovenous extracorporeal membrane oxygenation to facilitate tumor debulking and recanalization of the carina and mainstem bronchi. Neither patient had major complications or adverse events. These cases suggest that short-term extracorporeal membrane oxygenation is safe in patients undergoing complex resection or debulking of endobronchial lesions.

Role of Echocardiography in Transcatheter Mitral Valve Replacement in Native Mitral Valves and Mitral Rings.

Adaptation and evolution of transcatheter aortic valve replacement (TAVR) technologies has led to approval of TAVR for consideration in patients at intermediate risk for surgical aortic valve intervention. As TAVR becomes more mainstream, attention is shifting toward percutaneous mitral valve (MV) repair and transcatheter MV replacement (TMVR) techniques. Transcatheter heart valves (both purpose-built and off-label-use TAVR valves) are being implanted during TMVR procedures to treat clinically significant MV disease (native disease, degenerated bioprosthetic valves, and dysfunctional surgical MV annuloplasty repairs) when the risk of open heart MV surgery is prohibitive. The success of these high-risk procedures is directly related to accurate periprocedural imaging with echocardiography and other modalities. Although a multidisciplinary heart valve team approach is necessary for optimal patient selection, a multimodality team-based imaging approach and comprehensive understanding of the MV are required for safe procedural planning. Collaboration between noninvasive cardiac imagers and the intraprocedural interventional imaging team and translation of the periprocedural imaging to the implanting team are crucial to the success of TMVR technology. Currently, the TMVR procedures discussed here are conducted either as part of clinical research or off label. The US Food and Drug Administration-approved mitral valve-in-valve procedures for the treatment of degenerated mitral bioprosthetic valves are not discussed here.

Isolated mitral valve surgery risk in 77,836 patients from the Society of Thoracic Surgeons database.

BACKGROUND: Understanding the operative outcomes of mitral valve (MV) surgery across the spectrum of predicted risk of mortality (PROM) is necessary to determine the best use of novel percutaneous approaches. METHODS: The Society of Thoracic Surgeons Adult Cardiac Surgery Database was utilized to study isolated MV operations during two time periods: era 1 (2002 to 2006, n = 37,743) and era 2 (2007 to 2010, n = 40,093). In each era, four PROM groups were defined: low risk (PROM 0% to <4%); intermediate risk (PROM 4% to <8%); high risk (PROM 8% to <12%); and extreme risk (PROM ≥ 12%). In each risk group, mortality rates and observed to expected mortality ratios were compared across eras. RESULTS: A total of 63,645 cases (82%) were classified as low risk, 8,032 (10%) as intermediate risk, 2,765 (4%) as high risk, and 3,394 (4%) as extreme risk. Sixty-seven percent of MV repairs (n = 30,488) and 18% of MV replacements (n = 5,749) had a PROM less than 1%. PROM less than 4% was seen for 93% of MV repairs (n = 42,196) and 66% of replacements (n = 21,449). Across the two eras, the MV repair rate increased from 54.8% to 61.8% (p = 0.0017); and a significant reduction in operative mortality was observed in high risk and extreme risk cohorts (p < 0.05). CONCLUSIONS: The frequency with which MV repair for isolated MV disease is performed has increased over time and is associated with very low early mortality. A significant reduction in mortality among patients at highest risk has occurred, and must be considered as patients are evaluated for percutaneous therapies.

Simple technique to verify CO(2) diffusion with the CarbonAid™ device.

It has become common practice in cardiac surgery to flood the operative field with CO(2) to facilitate deairing of the heart. However, CO(2) delivery is variable and verification of CO(2) delivery can be challenging. We report a simple, reliable method to confirm CO(2) delivery. This technique ensures that the benefits of CO(2) delivery are provided to the patient during the operation.

Left atrial appendage occlusion: lessons learned from surgical and transcatheter experiences.

Since the 1950s, the pathophysiologic role of the left atrial appendage (LAA) has been known in thromboembolic disease. A variety of surgical techniques have been described to close the LAA, with various degrees of efficacy. Today, transcatheter devices for LAA occlusion may offer a less invasive solution. This review looks at the surgical experience with LAA occlusion, with a focus on the techniques of closure, the prospects for stroke reduction, and the percutaneous trials completed so far, to formulate some meaningful conclusions about the status of LAA closure today.

Effect of the effluent released from the canine internal mammary artery after intraluminal and extraluminal perfusion of acetylcholine and adenosine diphosphate.

Segments of the canine internal mammary artery (35 mm in length) were suspended in vitro in an organ chamber containing physiological salt solution (95% O2/5% CO2, pH = 7.4, 37 degrees C). Segments were individually cannulated and perfused at 5 ml/minute using a roller pump. Vasorelaxant activity of the effluent from the perfused internal mammary arteries was bioassayed by measuring the decrease in tension induced by the effluent of the coronary artery endothelium-free ring which had been contracted with prostaglandin F2alpha (2 x 10(-6) M). Intraluminal perfusion of adenosine diphosphate (10(-5) M) induced significant increase in relaxant activity in the effluent from the perfused blood vessel. However, when adenosine diphosphate (10(-5) M) was added extraluminally to the internal mammary artery, no change in relaxant activity in the effluent was noted. In contrast, acetylcholine produced significant increase in the relaxant activity on the effluent of the perfused internal mammary artery with both intraluminal and extraluminal perfusion. The intraluminal and extraluminal release of endothelium-derived relaxing factor (EDRF) by acetylcholine (10(-5) M) can be inhibited by site-specific administration of atropine (10(-5) M). These experiments indicate that certain agonists can induce the release of EDRF only by binding to intravascular receptors while other agonists can induce endothelium-dependent vasodilatation by acting on neural side receptors.

High-frequency ultrasonic waves cause endothelial dysfunction on canine epicardial coronary arteries.

OBJECTIVE: Application of ultrasound energy by an endarterectomy probe can facilitate the removal of atheromatous plaque, but the effect of this procedure on surrounding vessel structure and function is still a matter of experimental investigations. METHODS: To determine whether ultrasound energy impairs the production of nitric oxide or damages vascular smooth muscle function, isolated canine epicardial coronary artery segments were exposed to either high (25 W) or low (0-10 W) ultrasonic energy outputs, for 15 seconds, using an endarterectomy device prototype. After exposure, segments of epicardial coronary artery were studied in organ chambers. The following drugs were used: adenosine diphosphate (ADP), acetylcholine (Ach) and sodium fluoride (NaF) to study endothelium-dependent relaxation and sodium nitroprusside (SNP) and isoproterenol to evaluate endothelium-independent relaxation. RESULTS: Application of high ultrasonic energy power impaired endothelium-dependent relaxation to ADP (10(-9)-10(-4) M), Ach (10(-9)-10(-4) M) and NaF (0.5-9.5 mM) in epicardial coronary arteries. However, low ultrasound energy output at the tip of the probe did not alter the endothelium-dependent relaxation (either maximal relaxation or EC50) to the same agonists. Vascular smooth muscle relaxation to isoproterenol (10(-9)-10(-5) M) or SNP (10(-9)-10(-6) M) was unaltered following exposure to either low or high ultrasonic energy outputs. CONCLUSION: These experiments currently prove that ultrasonic energy changes endothelial function of epicardial coronary arteries at high power. However, ultrasound does not alter the ability of vascular smooth muscle of canine epicardial coronary arteries to relax.

Ondas ultra-sônicas de alta freqüência causam disfunção endotelial em artérias coronárias caninas epicárdicas / High-frequency ultrasonic waves cause endothelial dysfunction on canine epicardial coronary arteries

OBJETIVO: Aplicação de energia por ultra-som pode facilitar a remoção da placa ateromatosa, mas o efeito desse procedimento em vasos próximos ainda é matéria de estudos experimentais. MÉTODOS: Para determinar se a energia ultra-sônica compromete a produção de óxido nítrico, segmentos de artérias coronárias caninas foram expostos a baixos (0-10 W) e altos (25 W) níveis de energia por 15 segundos, utilizando-se protótipo de aparelho para a realização de endarterectomia. Após exposição, segmentos das artérias coronarianas foram estudados em organ chambers. Para os ensaios farmacológicos foram utilizadas as seguintes drogas:difosfato de adenosina (ADP), acetilcolina (Ach) e fluoreto de sódio (NaF) para a avaliação do relaxamento dependente do endotélio. O nitroprussiato de sódio (NPS) e o isoproterenol foram utilizados para a avaliação do relaxamento independente do endotélio. RESULTADOS: A aplicação de alta energia ultra-sônica comprometeu o relaxamento dependente do endotélio induzido por ADP (10-9 - 10-4 M), Ach (10-9 - 10-4 M) e NaF (0,5 -9,5 mM) em artérias coronarianas epicárdicas. Entretanto, baixos valores de energia ultra-sônica não alteraram o relaxamento dependente do endotélio (nem o relaxamento máximo e nem a EC50) induzido pelos mesmos agonistas. O relaxamento da musculatura lisa vascular induzido por isoproterenol (10-9 - 10-5 M) ou NPS (10-9 - 10-6 M) não foi comprometido, tanto por baixos, quanto por altos níveis de energia ultra-sônica. CONCLUSÃO: Os experimentos demonstram que altas energias ultra-sônicas alteram a função endotelial. Entretanto, o ultra-som não altera a habilidade de relaxamento da musculatura lisa vascular de artérias caninas epicárdicas.

OBJECTIVE: Application of ultrasound energy by an endarterectomy probe can facilitate the removal of atheromatous plaque, but the effect of this procedure on surrounding vessel structure and function is still a matter of experimental investigations. METHODS: To determine whether ultrasound energy impairs the production of nitric oxide or damages vascular smooth muscle function, isolated canine epicardial coronary artery segments were exposed to either high (25 W) or low (0-10 W) ultrasonic energy outputs, for 15 seconds, using an endarterectomy device prototype. After exposure, segments of epicardial coronary artery were studied in organ chambers. The following drugs were used: adenosine diphosphate (ADP), acetylcholine (Ach) and sodium fluoride (NaF) to study endothelium-dependent relaxation and sodium nitroprusside (SNP) and isoproterenol to evaluate endothelium-independent relaxation. RESULTS: Application of high ultrasonic energy power impaired endothelium-dependent relaxation to ADP (10-9 - 10-4 M), Ach (10-9 - 10-4 M) and NaF (0.5 - 9.5 mM) in epicardial coronary arteries. However, low ultrasound energy output at the tip of the probe did not alter the endothelium-dependent relaxation (either maximal relaxation or EC50) to the same agonists. Vascular smooth muscle relaxation to isoproterenol (10-9 - 10-5 M) or SNP (10-9 - 10-6 M) was unaltered following exposure to either low or high ultrasonic energy outputs. CONCLUSION: These experiments currently prove that ultrasonic energy changes endothelial function of epicardial coronary arteries at high power. However, ultrasound does not alter the ability of vascular smooth muscle of canine epicardial coronary arteries to relax.

Endothelium-dependent vasodilation during acute rejection in dogs.

BACKGROUND: Acute rejection, which is a major cause of death after cardiac transplantation, is associated with increased coronary artery resistance and decreased coronary blood flow, leading to congestive heart failure. MATERIALS AND METHODS: To examine the contribution of endothelium-derived vasoactive factors on coronary artery tone during acute rejection, dogs underwent orthotopic heart transplantation without immunosuppression. Plasma levels of endothelin, a potent endogenous vasoconstrictor peptide, and atrial natriuretic peptide, an endogenous coronary vasodilator of cardiac origin, were measured daily by radioimmunoassay until sacrifice. RESULTS: Over 7 days, all animals developed acute rejection accompanied by progressive increases in plasma endothelin (10 +/- 3 to 25 +/- 4 pg/ml, n = 6, P < 0.05) and atrial natriuretic peptide (57 +/- 10 to 188 +/- 42 pg/ml, n = 6, P < 0.05). However, in organ chamber experiments, coronary artery segments from rejecting hearts exhibited normal endothelium-dependent vasodilation to acetylcholine, adenosine diphosphate, and the calcium ionophore A23187. In addition, coronary arteries exhibited normal relaxation to sodium nitroprusside (cyclic guanosine monophosphate-dependent) and isoproterenol (cyclic adenosine monophosphate-dependent). CONCLUSIONS: In early, untreated acute rejection after orthotopic heart transplantation, graft dysfunction is not associated with impaired endothelium-dependent coronary artery vasodilation but may result from enhanced production of endothelin, a potent vasoconstrictor.

Endothelium-dependent relaxation in response to poly-L-arginine in canine coronary arteries: implications about hyperpolarization as a mechanism of vasodilatation.

OBJECTIVE: To study the mechanism by which poly-L-arginine mediates endothelium-dependent relaxation. METHODS: Vascular segments with and without endothelium were suspended in organ chambers filled with control solution maintained at 37 C and bubbled with 95% O2 / 5% CO2. Used drugs: indomethacin, acetycholine, EGTA, glybenclamide, ouabain, poly-L-arginine, methylene blue, N G-nitro-L-arginine, and verapamil and N G-monomethyl-L-arginine. Prostaglandin F2 and potassium chloride were used to contract the vascular rings. RESULTS: Poly-L-arginine (10-11 to 10-7 M) induced concentration-dependent relaxation in coronary artery segments with endothelium. The relaxation to poly-L-arginine was attenuated by ouabain, but was unaffected by glybenclamide. L-NOARG and oxyhemoglobin caused attenuation, but did not abolish this relaxation. Also, the relaxations was unaffected by methylene blue, verapamil, or the presence of a calcium-free bathing medium. The endothelium-dependent to poly-L-arginine relaxation was abolished only in vessels contracted with potassium chloride (40 mM) in the presence of L-NOARG and indomethacin. CONCLUSION: These experiments indicate that poly-L-arginine induces relaxation independent of nitric oxide.

Endothelium-dependent relaxation to poly-L-arginine in canine coronary arteries.

The endothelium-dependent relaxation elicited by poly-L-arginine was investigated in canine coronary arteries. Poly-L-arginine (10(-11) to 10(-7) M) induced concentration-dependent endothelium-dependent relaxation in segments of canine coronary arteries incubated with indomethacin. In the presence of indomethacin, arteries contracted with prostaglandin F2alpha and exposed also to ouabain, oxyhemoglobin, or N(omega)-nitro-L-arginine, as well as those contracted with 20 mM of KCl, presented reduced endothelium-dependent relaxation to poly-L-arginine. The combination of N(omega)-nitro-L-arginine with indomethacin produced further reduction of endothelium-dependent relaxation in arteries contracted with prostaglandin F2alpha as well as in arteries contracted with 20 mM of KCl. However, only quinacrine or calmidazolium, both in presence of N(omega)-nitro-L-arginine plus indomethacin, abolished the endothelium-dependent relaxation elicited by poly-L-arginine. The relaxation to poly-L-arginine was not significantly affected by glybenclamide. The present study demonstrates that in addition to the prostacyclin and nitric oxide-dependent mechanisms, poly-L-arginine also elicits endothelium-dependent relaxation in canine coronary arteries, stimulating the release of endothelial relaxing factor(s) produced by the phospholipase A2 pathway, but independent of the cyclooxygenase pathway, which may cause hyperpolarization of the vascular smooth muscle.

Relaxamento dependente do endotélio causado pela Poli-L-Arginia. Implicações sobre a hiperpolarizaçäo como mecanismo de vasodilataçäo / Endothelium-dependent relaxation in response to poly-L-arginine in canine coronary arteries: implications about hyperpolarization as a mechanism of vasodilatation

OBJECTIVE: To study the mechanism by which poly-L-arginine mediates endothelium-dependent relaxation. METHODS: Vascular segments with and without endothelium were suspended in organ chambers filled with control solution maintained at 37ºC and bubbled with 95 percent O2 / 5 percent CO2. Used drugs: indomethacin, acetycholine, EGTA, glybenclamide, ouabain, poly-L-arginine, methylene blue, N G-nitro-L-arginine, and verapamil and N G-monomethyl-L-arginine. Prostaglandin F2á and potassium chloride were used to contract the vascular rings. RESULTS: Poly-L-arginine (10-11 to 10-7 M) induced concentration-dependent relaxation in coronary artery segments with endothelium. The relaxation to poly-L-arginine was attenuated by ouabain, but was unaffected by glybenclamide. L-NOARG and oxyhemoglobin caused attenuation, but did not abolish this relaxation. Also, the relaxations was unaffected by methylene blue, verapamil, or the presence of a calcium-free bathing medium. The endothelium-dependent to poly-L-arginine relaxation was abolished only in vessels contracted with potassium chloride (40 mM) in the presence of L-NOARG and indomethacin. CONCLUSION: These experiments indicate that poly-L-arginine induces relaxation independent of nitric oxide

Efeito da vasopressina em artérias coronárias epicárdicas caninas. Experimentos sobre a produção de óxido nítrico mediante a estimulação de receptores V1 / Effect of arginine vasopressin on the canine epicardial coronary artery. Experiments on V1-receptor-mediated production of nitric oxide

OBJECTIVE: To determine whether arginine vasopressin releases endothelium-derived nitric oxide (EDNO) from the epicardial coronary artery. METHODS: We studied segments of canine left circumflex coronary arteries suspended in organ chambers to measure isometric force. The coronary artery segments were contracted with prostaglandin F2alpha (2 x 10-6M) and exposed to a unique, strong arginine vasopressin concentration (10-6M) or titrated concentrations (10-9 a 10-5 M). RESULTS: The unique dose of arginine vasopressin concentration (10-6M) induced transient, but significant (p<0.05), relaxation in arterial segments with endothelium, and an increase, not significant, in tension in arteries without endothelium. Endothelium-dependent relaxation to arginine vasopressin was inhibited by Ng-monomethyl-L-arginine (L-NMMA, 10-5M) or N G-nitro-L-arginine (L-NOARG) (10-4M), 2 inhibitors of nitric oxide synthesis from L-arginine. Exogenous L-arginine (10-4M), but not D-arginine (10-4M), reversed the inhibitory effect of L-NMMA on vasopressin-mediated vasorelaxation. Endothelium dependent relaxation to vasopressin was also reversibly inhibited by the vasopressin V1-receptor blocker d(CH2)5Try(Me) arginine vasopressin (10-6M) (n=6, P<0.05). CONCLUSION: Vasopressin acts through V1 endothelial receptors to stimulate nitric oxide release from L-arginine

Reatividade vascular da artéria mamária interna: estudos farmacológicos comparativos entre artérias caninas direita e esquerda / Vascular reactivity of the internal mammary artery: comparative pharmacological studies between canine right and left arteries

Para estudos comparativos da reatividade vascular entre artéria mamária interna (AMI) canina direita e esquerda, realizaram-se experimentos "in vitro" utilizando-se banhos orgânicos ("organ chambers") e ensaios biológicos: 1) os produtos plaquetários ADP e 5-HT induziram, respectivamente, vasodilatação dependente e independente do endotélio; 2) os autacóides, bradicinina e histamina, também induziram vasodilatação, respectivamente, dependente e independente do endotélio; 3) o A23187, vasodilatador independente de receptor, induziu relaxamentos dependentes do endotélio; 4) dopamina, dobutamina, papaverina e a poli-L-arginina induziram vasodilatações independentes do endotélio; 5) a NOR induziu intensa vasoconstrição comparável à causada pelo KCI e pela endotelina; 6) em 83 porcento de 24 ensaios, a liberação basal de NO foi maior na AMI esquerda, em comparação com a AMI direita; 7) ensaios biológicos de AMIs demonstraram a importância da PGI2 nas condições de hipóxia, uma vez que a indometacina aboliu vasodilatação adicional em resposta à hipóxia em condições de vasodilatação induzida pela liberação basal de NO; 8) não ocorreram diferenças significantes de resposta, comparando-se estudos realizados em AMIs direita e esquerda

Efeito protetor da criocardioplegia cristalóide na isquemia global e reperfusäo durante circulaçäo extracorpórea: um mecanismo dependente do endotélio? / Protective effect of crystalloid cryocardioplegia in the global ischemia and reperfusion during extracorporeal circulation: an endothelium-dependent mechanism?

Estudos prévios demonstraram que o comprometimento da produçäo de EDRF/NO mediada por receptores, após isquemia global e reperfusäo, possa ser devido a uma disfunçäo de G-proteínas que liga os receptores da célula endotelial à via da síntese de EDRF/NO. O presente trabalho experimental sugere que a criocardioplegia cristalóide, associada a hipotermia tópica, previne ou pode reverter, em parte, a disfunçäo endotelial nas mesmas condiçöes. Mais estudos seräo necessários para conclusöes mais definitivas, pois as análises estatísticas mais acuradas sugeriram aumento da amostragem. Este detalhe talvez seja devido às grandes dificuldades de uniformizaçäo relacionada a este tipo de experimentos. Além disso, demonstrou-se pela primeira vez que a hipotermia, por si só, pode estimular a liberaçäo de EDRF/NO pelo endotélio vascular. Isto sugere que o endotélio possa ser um importante sensor de mudanças da temperatura sangüínea e tem importantes implicaçöes para o entendimento da fisiologia da CEC e dos mecanismos locais de auto-regulaçäo.

Cardioplegia cristalóide, barotrauma e funçäo endotelial: consideraçöes experimentais / Crystalloid cardioplegia, barotrauma and endothelium function: experimental considerations

O presente ensaio experimental estudou o efeito da infusao de soluçao cardioplégica cristalóide a altas pressoes sobre a funçao endotelial de artérias epicárdicas de caes. Nao se encontraram alteraçoes a nível de receptores (curvas dose-respostas à ACH e ADP; da transduçao do sinal iniciado nos receptores/sitema de G-proteínas (fluoreto de sódio) e nos processos intracelulares da produçao de EDRF/NO (fosfolipase C e ionóforo do cálcio A23187). A funçao da musculatura lisa vascular nao foi afetada quando se analisaram as respostas relaxantes (nitroprussiato de sódio e isoproterenol) e contráteis (KCI e prostaglandina 2alfa). Estes achados permitem as seguintes consideraçoes especulativas: a) O barotrauma produzido pela infusao da cardioplegia cristalóide a altas pressoes ocorreria apenas em circulaçoes coronarianas previamente doentes? b) Uma vez que as infusoes duraram de 2 a 3 minutos, seria o barotrauma coronariano um fenômeno dependente do tempo de infusao? c) Para que ocorra o barotrauma seriam necessários níveis mais elevados de Potássio? d) Questionara existência do fenômeno do barotrauma coronariano produzido pela infusao de soluçoes cadioplégicas pelo menos nas condiçoes experimentais utilizadas. e) A metodologia empregada estuda apenas as reatividades vasculares de artérias coronarias epicárdicas. estas artérias seriam menos sensíveis aos efeitos da pressao de infusao da cardioplegia do que a microcirculaçao coronariana? f) Seria a circulaçao coronária do cao menos sensível a altas pressoes do que do homem? Estas observaçoes experimentais sugerem que a infusao de cardioplegia cristalóide, moderadamente hipocalêmica, a altas pressoes em um tempo de 2 a 3 minutos, nao interfere com a produçao de EDRF/NO pelo endotélio de coronárias epicárdicas do cao.

Oxido nítrico e substância vasoativas derivadas do endotélio: papel no controle do tônus vascular / Nitric oxide and endothelium-derived vasoactive factors: role inthe vascular tone control

O endotélio de artérias e veias vem sendo estudado, há muito tempo, por médicos e pesquisadores que lidam com doenças cardiovasculares ou complicaçöes cardiovasculares da idade avançada.Entretanto, a visäo globalda funçäo endotelial näo foi possível até duas décadas atrás, quando se testemunhou a descoberta da produçäo da prostaciclina, do óxido nítrico (NO) derivado do endotélio ede outros fatores vasoativos.Longe de ser uma barreira passiva de interface entre o fuxo sanguíneo e o corpo, o endotélio deve ser considerado um sistema orgânico cuja funçäo é crítica na manutençäo da anticoagulaçäo sanguínea "in vivo", na manutançäo do tônus vascular e na regulaçäo da perfusäo.Acresça-se que a lesäo ou disfunçäo endotelial é uma via comum a diversas doenças cardiovasculares, incluindo a aterosclerose, as doenças vasoespásticas e a hipertensäo arterial.Este texto tem a finalidade de revisar os fatores vasoativos produzidos pelo endotélioe discutir aspectos da regulaçäo parácrina do tônus vascular.Seräo revisados os fatores relaxantes (PGI2-prostaciclina; EDRF/NO - fator relaxante do endotélio/óxido nítrico; e EDHF -fator hiperpolarizante derivado do endotélio) e os fatores contráteis derivados do endotélio (EDCFs).Após a revisäo desses fatores, seräo discutidas, de forma crítica, suas açöes isoladas e/ou sinérgicas na regulaçäo do tônus vascular.