Resting Heart Rate Affects Heart Response to Cold-Water Face Immersion Associated with Apnea.

The regular cardiac response to immersion of the face in cold water is reduction in heart rate (HR). The highly individualized and unpredictable course of the cardiodepressive response prompted us to investigate the relationship between the cardiac response to face immersion and the resting HR. The research was conducted with 65 healthy volunteers (37 women and 28 men) with an average age of 21.13 years (20-27 years) and a BMI of 21.49 kg/m2 (16.60-28.98). The face-immersion test consisted of stopping breathing after maximum inhaling and voluntarily immersing the face in cold water (8-10 °C) for as long as possible. Measurements included determination of minimum, average, and maximum HR at rest and minimum and maximum HR during the cold-water face-immersion test. The results indicate a strong relationship between the cardiodepressive reaction of the immersion of the face and the minimum HR before the test, as well as a relationship between the maximum HR during the test and the maximum HR at rest. The results also indicate a strong influence of neurogenic HR regulation on the described relationships. The parameters of the basal HR can, therefore, be used as prognostic indicators of the course of the cardiac response of the immersion test.

Heart Rate Variability at Rest Predicts Heart Response to Simulated Diving.

A characteristic feature of the cardiac response to diving is the uncertainty in predicting individual course. The aim of the study was to determine whether resting regulatory heart rate determinants assessed before diving may be predictors of cardiac response in a simulated diving test. The research was conducted with 65 healthy volunteers (37 women and 28 men) with an average age of 21.13 years (20-27 years) and a BMI of 21.49 kg/m2 (16.60-28.98). The simulated diving test consisted of stopping breathing after maximum inhaling and voluntarily immersing the face in water (8-10 °C) for as long as possible. The measurements included heart rate variability (HRV) analysis before diving and determination of the course of the cardiac response to diving-minimum and maximum heart rate (HR). The results indicate that minimum HR during diving (MIN_div) is dependent on the short-term HRV measures, which proves the strong influence of the parasympathetic system on the MIN_div. The lack of dependence of MIN_div on short-term HRV in women may be associated with differences in neurogenic HR regulation in women and men. In conclusion, cardiac response to simulated diving is strictly dependent on the autonomic regulation of the heart rhythm under resting conditions. The course of the cardiac response to diving and its relationship with resting HRV appears to be gender dependent.

Mild poikilocapnic hypoxia increases very low frequency haemoglobin oxygenation oscillations in prefrontal cortex.

BACKGROUND: The aim of the study was to investigate the effect of mild cerebral hypoxia on haemoglobin oxygenation (HbO2), cerebrospinal fluid dynamics and cardiovascular physiology. To achieve this goal, four signals were recorded simultaneously: blood pressure, heart rate / electrocardiogram, HbO2 from right hemisphere and changes of subarachnoid space (SAS) width from left hemisphere. Signals were registered from 30 healthy, young participants (2 females and 28 males, body mass index = 24.5 ± 2.3 kg/m2, age 30.8 ± 13.4 years). RESULTS: We analysed the recorded signals using wavelet transform and phase coherence. We demonstrated for the first time that in healthy subjects exposed to mild poikilokapnic hypoxia there were increases in very low frequency HbO2 oscillations (< 0.052 Hz) in prefrontal cortex. Additionally, SAS fluctuation diminished in the whole frequency range which could be explained by brain oedema. CONCLUSIONS: Consequently the study provides insight into mechanisms governing brain response to a mild hypoxic challenge. Our study supports the notion that HbO2 and SAS width monitoring might be beneficial for patients with acute lung disease.

Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice.

BACKGROUND: The goal of this study was to assess the effect of melatonin on blood redox systems in mice simultaneously exposed to ethanol and low-dose lipopolysaccharide (LPS). METHODS: Oxidative stress parameters were assessed in eight groups: untreated control, melatonin (10 mg kg-1, 10 days), LPS (injected once intraperitoneally at a dose of 150 µg per mouse), LPS with previous melatonin treatment, acute ethanol-induced stress (AES, 0.75 g kg-1 per day, 10 days), AES with previous melatonin treatment, LPS- and AES-induced toxicity, and melatonin treatment. RESULTS: Both ethanol and LPS induced oxidative stress. The combination of these two factors was even more toxic to the organism. Melatonin stabilized erythrocyte membranes and decreased the high level of free radical oxidation at the initial and final stages. Furthermore, melatonin limited protein damage through maintenance in the functional ability of the blood redox system to counteract pathological conditions. CONCLUSIONS: Melatonin limited the negative effects associated with alcohol consumption and low-intensity inflammation.

Mild poikilocapnic hypoxia increases very low frequency haemoglobin oxygenation oscillations in prefrontal cortex

BACKGROUND: The aim of the study was to investigate the effect of mild cerebral hypoxia on haemoglobin oxygenation (HbO2), cerebrospinal fluid dynamics and cardiovascular physiology. To achieve this goal, four signals were recorded simultaneously: blood pressure, heart rate / electrocardiogram, HbO2 from right hemisphere and changes of subarachnoid space (SAS) width from left hemisphere. Signals were registered from 30 healthy, young participants (2 females and 28 males, body mass index = 24.5 ± 2.3 kg/m2, age 30.8 ± 13.4 years). RESULTS: We analysed the recorded signals using wavelet transform and phase coherence. We demonstrated for the first time that in healthy subjects exposed to mild poikilokapnic hypoxia there were increases in very low frequency HbO2 oscillations (< 0.052 Hz) in prefrontal cortex. Additionally, SAS fluctuation diminished in the whole frequency range which could be explained by brain oedema. CONCLUSIONS: Consequently the study provides insight into mechanisms governing brain response to a mild hypoxic challenge. Our study supports the notion that HbO2 and SAS width monitoring might be beneficial for patients with acute lung disease.

Comparison of near infrared spectroscopy (NIRS) and near-infrared transillumination-backscattering sounding (NIR-T/BSS) methods.

The aim of the study was to compare simultaneously recorded a NIR-T/BSS and NIRS signals from healthy volunteers. NIR-T/BSS is a device which give an ability to non-invasively detect and monitor changes in the subarachnoid space width (SAS). Experiments were performed on a group of 30 healthy volunteers (28 males and 2 females, age 30.8 ± 13.4 years, BMI = 24.5 ± 2.3 kg/m2). We analysed recorded signals using analysis methods based on wavelet transform (WT) for the wide frequency range from 0.0095 to 2 Hz. Despite the fact that both devices use a similar radiation source both signals are distinct from each other. We found statistically significant differences for WT amplitude spectra between both signals. Additionally, we showed different relationships of both signals to blood pressure. Collectively, based on the present findings and those of previous studies, we can conclude that the combination of NIR-T/BSS or NIRS signals and time-frequency analysis opens new frontiers in science, and give possibility to understand and diagnosis of various neurodegenerative and ageing related diseases to improve diagnostic procedures and patient prognosis.

Dietary Fat and Cancer-Which Is Good, Which Is Bad, and the Body of Evidence.

A high-fat diet (HFD) induces changes in gut microbiota leading to activation of pro-inflammatory pathways, and obesity, as a consequence of overnutrition, exacerbates inflammation, a known risk factor not only for cancer. However, experimental data showed that the composition of dietary fat has a greater impact on the pathogenesis of cancer than the total fat content in isocaloric diets. Similarly, human studies did not prove that a decrease in total fat intake is an effective strategy to combat cancer. Saturated fat has long been considered as harmful, but the current consensus is that moderate intake of saturated fatty acids (SFAs), including palmitic acid (PA), does not pose a health risk within a balanced diet. In regard to monounsaturated fat, plant sources are recommended. The consumption of plant monounsaturated fatty acids (MUFAs), particularly from olive oil, has been associated with lower cancer risk. Similarly, the replacement of animal MUFAs with plant MUFAs decreased cancer mortality. The impact of polyunsaturated fatty acids (PUFAs) on cancer risk depends on the ratio between ω-6 and ω-3 PUFAs. In vivo data showed stimulatory effects of ω-6 PUFAs on tumour growth while ω-3 PUFAs were protective, but the results of human studies were not as promising as indicated in preclinical reports. As for trans FAs (TFAs), experimental data mostly showed opposite effects of industrially produced and natural TFAs, with the latter being protective against cancer progression, but human data are mixed, and no clear conclusion can be made. Further studies are warranted to establish the role of FAs in the control of cell growth in order to find an effective strategy for cancer prevention/treatment.

Current understanding of the effects of inspiratory resistance on the interactions between systemic blood pressure, cerebral perfusion, intracranial pressure, and cerebrospinal fluid dynamics.

Negative intrathoracic pressure (nITP) is generated by the respiratory muscles during inspiration to overcome inspiratory resistance, thus enabling lung ventilation. Recently developed noninvasive techniques have made it possible to assess the effects of nITP in real time in several physiological aspects such as systemic blood pressure (BP), intracranial pressure (ICP), and cerebral blood flow (CBF). It has been shown that nITP from 0 to -20 cmH2O elevates BP and diminishes ICP, which facilitates brain perfusion. The effects of nITP from -20 to -40 cmH2O on BP, ICP, and CBF remain largely unrecognized, yet even nITP at -40 cmH2O may facilitate CBF by diminishing ICP. Importantly, nITP from -20 to -40 cmH2O has been documented in adults in commonly encountered obstructive sleep apnea, which justifies research in this area. Recent revelations about interactions between ICP and BP have opened up new fields of research in physiological regulation and the pathophysiology of common diseases, such as hypertension, brain injury, and respiratory disorders. A better understanding of these interactions may translate directly into new therapies in various fields of clinical medicine.

Liver mitochondrial respiratory plasticity and oxygen uptake evoked by cobalt chloride in rats with low and high resistance to extreme hypobaric hypoxia.

High-altitude intolerance and consequently high-altitude sickness, is difficult to predict. Liver is an essential organ in glucose and lipid metabolism, and may play key role in the adaptation to high altitude. In response to extreme high altitude, mitochondrial respiration exhibits changes in substrate metabolism, mitochondrial electron transport chain activity, and respiratory coupling. We determined the cobalt chloride (CoCl2) effects on liver mitochondrial plasticity and oxygen uptake in rats with low resistance (LR) and high resistance (HR) to extreme hypobaric hypoxia. The polarographic method proposed by Chance and Williams was used as a simple and effective tool to trace mitochondrial functionality and oxygen consumption. HR rats had more efficient processes of NADH- and FAD-generated mitochondrial oxidation. CoCl2 promoted more efficient NADH-generated and diminished less efficient FAD-generated mitochondrial respiratory reactions in HR rats. CoCl2 diminished both aerobic and anaerobic processes in LR rats. Glutamate and pyruvate substrates of NADH-generated mitochondrial pathways were highly affected by CoCl2. Red blood cells acted as cobalt depots in HR and LR rats. We have unveiled several mechanisms leading to differentiated mitochondrial respiratory responses to hypobaric hypoxia in LR and HR rats. Our study strongly supports the existence of adaptive liver mitochondrial plasticity to extreme hypoxia.

Central sympathetic nervous system reinforcement in obstructive sleep apnoea.

The available studies on cerebrovascular reactivity and cerebral oxygenation in obstructive sleep apnoea (OSA) patients brought conflicting results, yet the overall evidence suggests that resting state cerebral perfusion is diminished in these patients. Interestingly, in a group of healthy professional breath-hold divers who are exercising very long apnoeas - episodes corresponding to the ones observed in patients with OSA - demonstrated that cerebral oxygenation may remain stable at the expense of extreme sympathetic nervous system (SNS) activation. In the present review we address several mechanisms that could potentially explain these discrepancies. We focus in depth on mechanisms of central SNS reinforcement in OSA including dysfunctional baroreflex response, and inflammatory processes within the brain centres controlling the cardiovascular system. Additionally, novel insights into physiology of cerebral blood flow regulation are proposed, including the role of short-term blood pressure changes, heart rate fluctuations and baroreflex alterations. Finally, a potential role of increased blood flow pulsatility in cerebrospinal fluid circulation changes and its influence on SNS drive is highlighted. The presented review provides insights into how sympathetic nervous system reinforcement in OSA promotes maladaptive mechanisms that could alter cerebral perfusion regulation, and result in functional and structural cerebral changes.

Increased inspiratory resistance affects the dynamic relationship between blood pressure changes and subarachnoid space width oscillations.

BACKGROUND AND OBJECTIVE: Respiration is known to affect cerebrospinal fluid (CSF) movement. We hypothesised that increased inspiratory resistance would affect the dynamic relationship between blood pressure (BP) changes and subarachnoid space width (SAS) oscillations. METHODS: Experiments were performed in a group of 20 healthy volunteers undergoing controlled intermittent Mueller Manoeuvres (the key characteristic of the procedure is that a studied person is subjected to a controlled, increased inspiratory resistance which results in marked potentiation of the intrathoracic negative pressure). BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography; oxyhaemoglobin saturation with an ear-clip sensor; end-tidal CO2 with a gas analyser; cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a new method i.e. near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the BP and SAS oscillations coupling. RESULTS: Initiating Mueller manoeuvres evoked cardiac SAS component decline (-17.8%, P<0.001), systolic BP, diastolic BP and HR increase (+6.3%, P<0.001; 6.7%, P<0.001 and +2.3%, P<0.05, respectively). By the end of Mueller manoeuvres, cardiac SAS component and HR did not change (+2.3% and 0.0%, respectively; both not statistically significant), but systolic and diastolic BP was elevated (+12.6% and +8.9%, respectively; both P<0.001). With reference to baseline values there was an evident decrease in wavelet coherence between BP and SAS oscillations at cardiac frequency in the first half of the Mueller manoeuvres (-32.3%, P<0.05 for left hemisphere and -46.0%, P<0.01 for right hemisphere) which was followed by subsequent normalization at end of the procedure (+3.1% for left hemisphere and +23.1% for right hemisphere; both not statistically significant). CONCLUSIONS: Increased inspiratory resistance is associated with swings in the cardiac contribution to the dynamic relationship between BP and SAS oscillations. Impaired cardiac performance reported in Mueller manoeuvres may influence the pattern of cerebrospinal fluid pulsatility.

Acute hypoxia diminishes the relationship between blood pressure and subarachnoid space width oscillations at the human cardiac frequency.

BACKGROUND: Acute hypoxia exerts strong effects on the cardiovascular system. Heart-generated pulsatile cerebrospinal fluid motion is recognised as a key factor ensuring brain homeostasis. We aimed to assess changes in heart-generated coupling between blood pressure (BP) and subarachnoid space width (SAS) oscillations during hypoxic exposure. METHODS: Twenty participants were subjected to a controlled decrease in oxygen saturation (SaO2 = 80%) for five minutes. BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography, oxyhaemoglobin saturation with an ear-clip sensor, end-tidal CO2 with a gas analyser, and cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a recently-developed method called near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the relationship between BP and SAS oscillations. RESULTS: Gradual increases in systolic, diastolic BP and HR were observed immediately after the initiation of hypoxic challenge (at fifth minute +20.1%, +10.2%, +16.5% vs. baseline, respectively; all P<0.01), whereas SAS remained intact (P = NS). Concurrently, the CBFV was stable throughout the procedure, with the only increase observed in the last two minutes of deoxygenation (at the fifth minute +6.8% vs. baseline, P<0.05). The cardiac contribution to the relationship between BP and SAS oscillations diminished immediately after exposure to hypoxia (at the fifth minute, right hemisphere -27.7% and left hemisphere -26.3% vs. baseline; both P<0.05). Wavelet phase coherence did not change throughout the experiment (P = NS). CONCLUSIONS: Cerebral haemodynamics seem to be relatively stable during short exposure to normobaric hypoxia. Hypoxia attenuates heart-generated BP SAS coupling.

Stress Response, Brain Noradrenergic System and Cognition.

Locus coeruleus is a critical component of the brain noradrenergic system. The brain noradrenergic system provides the neural substrate for the architecture supporting the interaction with, and navigation through, an external world complexity. Changes in locus coeruleus tonic and phasic activity and the interplay between norepinephrine and α1- and α2-adrenoceptors in the prefrontal cortex are the key elements of this sophisticated architecture. In this narrative review we discuss how the brain noradrenergic system is affected by increased exposure to corticotropin-releasing hormone triggered by stress response. In particular, we present the mechanisms responsible for thinking inflexibility often observed under highly stressful conditions. Finally, the main directions for future research are highlighted.

Pial artery and subarachnoid width response to apnoea in normal humans.

BACKGROUND: Little is known about intracranial pressure (ICP)-cerebral haemodynamic interplay during repetitive apnoea. A recently developed method based on near-infrared transillumination/backscattering sounding (NIR-T/BSS) noninvasively measures changes in pial artery pulsation (cc-TQ) as well as subarachnoid width (sas-TQ) in humans. METHOD: We tested the complex response of the pial artery and subarachnoid width to apnoea using this method. The pial artery and subarachnoid width response to consecutive apnoeas lasting 30, 60 s and maximal breath-hold (91.1 ±â€Š23.1 s) were studied in 20 healthy volunteers. The cc-TQ and sas-TQ were measured using NIR-T/BSS; cerebral blood flow velocity (CBFV), pulsatility index and resistive index were measured using Doppler ultrasound of the left internal carotid artery; heart rate (HR) and beat-to-beat SBP and DBP blood pressure were recorded using a Finometer; end-tidal CO2 (EtCO2) was measured using a medical gas analyser. RESULTS: Apnoea evoked a multiphasic response in blood pressure, pial artery compliance and ICP. First, SBP declined, which was accompanied by an increase in cc-TQ and sas-TQ. Directly after these changes, SBP exceeded baseline values, which was followed by a decline in cc-TQ and the return of sas-TQ to baseline. During these initial changes, CBFV remained stable. Towards the end of the apnoea, BP, cc-TQ and CBFV increased, whereas pulsatility index, resistive index and sas-TQ declined. Changes in sas-TQ were linked to changes in EtCO2, HR and SBP. CONCLUSION: Apnoea is associated with ICP swings, closely reflecting changes in EtCO2, HR and peripheral BP. The baroreflex influences the pial artery response.

Brain inflammation and hypertension: the chicken or the egg?

Inflammation of forebrain and hindbrain nuclei controlling the sympathetic nervous system (SNS) outflow from the brain to the periphery represents an emerging concept of the pathogenesis of neurogenic hypertension. Angiotensin II (Ang-II) and prorenin were shown to increase production of reactive oxygen species and pro-inflammatory cytokines (interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α)) while simultaneously decreasing production of interleukin-10 (IL-10) in the paraventricular nucleus of the hypothalamus and the rostral ventral lateral medulla. Peripheral chronic inflammation and Ang-II activity seem to share a common central mechanism contributing to an increase in sympathetic neurogenic vasomotor tone and entailing neurogenic hypertension. Both hypertension and obesity facilitate the penetration of peripheral immune cells in the brain parenchyma. We suggest that renin-angiotensin-driven hypertension encompasses feedback and feedforward mechanisms in the development of neurogenic hypertension while low-intensity, chronic peripheral inflammation of any origin may serve as a model of a feedforward mechanism in this condition.

Assessing changes in pial artery resistance and subarachnoid space width using a non-invasive method in healthy humans during the handgrip test.

The aim of this study was to assess the influence of the handgrip test (HGT) on: (1) pial artery pulsation (cc-TQ), (2) subarachnoid space (SAS) width (sas-TQ) and (3) the relationship between peripheral blood pressure (BP), heart rate (HR), cerebral blood flow velocity (CBFV), resistive index (RI), cc-TQ and sas-TQ. The study was performed on 29 healthy volunteers (11 men and 18 women) with a mean age of 29.3 ± SE 4.0. HGT was performed in the sitting position at 30% of maximal voluntary contraction. cc-TQ and sas-TQ were registered using near-infrared transillumination/backscattering sounding (NIR-T/BSS); BP and heart rate (HR) were measured using a Finapres monitor. CBFV and RI were recorded using a transcranial Doppler. A significant reduction in cc-TQ (-34.3%, P<0.0001) and sas-TQ (-12.9%, P<0.001) were observed, while mean arterial pressure and HR increased (+34.8%, P<0.0001 and +7.9%, P<0.0001, respectively). There was no significant change in CBFV (+1.0 percent) while RI increased (+12.0 percent, P<0.05). Correlation and regression analysis did not reveal any interdependencies between the investigated variables. HGT evoked a significant increase in pial artery resistance, with a simultaneous decrease in the width of the SAS. A decrease in pial artery compliance should be seen as protective mechanism against acute BP elevation, most likely mediated by sympathetic activation. NIR-T/BSS recordings allowed for non-invasive assessments of changes in pial artery compliance, and were consistent with data from the literature and physiological knowledge.

Effects of acute hypercapnia on the amplitude of cerebrovascular pulsation in humans registered with a non-invasive method.

AIM: The aim of the study was to assess non-invasively the effects of acute hypercapnia on the amplitude of cerebrovascular pulsation (CVP) in humans. METHODS: Experiments were carried out in four male volunteers aged 25, 26, 31 and 49. Changes in blood flow through the pial arteries were induced using two interventions: (A) breathing a gas mixture containing 5% CO(2) for 2 minutes and (B) intravenous administration of 1g acetazolamide. The amplitude of CVP and width of subarachnoid space (SAS) were measured non-invasively using near-infrared transillumination/backscattering sounding (NIR-T/BSS), while cerebral blood flow was assessed by single photon emission computed tomography (SPECT) and mean blood flow velocity in the left anterior cerebral artery by transcranial Doppler. RESULTS: Inhalation of a gas mixture containing 5% CO(2) evoked an increase in the amplitude of CVP (202.5% ± SE 10.1), normalized number of counts (22.6% ± SE 3.5%) and mean blood flow velocity in the left cerebral anterior artery (37.6%± SE 11.7%), while resistive index decreased (-8.7% ± SE 2.3%) and the width of SAS decreased (-8.0 ± SE 0.45). Acetazolamide also produced an increase in the amplitude of CVP (23.7% ± SE 5.4%), normalized number of counts (7.9% ± SE 1.1%), and mean blood flow velocity in the left cerebral anterior artery (62.8% ± SE 13.7%), while resistive index decreased (-7.9% ± SE 1.7%), and the width of SAS decreased (-13.4% ± SE 3.4%). CONCLUSION: Acute hypercapnia causes an increase in the amplitude of CVP pulsation in humans. NIR-T/BSS allows for non-invasive bedside monitoring of the amplitude of CVP. NIR-T/BSS is consistent with transcranial Doppler and SPECT.

Use of Near Infrared Transillumination / Back Scattering Sounding (NIR-T/BSS) to assess effects of elevated intracranial pressure on width of subarachnoid space and cerebrovascular pulsation in animals.

The objective was to assess changes in the width of the subarachnoid space (SAS) and amplitude of cerebrovascular pulsation (CVP) during acute elevation of intracranial pressure (ICP) using Near Infrared Transillumination/Back Scattering Sounding (NIR-T/BSS). Changes in the width of the SAS and amplitude of CVP were observed in rabbits during experimental ICP elevation induced by: (1) quick injections of saline into the subdural space of the spinal cord, and (2) distension of a surgical catheter balloon placed intracranially in the subdural space. The amplitude of CVP was also assessed during acute elevation of blood pressure in the intracranial portion of the internal carotid artery (ICA) induced by adrenaline. Each of the injections of saline caused a transient rise in the width of the SAS and amplitude of CVP. The amplitude of the increase in CVP was dependent on changes in blood pressure in the ICA (r=-0.82, P<0.01). Distension of the intracranial balloon resulted in elimination of the respiratory oscillations in the CVP and increased its systolic-diastolic amplitude. An increase in the amplitude of CVP was evoked by adrenaline without an increase in the carotid blood flow. We demonstrated that during elevation of ICP the amplitude of CVP depends on blood pressure rather than on blood flow in large cerebral vessels. Elimination of the respiratory oscillations by a minute ("sub-critical") ICP increase may be used as an early indicator of rising ICP. The direction of changes recorded using NIR-T/BSS was consistent with changes recorded using tensometric transducers.

Effects of the Valsalva maneuver on pial artery pulsation and subarachnoid width in healthy adults.

AIM: The objective was to characterize the effects of Valsalva maneuver (VM) on the amplitude of cerebrovascular pulsation (CVP), and to explore the direct interactions between the cerebral vasculature and the cerebrospinal fluid compartment in VMIII. METHODS: Twenty-nine healthy volunteers between the ages of 25 and 40 (29.3 ± SE 4.0) were studied. Changes in the amplitude of CVP (cc-TQ) and width of subarachnoid space (SAS; sas-TQ) were recorded with NIR-T/BSS sensor. Changes in arterial blood pressure (ABP) and heart rate were measured using Finapres. Cerebral blood flow velocity (CBFV) in the left middle cerebral artery was recorded with transcranial doppler. RESULTS: sas-TQ remained unchanged, while cc-TQ increased in VMI (+40% vs. baseline). In VMIIa, sas-TQ increase (+3.4% vs. baseline) and deep decrease in cc-TQ (-81% vs. baseline) were observed. sas-TQ decrease started in VMIIb (-2.7% vs. baseline), with simultaneous slight increase in cc-TQ (-58% vs. baseline). In VMIII deep sas-TQ decrease (-6.2% vs. baseline) was associated with huge increase in cc-TQ (+110% vs. baseline; r=-0.56, p<0.01). During VMIV sas-TQ increased (-4.8% vs. baseline) while cc-TQ decreased (+38% vs. baseline). The drop of cc-TQ in VMIIa was significantly greater than corresponding changes in CBFV and ABP. Increase in cc-TQ in VMIII preceded CBFV and ABP changes in VMIV. CONCLUSION: The VM evokes significant changes in the amplitude of CVP. Changes in small vessel pulsation precede changes in CBFV. There are direct interactions between cc-TQ and sas-TQ in VMIII. NIR-T/BSS allows for continuous, non-invasive monitoring of the amplitude of CVP and width of the SAS.

Flow-induced changes in pial artery compliance registered with a non-invasive method in rabbits.

AIM: This study was performed: 1) to assess the relationship between blood flow velocity in the internal carotid artery (CBF(ICA)) and pial artery pulsation (cc-TQ) and 2) to evaluate flow-induced changes in pial artery compliance. METHODS: Experiments were performed on 10 crossbred male rabbits. Heart rate (HR), blood pressure (BP), left ventricle ejection fraction (LVEF), CBF(ICA), the systolic-diastolic blood volume fraction in the brain circulation (CBF(SDF)) and cc-TQ were recorded after glucagon and acetazolamide administration. cc-TQ was measured with near-infrared transillumination back scattering sounding (NIR-T/BSS), LVEF and CBF(SDF) with gated scintigraphy and BP and CBF(ICA) with electromagnetic pressure and flow transducers, respectively. Doses of drugs were chosen to exert a haemodynamic effect but not change BP or intracranial pressure. RESULTS: Acetazolamide and glucagon evoked significant increases in cc-TQ, CBF(SDF), CBF(ICA), LVEF and HR. The following interdependencies were found: 1) changes after acetazolamide administration compared to baseline: CBF(SDF) vs. LVEF (r=0.73, p<0.05), cc-TQ vs. CBF(SDF) (r=-0.67, p<0.05), cc-TQ vs. LVEF (r=-0.76, p<0.05), 2) changes after glucagon administration compared to baseline: CBF(ICA) vs. BP (r=0.73, p<0.05), CBF(SDF) vs. LVEF (r=0.87, p<0.05), cc-TQ vs. HR (r=0.85, p<0.05), cc-TQ vs. CBF(ICA) (r=-0.74, p<0.05). CONCLUSION: In the absence of systemic BP changes, pial arteries are significantly affected by changes in CBF(ICA). Pial arteries counteract changes in CBF(ICA) and CBF(SDF). The ability of pial arteries to stabilise CBF(ICA) is impaired after acetazolamide administration. Changes in cardiac output directly affect the brain's microcirculation. NIR-T/BSS recordings allow for non-invasive assessment of changes in pial artery compliance.