Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

1975 ◽  
Vol 49 (2) ◽  
pp. 157-169
Author(s):  
N. N. Stanley ◽  
B. G. Salisbury ◽  
L. C. McHenry ◽  
N. S. Cherniack
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Liver Failure ◽  
Metabolic Rate ◽  
Ventilatory Response ◽  
Cerebral Metabolism ◽  
Experimental Production ◽  
Arterial Blood ◽  
Ventilatory Response To Co2

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial Pco2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased Pco2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated Pco2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the Pco2 is increased.

Cerebral Blood Flow, Cerebral Metabolism and Cerebrospinal Fluid Biochemistry in Brain-Injured Patients after Exposure to Hyperbaric Oxygen

1976 ◽  
Vol 14 (5) ◽  
pp. 351-364 ◽  
Author(s):  
François Artru ◽  
Bernard Philippon ◽  
Françoise Gau ◽  
Michel Berger ◽  
Raymond Deleuze
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Hyperbaric Oxygen ◽  
Cerebral Metabolism ◽  
Brain Injured ◽  
Injured Patients

scholarly journals The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Cerebrovascular Function

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.

scholarly journals Increasing cerebral blood flow reduces the severity of central sleep apnea at high altitude

2018 ◽  
Vol 124 (5) ◽  
pp. 1341-1348 ◽  
Author(s):  
Keith R. Burgess ◽  
Samuel J. E. Lucas ◽  
Katie M. E. Burgess ◽  
Kate E. Sprecher ◽  
Joseph Donnelly ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sleep Apnea ◽  
Healthy Volunteers ◽  
High Altitude ◽  
Ventilatory Response ◽  
Central Sleep Apnea ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Central Chemoreceptors

Earlier studies have indicated an important role for cerebral blood flow in the pathophysiology of central sleep apnea (CSA) at high altitude, but were not decisive. To test the hypothesis that pharmacologically altering cerebral blood flow (CBF) without altering arterial blood gas (ABGs) values would alter the severity of CSA at high altitude, we studied 11 healthy volunteers (8M, 3F; 31 ± 7 yr) in a randomized placebo-controlled single-blind study at 5,050 m in Nepal. CBF was increased by intravenous (iv) acetazolamide (Az; 10 mg/kg) plus intravenous dobutamine (Dob) infusion (2–5 μg·kg−1·min−1) and reduced by oral indomethacin (Indo; 100 mg). ABG samples were collected and ventilatory responses to hypercapnia (HCVR) and hypoxia (HVR) were measured by rebreathing and steady-state techniques before and after drug/placebo. Duplex ultrasound of blood flow in the internal carotid and vertebral arteries was used to measure global CBF. The initial 3–4 h of sleep were recorded by full polysomnography. Intravenous Az + Dob increased global CBF by 37 ± 15% compared with placebo ( P < 0.001), whereas it was reduced by 21 ± 8% by oral Indo ( P < 0.001). ABGs and HVR were unchanged in both interventions. HCVR was reduced by 28% ± 43% ( P = 0.1) during intravenous Az ± Dob administration and was elevated by 23% ± 30% ( P = 0.05) by Indo. During intravenous Az + Dob, the CSA index fell from 140 ± 45 (control night) to 48 ± 37 events/h of sleep ( P < 0.001). Oral Indo had no significant effect on CSA. We conclude that increasing cerebral blood flow reduced the severity of CSA at high altitude; the likely mechanism is via a reduction in the background stimulation of central chemoreceptors.NEW & NOTEWORTHY This work is significant because it shows convincingly for the first time in healthy volunteers that increasing cerebral blood flow will reduce the severity of central sleep apnea in a high-altitude model, without the potentially confounding effects of altering partial pressure of arterial carbon dioxide or the ventilatory response to hypoxia. The proposed mechanism of action is that of increasing the removal of locally produced CO2from the central chemoreceptors, causing the reduction in hypercapnic ventilatory response, hence reducing loop gain.

scholarly journals REGULATION OF CEREBRAL BLOOD FLOW IN HUMANS: PHYSIOLOGY AND CLINICAL IMPLICATIONS OF AUTOREGULATION

2021 ◽  
Author(s):  
Jurgen A.H.R. Claassen ◽  
Dick H.J. Thijssen ◽  
Ronney B Panerai ◽  
Frank M. Faraci
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Function ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Blood Gases ◽  
Clinical Implications ◽  
Arterial Blood ◽  
The Impact

Brain function critically depends on a close matching between metabolic demands, appropriate delivery of oxygen and nutrients, and removal of cellular waste. This matching requires continuous regulation of cerebral blood flow (CBF), which can be categorized into four broad topics: 1) autoregulation, which describes the response of the cerebrovasculature to changes in perfusion pressure, 2) vascular reactivity to vasoactive stimuli [including carbon dioxide (CO2)], 3) neurovascular coupling (NVC), i.e., the CBF response to local changes in neural activity (often standardized cognitive stimuli in humans), and 4) endothelium-dependent responses. This review focuses primarily on autoregulation and its clinical implications. To place autoregulation in a more precise context, and to better understand integrated approaches in the cerebral circulation, we also briefly address reactivity to CO2 and NVC. In addition to our focus on effects of perfusion pressure (or blood pressure), we describe the impact of select stimuli on regulation of CBF (i.e., arterial blood gases, cerebral metabolism, neural mechanisms, and specific vascular cells), the inter-relationships between these stimuli, and implications for regulation of CBF at the level of large arteries and the microcirculation. We review clinical implications of autoregulation in aging, hypertension, stroke, mild cognitive impairment, anesthesia, and dementias. Finally, we discuss autoregulation in the context of common daily physiological challenges, including changes in posture (e.g., orthostatic hypotension, syncope) and physical activity.

Cerebrospinal fluid ionic regulation, cerebral blood flow, and glucose use during chronic metabolic alkalosis

1989 ◽  
Vol 257 (4) ◽  
pp. H1220-H1227 ◽  
Author(s):  
H. Schrock ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Metabolic Alkalosis ◽  
Glucose Utilization ◽  
Cerebral Metabolism ◽  
Brain Structures ◽  
Cerebral Glucose Utilization ◽  
K Concentration ◽  
Low K

Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-[14C]antipyrine and 2-[14C]deoxy-D-glucose method. The treatment induced moderate [15 days, base excess (BE) 16 mM] to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow was detectable in most brain structures when compared with controls. Cerebrospinal fluid (CSF) K+ and H+ concentrations were significantly decreased. During severe hypochloremic alkalosis, cerebral blood flow was decreased by 19% and cerebral glucose utilization by 24% when compared with the control values. The decrease in cerebral blood flow during severe metabolic alkalosis is attributed mainly to the decreased cerebral metabolism and to a lesser extent to a further decrease of the CSF H+ concentration. CSF K+ concentration was not further decreased. The results show an unaltered cerebral blood flow and glucose utilization together with a decrease in CSF H+ and K+ concentrations at moderate metabolic alkalosis and a decrease in cerebral blood flow and glucose utilization together with a further decreased CSF H+ concentration at severe metabolic alkalosis.

Cerebrospinal fluid production and its relationship to cerebral metabolism and cerebral blood flow

1959 ◽  
Vol 197 (4) ◽  
pp. 825-828 ◽  
Author(s):  
Edgar A. Bering
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Choroid Plexus ◽  
Cerebral Metabolism ◽  
Oxygen Metabolism ◽  
Csf Flow ◽  
Constant Composition ◽  
Fluid Production

The cerebrospinal fluid production has been studied in the dog under conditions of maximum obtainable flow rates from the cisterna magna. Under these conditions the fluid had constant composition and was assumed to represent the cerebrospinal fluid in the intact state. Cerebral blood flow and cerebral oxygen consumption were measured by the method of Kety and Schmidt. The only significant correlations found were with oxygen consumption when the CSF flow rate was in terms of brain weight and with cerebral blood flow and cerebral vascular resistance when CSF flow was in terms of choroid plexus weight. A combined regression equation was calculated which satisfactorily accounted for the observed CSF flow: CSF cu mm/min. = .128 x CMRO2 x brain wgt. + 0.15 x CVR x choroid plexus wt. This suggested separate physiological processes, one correlated with oxygen metabolism and one with hydrodynamic factors of the cerebral blood flow. The data demonstrated that the choroid plexus alone could not have accounted for the entire CSF flow and some must have come from another source, presumably the brain.

Autoregulation of cerebral blood flow and its relation to cerebrospinal fluid pH

1976 ◽  
Vol 231 (3) ◽  
pp. 929-935 ◽  
Author(s):  
MJ Hernandez-Perez ◽  
DK Anderson
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Internal Carotid ◽  
Flow Transducer ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Before And After

Internal carotid artery blood flow (IFBF) was determined in each of nine Macaca mulatta by means of a flow transducer implanted around an internal carotid artery. The monkeys were lightly anesthetized, intubated, and paralyzed. Normoxia and normocarbia were maintained stable throughout the experiment. ICBF was monitored while mean arterial blood pressure (MABP) was lowered by withdrawal of blood. MABP was kept within the known limits of autoregulation in order not to compromise CBF. Cerebrospinal fluid (CSF) from the cisterna magna was analyzed for pH PCO2, and PO2 before and after a 30-min hypotensive period in which MABP was lowered from 116 +/- 4 to 70 +/- 2 mmHg (mean +/- SE). Corresponding HCO3- concentrations were calculated. The decrease in MABP did not result in a significant reduction in ICBF but elicited a 37% reduction in calculated cerebrovascular resistance, indicating normal autoregulation. Mena CSF pH was not significantly decreased (P less than 0.05); it changed from 7.320 +/- 0.010 to 7.317 +/- 0.010 after the induced hypotensive period. Thus CSF pH does not appear to have a significant role in cerebral blood flow autoregulation.

Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans

2002 ◽  
Vol 93 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Lars Nybo ◽  
Kirsten Møller ◽  
Stefanos Volianitis ◽  
Bodil Nielsen ◽  
Niels H. Secher
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Core Temperature ◽  
Prolonged Exercise ◽  
Cerebral Metabolism ◽  
Cycle Ergometer ◽  
Carbon Dioxide Tension ◽  
Cerebral Metabolic Rate ◽  
Exercise In Humans

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9°C; control) or when severe hyperthermia had developed (core temperature = 39.5°C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 ± 4 vs. 51 ± 4 ml · 100 g−1· min−1; P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q10(temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.

Preservation of the Ratio of Cerebral Blood Flow/Metabolic Rate for Oxygen during Prolonged Anesthesia with Isoflurane, Sevoflurane, and Halothane in Humans

1996 ◽  
Vol 84 (3) ◽  
pp. 555-561 ◽  
Author(s):  
Yasuhiro Kuroda ◽  
Mari Murakami ◽  
Junko Tsuruta ◽  
Toshisuke Murakawa
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Animal Studies ◽  
Prolonged Exposure ◽  
Volatile Anesthetic ◽  
Volatile Anesthetics ◽  
Dependent Manner ◽  
Arterial Blood ◽  
Over Time

Background In several animal studies, an increase in cerebral blood flow (CBF) produced by volatile anesthetics has been reported to resolve over time during prolonged anesthesia. It is important to investigate whether this time-dependent change of CBF takes place in humans, especially in clinical situations where surgery is ongoing under anesthesia. In this study, to evaluate the effect of prolonged exposure to volatile anesthetics (isoflurane, sevoflurane, and halothane), the CBF equivalent (CBF divided by cerebral metabolic rate for oxygen (CMRO2) was determined every 20 min during anesthesia lasting more than 4h in patients. Methods Twenty-four surgical patients were assigned to three groups at random to receive isoflurane, sevoflurane, or halothane (8 patients each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 MAC before surgery and then 1.5 MAC for the 3 h of surgical procedure. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 60 mmHg, using phenylephrine infusion, if necessary. CBF equivalent was calculated every 20 min as the reciprocal of arterial-jugular venous oxygen content difference. Results CBF equivalent at 0.5 MAC of isoflurane, halothane, and sevoflurane was 21 +/- 4, 20 +/- 3, and 21 +/- 5 ml blood/ml oxygen, respectively. All three examined volatile anesthetics significantly (P&lt;0.01) increased CBF equivalent in a dose-dependent manner (0.5, 1.0, 1.5 MAC). AT 1.5 MAC, the increase of CBF equivalent with all anesthetics was maintained increased with minimal fluctuation for 3 h. The mean value of CBF equivalent at 1.5 MAC in the isoflurane group (45 +/- 8) was significantly (P&lt;0.01) greater than those in the halothane (32 +/- 8) and sevoflurane (31 +/- 8) groups. Electroencephalogram was found to be relatively unchanged during observation periods at 1.5 MAC. Conclusions These results demonstrate that CBF/CMRO2 ratio is markedly increased above normal and maintained during prolonged inhalation of volatile anesthetics in humans. It is impossible to determine whether these data indicate a stable CBF or whether CBF and CMRO2 are changing in parallel during the observation period. The unchanging electroencephalographic pattern suggests that the former possibility is more likely and that the increase of CBF produced by volatile anesthetics is maintained over time without decay, which has been reported in several animal studies. It also is suggested that isoflurane possesses greater capability to maintain global CBF relative to CMRO(2) than does halothane or sevoflurane. time.)

Intracranial pressure, cerebral blood flow, and cerebrospinal fluid formation during hyperammonemia in cat

1986 ◽  
Vol 65 (1) ◽  
pp. 86-91 ◽  
Author(s):  
Adam Chodobski ◽  
Joanna Szmydynger-Chodobska ◽  
Anna Urbańska ◽  
Ewa Szczepańska-Sadowska
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Ammonium Acetate ◽  
Formation Rate ◽  
Ammonia Level ◽  
Blood Ammonia ◽  
Blood Ammonia Level ◽  
Arterial Blood ◽  
Csf Formation Rate

✓ Intracranial pressure (ICP), cerebral blood flow (CBF), and the cerebrospinal fluid (CSF) formation rate were examined in anesthetized cats during ammonia intoxication. Hyperammonemia, evoked by intravenous infusion of ammonium acetate, caused a significant increase in ICP when the arterial blood ammonia level exceeded 400 µmol ⋅ liter−1. A progressive elevation of blood ammonia concentration was followed by a gradual rise in CBF, measured by the xenon-133 clearance technique. At an arterial blood ammonia level exceeding 500 µmol ⋅ liter−1, the CBF reached a plateau at 30% above the mean control value. Increase in ICP correlated weakly, but significantly, with the increase in CBF (R = 0.489, p < 0.005). Elevation of the arterial blood ammonia level to 780.4 ± 25.5 µmol ⋅ liter−1 for 2 hours elicited a significant gradual increase in CSF formation rate, measured by the ventriculocisternal perfusion method with iodine-125-albumin as an indicator substance. A maximum increase in CSF flow of 81% was noted at the end of the ammonium acetate infusion. It is suggested that hyperammonemia increases ICP both by cerebral vasodilatation and by enhancement of the CSF formation rate.

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