scholarly journals Canine Cerebral Metabolism and Blood Flow during Hypoxemia and Normoxic Recovery from Hypoxemia

1981 ◽  
Vol 1 (3) ◽  
pp. 277-283 ◽  
Author(s):  
Alan A. Artru ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cell Damage ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Oxygen Demand ◽  
Brain Biopsy ◽  
Brain Cell ◽  
Blood Oxygen ◽  
Sagittal Sinus ◽  
Arterial Blood

There are conflicting reports regarding the effects of hypoxemia on the cerebral metabolic rate for oxygen (CMRO2). Accordingly, we examined the changes in CMRO2 during normoxia, progressive hypoxia (PaO2 of 37, 27, and 23 mm Hg), and normoxic recovery from hypoxia, Measurements were made in dogs anesthetized with nitrous oxide (60–70%) and halothane (<0.1%) in oxygen. Arterial-cerebral venous blood oxygen content differences and cerebral blood flow (CBF) were measured simultaneously, the latter by a technique (collection of sagittal sinus outflow) previously validated for conditions of near-maximal CBF, The duration of each of the three hypoxic exposures was approximately 10 min. CMRO2 was significantly decreased (14%) only when the arterial blood oxygen tension was reduced to 23 mm Hg. CBF increased progressively to a maximum of 153% of control. Posthypoxemic brain biopsy values for cerebral metabolites obtained 40 min after normoxemia had been restored were normal. These results, in conjunction with an unchanged CMRO2 at 40 min normoxic recovery, suggest that no gross irreversible brain cell damage occurred. We conclude that with progressive hypoxemia. CMRO2 remains stable until oxygen demand exceeds oxygen delivery, resulting there after in a progressive reduction in CMRO2.

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.

Altering blood flow does not reveal differences between nitrogen and helium kinetics in brain or in skeletal miracle in sheep

2015 ◽  
Vol 118 (5) ◽  
pp. 586-594 ◽  
Author(s):  
David J. Doolette ◽  
Richard N. Upton ◽  
Cliff Grant
Keyword(s):  
Blood Flow ◽  
Hind Limb ◽  
Femoral Vein ◽  
Venous Blood ◽  
Compartmental Models ◽  
Arterial Blood Gas ◽  
Blood Flows ◽  
Sagittal Sinus ◽  
Oxygen Breathing ◽  
Arterial Blood

In underwater diving, decompression schedules are based on compartmental models of nitrogen and helium tissue kinetics. However, these models are not based on direct measurements of nitrogen and helium kinetics. In isoflurane-anesthetized sheep, nitrogen and helium kinetics in the hind limb ( n = 5) and brain ( n = 5) were determined during helium-oxygen breathing and after return to nitrogen-oxygen breathing. Nitrogen and helium concentrations in arterial, femoral vein, and sagittal sinus blood samples were determined using headspace gas chromatography, and venous blood flows were monitored continuously using ultrasonic Doppler. The experiment was repeated at different states of hind limb blood flow and cerebral blood flow. Using arterial blood gas concentrations and blood flows as input, parameters and model selection criteria of various compartmental models of hind limb and brain were estimated by fitting to the observed venous gas concentrations. In both the hind limb and brain, nitrogen and helium kinetics were best fit by models with multiexponential kinetics. In the brain, there were no differences in nitrogen and helium kinetics. Hind limb models fit separately to the two gases indicated that nitrogen kinetics were slightly faster than helium, but models with the same kinetics for both gases fit the data well. In the hind limb and brain, the blood:tissue exchange of nitrogen is similar to that of helium. On the basis of these results, it is inappropriate to assign substantially different time constants for nitrogen and helium in all compartments in decompression algorithms.

Cerebral blood flow and oxygen consumption in the newborn dog

1978 ◽  
Vol 234 (5) ◽  
pp. R209-R215
Author(s):  
M. J. Hernandez ◽  
R. W. Brennan ◽  
R. C. Vannucci ◽  
G. S. Bowman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Superior Sagittal Sinus ◽  
Venous Blood ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Newborn Brain ◽  
Arterial Blood

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.

Effect of two methods of hand heating on body temperature, forearm blood flow, and deep venous oxygen saturation

1990 ◽  
Vol 259 (5) ◽  
pp. E639-E643 ◽  
Author(s):  
I. W. Gallen ◽  
I. A. Macdonald
Keyword(s):  
Blood Flow ◽  
Body Temperature ◽  
Oxygen Content ◽  
Forearm Blood Flow ◽  
Venous Blood ◽  
Blood Oxygen ◽  
Left Hand ◽  
Venous Oxygen Saturation ◽  
Baseline Values ◽  
Healthy Females

Two methods of hand heating [warmed blanket 40 degrees C (WB) and warm-air box 55 degrees C (WA)] were compared with the effect of no heating (control) in six healthy females. After 30 min baseline, the left hand was either heated for 1 h or not heated. Measurements were made of skin temperature (ST), core temperature (CT), right forearm (FBF) and skin blood flow (SBF), and right forearm deep venous blood oxygen content with and without occlusion of the hand circulation. CT rose above baseline in WB (by +0.2 degrees C, P less than 0.01) but not with control or WA. Abdominal ST rose only with WB (by +0.66 degrees C above baseline, P less than 0.01). FBF increased above baseline values with both WA (by +10 ml.l forearm-1.min-1) and WB (by +12 ml.l forearm-1.min-1), but neither was significantly greater than the control. SBF increased above baseline only with WB (by +202 mV, P less than 0.01), and this was significantly greater than control SBF. With an occluded hand circulation, deep venous oxygen content rose above baseline values with WB only (+6.0%, P less than 0.01) but was not greater than control with either method of hand heating. We conclude that using a warm-air box has less effect than a heated blanket on the measured variables.

A field versus laboratory study of blood oxygen status in normoxic crabs at different temperatures

1996 ◽  
Vol 74 (3) ◽  
pp. 423-430 ◽  
Author(s):  
J.-C. Massabuau ◽  
J. Forgue
Keyword(s):  
Wide Spectrum ◽  
Venous Blood ◽  
Carcinus Maenas ◽  
Blood Oxygen ◽  
Arterial Blood ◽  
Field Versus ◽  
Partial Pressures ◽  
Different Temperatures ◽  
Head Pressure ◽  
Oxygen Status

The blood oxygen status of two species of active crabs (Carcinus maenas and Necora puber) was studied in the field and compared with the results of previous laboratory experiments performed on a wide spectrum of physiologically different water-breathers. The aim was to determine whether, as in the laboratory, the functioning of the O2 supply system in the field could be based on maintaining the arterial [Formula: see text] in the low range, 1–3 kPa. The O2 partial pressures and concentrations in the arterial and venous blood, arterial blood pH, and blood respiratory pigment concentration were measured in normoxic water at various temperatures ranging from 10 to 20 °C and in various seasons. In the field, [Formula: see text] values in normoxic C. maenas and N. puber were in the low range, 1–3 kPa, independently of temperature, season, and blood haemocyanin concentration. It is concluded that in the field as in the laboratory, [Formula: see text] values mainly in the low range provide a head pressure sufficient to meet O2 needs. The changes that appear to occur in other respiratory variables are discussed in relation to field versus laboratory conditions and temperature differences. The consequences for analysing problems of hypoxaemia in hypoxic waters or situations are discussed.

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Venous Blood ◽  
Reference Sample ◽  
Venous Hypertension ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Systemic and hepatic hemodynamic changes in acute liver injury

1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Venous Blood ◽  
Marked Change ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Subsequent Increase ◽  
Arterial Blood

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

Adrenal catecholamines in E. coli endotoxin shock

1961 ◽  
Vol 16 (2) ◽  
pp. 348-350 ◽  
Author(s):  
Florian Nykiel ◽  
Vincent V. Glaviano
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
Endotoxin Shock ◽  
Mean Blood Pressure ◽  
E Coli ◽  
Arterial Blood ◽  
Splanchnic Nerves

In dogs with left adrenal cannulation, administration of 1 mg/kg of purified E. coli endotoxin resulted in a decrease in mean blood pressure and adrenal blood flow. These changes were accompanied by significant increases in levels of epinephrine in adrenal venous blood. Release of epinephrine by the adrenals in endotoxin shock was due to a neurogenic mechanism, since sectioning of the splanchnic nerves prevented secretion of epinephrine. The rise in epinephrine output from an intact adrenal was noted to occur only in the presence of a significant decrease in arterial blood pressure; therefore endotoxin causes adrenal stimulation from reflexes initiated by the hypothalamus or peripheral baroreceptors. Submitted on September 20, 1960

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.

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