Hydrogen ion concentration and oxygen uptake in an isolated canine hindlimb

1976 ◽  
Vol 40 (1) ◽  
pp. 1-5 ◽  
Author(s):  
A. H. Harken

Oxygen utilization (VO2) and lactate production by an isolated perfused canine hindlimb was evaluated at various hydrogen ion concentrations. A membrane lung perfusion system was established such that blood flow and temperature could be fixed at normal levels. Oxygen, nitrogen, and carbon dioxide (CO2) gas flows to the membrane lung were independently regulated to provide a fixed arterial oxygen content (CaO2). By changing CO2 flow, the pH of the arterial blood was varied between 6.9 and 7.6 at 10-min intervals. The mean O2 delivery (CaO2 X blood flow) was between 16.3 ML O2/min and 20.5 ml O2/min. Standard error of the mean in each dog, however, was less than 0.4 ml O2/min. VO2 was linearly related to the pH of the perfusing blood: VO2% = 100.1 pH - 643 (r = 0.866). Oxygen consumption was inversely related to PCO2: VO2% = -0.62 PCO2 + 124, but the correlation was less good (r = 0.729). Lactate production was linearly related to the pH of the perfusing blood (above a pH of 7.4): lactate produced = 22.5 pH - 162.5 (r = 0.75). At a pH below 7.4, lactate was not produced. Oxygen consumption of skeletal muscle appears critically dependent on extracellular fluid pH. A change in pH of 0.1 alters VO2 almost exactly 10%. Alkalosis is a potent stimulus to lactic acid production by skeletal muscle.

1983 ◽  
Vol 61 (2) ◽  
pp. 178-182 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius–plantaris muscle group was isolated. Cardiac output [Formula: see text], muscle blood flow [Formula: see text], total body and muscle oxygen uptake [Formula: see text] were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle [Formula: see text], [Formula: see text], and [Formula: see text] were increased in both groups at 30 min of anemia. By 60 min, [Formula: see text] and [Formula: see text] declined to preanemic control values in the moderate anemia group; whole body [Formula: see text] was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle [Formula: see text] showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle [Formula: see text] during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle [Formula: see text] response was related to the decrease in arterial oxygen transport.


1981 ◽  
Vol 50 (2) ◽  
pp. 450-455 ◽  
Author(s):  
B. R. Grubb

Birds are known to be much more tolerant than mammals to high altitude [low oxygen pressure (PO2)], and it is therefore of interest to know the responses of their muscles to low oxygen. We studied the influence of hypoxia on the rate of blood flow, oxygen extraction, and oxygen consumption (VO2) in resting hindlimb muscle of ducks. We found that during normoxia the VO2 in this muscle mass was similar to resting mammalian red muscle. However, blood flow rate (45 ml x 100 g-1 x min-1) and venous PO2 (70 Torr) were much higher than in resting red or white mammalian muscle. Hypoxia down to 35-40 Torr resulted in no change in blood flow, but oxygen extraction increased dramatically as arterial PO2 fell below 70 Torr. The resting VO2 was maintained even at the lowest arterial oxygen content (5 ml/100 ml). From these experiments it appears as though duck skeletal muscle has a "luxuriant" resting blood flow rate that is sufficient to supply skeletal muscle with adequate oxygen.


1990 ◽  
Vol 258 (6) ◽  
pp. H1856-H1864
Author(s):  
D. Bernstein ◽  
D. F. Teitel

We studied the interrelationships among myocardial oxygenation, cardiac output, and systemic oxygenation during acute progressive hypoxemia in the paralyzed and mechanically ventilated lamb. Fractional inspired concentration of oxygen was reduced in five steps to a minimum of 0.05, decreasing arterial oxygen content (CaO2) from 10.9 +/- 2.4 to 2.8 +/- 0.5 ml/dl. Heart rate and stroke volume did not change at any step so that systemic oxygen transport decreased with CaO2. Systemic oxygen consumption fell at CaO2 less than 6 ml/dl. Left ventricular blood flow at maximal hypoxemia increased 277% (249 +/- 27 to 938 +/- 118 ml.min-1.100 g-1) so that left ventricular oxygen delivery and oxygen consumption were maintained. Evidence of anaerobic metabolism occurred when CaO2 was less than four (increase in arterial lactate and hypoxanthine), whereas at this level there was no evidence of inadequate myocardial oxygenation as determined by normal subepicardial: subendocardial blood flow and absence of net lactate production, although coronary sinus PO2 decreased. Although myocardial, cerebral, and adrenal blood flows increased, there was no redistribution of blood flow away from the viscera and skin.


1958 ◽  
Vol 193 (1) ◽  
pp. 147-150 ◽  
Author(s):  
René Wégria ◽  
J. Nakano ◽  
J. C. McGiff ◽  
D. F. Rochester ◽  
M. R. Blumenthal ◽  
...  

In the anesthetized dog, acute arteriovenous fistulae sufficient to increase the cardiac output by from 16 to 130% resulted in an increase in the coronary blood flow even in the presence of a definite and even marked drop in the mean arterial blood pressure. The arteriovenous fistulae also resulted in an increase of the cardiac work and oxygen consumption as well as the cardiac efficiency.


1984 ◽  
Vol 246 (2) ◽  
pp. G195-G203
Author(s):  
R. H. Gallavan ◽  
Y. Tsuchiya ◽  
E. D. Jacobson

The purpose of this study was to determine the effects of nicotine on intestinal blood flow and oxygen consumption. The intravenous infusion of nicotine at doses corresponding to those experienced by smokers produced a transient increase in systemic arterial blood pressure and mesenteric blood flow. Subsequently a steady-state response developed that consisted of a reduction in mesenteric blood flow due to both a decrease in blood pressure and an increase in intestinal vascular resistance. This increase in resistance was probably due to increased levels of circulating catecholamines. The intra-arterial infusion of nicotine into the intestinal circulation at doses experienced by the average smoker had no effect on either intestinal blood flow or oxygen consumption. Similarly, under in vitro conditions nicotine had no direct effect on intestinal vascular smooth muscle tension. Thus, nicotine appears to reduce intestinal blood flow indirectly as a result of its systemic effects.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Nicolas Polge ◽  
fanny lidouren ◽  
Matthias Kohlhauer ◽  
...  

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined. Hypothesis: We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75 vs 80-90 mmHg) in a porcine model of E-CPR. Methods: Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75 vs 80-90 mmHg, respectively). Animals were followed during 120 min after ROSC. Results: Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8 vs 54±6 L O 2 /min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP. Conclusion: Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR. Figure: Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)


1977 ◽  
Vol 43 (2) ◽  
pp. 204-210 ◽  
Author(s):  
A. Capderou ◽  
J. Polianski ◽  
J. Mensch-Dechene ◽  
L. Drouet ◽  
G. Antezana ◽  
...  

An impairment of gluconeogenesis has been proposed to explain the low arterial blood glucose of highlanders. Therefore, we studied splanchnic blood flow, splanchnic uptake of oxygen and lactate, and output of glucose in nine normal and six anemic highlanders at an altitude of 3,750 m. Splanchnic blood flow, arteriovenous difference for oxygen, and oxygen consumption were comparable at rest in both groups and in lowlanders from the literature, whereas splanchnic output of glucose, and uptake of lactate were approximately twice those in lowlanders. After 10 min of mild exercise in 12 subjects (7 normals, 5 anemic), no significant changes in splanchnic hemodynamics and metabolism were found. During 29% oxygen breathing in 8 subjects (5 normals, 3 anemics), arterial lactate, splanchnic uptake of lactate and output of glucose fell to normal sea-level values. We concluded that splanchnic hemodynamics are similar in adapted highlanders and in lowlanders, and that there is no evidence of an impaired gluconeogenesis at the altitude of the present study.


1959 ◽  
Vol 197 (5) ◽  
pp. 1111-1114 ◽  
Author(s):  
Matthew N. Levy

Temperature was diminished in a stepwise fashion in the isolated kidney of the dog perfused from a peripheral artery of the original, normothermic animal. Decreased temperature resulted in an appreciable reduction of renal blood flow at constant arterial blood pressure. Increased blood viscosity and vasoconstriction were both responsible for this reduction of flow. Hypothermia also resulted in a reduction in arteriovenous oxygen difference which was roughly proportional to the centigrade temperature. Furthermore, hypothermia exerted a marked but reversible depression of the rate of oxidative metabolism. This effect was relatively more severe than the changes for the body as a whole at equivalent temperatures reported by other investigators.


1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.


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