scholarly journals STUDIES ON THE SUPRARENAL CORTEX

1933 ◽  
Vol 58 (1) ◽  
pp. 1-16 ◽  
Author(s):  
George A. Harrop ◽  
Albert Weinstein ◽  
Louis J. Soffer ◽  
John H. Trescher
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Gastrointestinal Tract ◽  
Respiratory Quotient ◽  
Capillary Permeability ◽  
Fatal Outcome ◽  
Arterial Blood

1. The basal oxygen consumption, respiratory quotient, blood flow, blood pressure, and the changes in concentration of the arterial blood were determined in suprarenalectomized dogs (a) when receiving injections of cortical extract (Swingle-Pfiffner), (b) during suprarenal insufficiency induced by withdrawal of the injections, and (c) during the period of recovery brought about by resumption of extract injections. 2. Reasons are advanced for the view that the hemoconcentration which occurs is probably due to loss of fluid through the kidneys, rather than by increased capillary permeability and loss into the tissues, or by loss through the gastrointestinal tract. 3. The loss of fluid from the plasma and tissues will explain the symptoms which follow withdrawal of injections of the hormone, as well as the fatal outcome. The assumption that the suprarenal cortex or its hormone has a detoxifying action upon some product of metabolism is thus rendered unnecessary.

Effects of nicotine on canine intestinal blood flow and oxygen consumption

1984 ◽  
Vol 246 (2) ◽  
pp. G195-G203
Author(s):  
R. H. Gallavan ◽  
Y. Tsuchiya ◽  
E. D. Jacobson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Muscle Tension ◽  
Intestinal Blood Flow ◽  
Mesenteric Blood Flow ◽  
State Response ◽  
Arterial Blood ◽  
Intestinal Circulation

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.

Oxygen consumption and blood flow in the hypothermic, perfused kidney

1959 ◽  
Vol 197 (5) ◽  
pp. 1111-1114 ◽  
Author(s):  
Matthew N. Levy
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Blood Viscosity ◽  
The Body ◽  
Peripheral Artery ◽  
Isolated Kidney ◽  
Arterial Blood ◽  
Oxygen Difference ◽  
Appreciable Reduction

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.

Circulatory effects of acute or chronic endotoxemia in rats

1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee
Keyword(s):  
Escherichia Coli ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gastrointestinal Tract ◽  
Peripheral Resistance ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Flow Changes ◽  
Fractional Distribution

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.

Effect of Arteriovenous Fistula on Mean Arterial Blood Pressure, Coronary Blood Flow, Cardiac Output, Oxygen Consumption, Work and Efficiency

1958 ◽  
Vol 193 (1) ◽  
pp. 147-150 ◽  
Author(s):  
René Wégria ◽  
J. Nakano ◽  
J. C. McGiff ◽  
D. F. Rochester ◽  
M. R. Blumenthal ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Arterial Blood Pressure ◽  
Coronary Blood Flow ◽  
Mean Arterial Blood Pressure ◽  
Arteriovenous Fistulae ◽  
Arterial Blood ◽  
The Mean

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.

Role of hypotension in decreasing cerebral blood flow in porcine endotoxemia

1987 ◽  
Vol 253 (4) ◽  
pp. H956-H964 ◽  
Author(s):  
C. F. Miller ◽  
M. J. Breslow ◽  
R. M. Shapiro ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Brain Stem ◽  
Lower Limit ◽  
Cerebral Autoregulation ◽  
Base Line ◽  
Arterial Blood

The role of reduced arterial blood pressure (MAP) in decreasing cerebral blood flow (CBF) during endotoxemia was studied in pentobarbital-anesthetized pigs. Microspheres (15 microns diam) were used to measure regional CBF changes during MAP manipulations in animals with and without endotoxin. Endotoxin (0.2 mg/kg iv) decreased MAP to 50 mmHg and decreased blood flow to the cortex and cerebellum without affecting cerebral cortical oxygen consumption (CMRO2). Elevating MAP from 50 to 70 mmHg during endotoxemia with norepinephrine (1.82 +/- 0.58 micrograms . kg-1 . min-1, iv) did not change cortical blood flow or CMRO2 but increased cerebellar blood flow. Brain stem blood flow was not affected by endotoxin or norepinephrine. When MAP was decreased to 50 mmHg by hemorrhage without endotoxin, no change in blood flow to cortex, cerebellum, or brain stem was observed from base-line levels. These results suggest that decreased MAP below a lower limit for cerebral autoregulation does not account for the decreased CBF observed after endotoxin.

Fetal myocardial oxygen and carbohydrate consumption during acutely induced hypoxemia

1982 ◽  
Vol 242 (4) ◽  
pp. H657-H661 ◽  
Author(s):  
D. J. Fisher ◽  
M. A. Heymann ◽  
A. M. Rudolph
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Cardiac Work ◽  
Arterial Blood ◽  
Lactate And Pyruvate ◽  
Arteriovenous Difference

Two days after catheter placement we measured the heart rate, arterial blood pressure, myocardial blood flow, and the myocardial consumption of oxygen, glucose, lactate, and pyruvate in 11 fetal sheep in utero. We then administered 8-10% oxygen to the ewe, producing a 50% decrease in oxygen content in the fetal ascending aortic blood. After 15 min of hypoxemia we repeated the measurements. Oxygen content in the fetal coronary sinus blood decreased significantly, but the arteriovenous difference of oxygen across the left ventricle also decreased during hypoxemia. Fetal myocardial blood flow increased 160% above the control level, and the myocardial oxygen consumption did not change. The systolic arterial blood pressure increased and the heart rate decreased, but cardiac work, as estimated by the rate-pressure product, was unchanged. As both fetal myocardial oxygen consumption and cardiac work did not change, myocardial oxygenation, the relationship between oxygen consumption and cardiac work, appears to be unchanged during this degree of hypoxemia. Although arterial blood glucose, lactate, and pyruvate concentrations increased significantly during hypoxemia, only the myocardial consumption of pyruvate increased; the arteriovenous difference of glucose and lactate decreased in proportion to the increase in myocardial blood flow. During hypoxemia, glucose consumption did not change, and lactate continued to be consumed rather than produced; thus it is apparent that fetal myocardial metabolism continued to be aerobic during this degree of hypoxemia. Complete oxidative combustion of the quantities of carbohydrates that were consumed would supply all of the substrate necessary to meet fetal myocardial energy demands both at rest and during hypoxemia.

Cerebral blood flow is reduced by N omega-nitro-L-arginine methyl ester during delayed hypoperfusion in cats

1994 ◽  
Vol 267 (1) ◽  
pp. H174-H181
Author(s):  
N. Clavier ◽  
J. R. Kirsch ◽  
P. D. Hurn ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Methyl Ester ◽  
Cerebral Oxygen ◽  
Physiological Variables ◽  
Arterial Blood ◽  
Subclavian Artery Occlusion ◽  
Cerebral Oxygen Consumption

We tested the hypothesis that decreased tonic release of nitric oxide (NO) or a NO-containing compound, during postischemic delayed hypoperfusion, would result in an impaired response of cerebral blood flow (CBF) to NO synthase inhibition. We measured CBF (microspheres), cerebral oxygen consumption, and physiological variables in 30 halothane-anesthetized cats. In 12 animals, complete cerebral ischemia (verified by midischemic CBF measurement) was produced for 12 min by brachiocephalic and left subclavian artery occlusion with hemorrhagic hypotension (mean arterial blood pressure = 40 mmHg). Steady-state hypoperfusion was present by 120 min of reperfusion (30 +/- 4% of baseline). Nonischemic animals (n = 12) were submitted to the same surgical procedures and anesthetic duration. N omega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv) or saline was administered 160 min after baseline measurements, equivalent to 140 min of reperfusion for animals treated with ischemia (n = 6 in each group). Blood pressure was controlled (aortic ligature) so that there was no change following L-NAME administration both in the ischemic and nonischemic groups. L-NAME reduced CBF during reperfusion in ischemic animals (from 37 +/- 2 to 24 +/- 2 ml.min-1 x 100 g-1) and in nonischemic animals (from 122 +/- 15 to 68 +/- 8 ml.min-1 x 100 g-1) with no change in cerebral oxygen consumption. In six additional cats, administration of L-arginine (250 mg/kg iv) reversed the effect of L-NAME. We conclude that tonic NO-mediated cerebral vasodilation occurs following transient global ischemia despite delayed hypoperfusion.

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