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.

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.

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.

Renal Response to Nonshocking Hemorrhage: the Role of Intrarenal Shunts

1958 ◽  
Vol 193 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Allan V. N. Goodyer ◽  
Louis R. Mattie ◽  
Allen Chetrick
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Body Weight ◽  
Arterial Pressure ◽  
The Body ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Renal Innervation ◽  
Aortic Obstruction

In anesthetized dogs, bleeding (1.5–3% of the body weight) was allowed while renal arterial pressure was maintained at constant levels by graded changes of mechanical aortic obstruction. The renal hematocrit decreased, (as measured with I131 albumin and acid hematin, and as compared to the blood hematocrit), primarily as a result of an increased renal plasma volume. These changes are correlated with previously identified alterations of sodium excretion, all independent of renal innervation or arterial blood pressure. It is proposed that hemorrhage may involve an intrarenal redistribution of blood flow favoring diversion of plasma to cell-poor capillaries or to lymphatic spaces.

Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose

1993 ◽  
Vol 264 (4) ◽  
pp. E504-E513 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
The Body ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Co2 Production ◽  
Arterial Blood ◽  
Splanchnic Oxygen

The contribution of the splanchnic tissues to the initial 2-h rise in whole body energy expenditure after ingestion of glucose or fructose was examined in healthy subjects. Indirect calorimetry and catheter techniques were employed to determine pulmonary gas exchange, cardiac output, splanchnic blood flow, splanchnic oxygen uptake, and blood temperatures before and for 2 h after ingestion of 75 g of either fructose or glucose in water solution or of water only. Fructose ingestion was found to increase total oxygen uptake by an average of 9.5% above basal levels; the corresponding increase for glucose was 8.8% and for water only 2.5%. The respiratory exchange ratio increased from 0.84 in the basal state to 0.97 at 45 min after fructose ingestion and rose gradually after glucose to 0.86 after 120 min. The average 2-h thermic effect, expressed as percent of ingested energy, was 5.0% for fructose and 3.7% for glucose (not significant). Splanchnic oxygen consumption did not increase measurably after ingestion of either fructose or glucose. The arterial concentration of lactate rose, arterial pH fell, and PCO2 remained essentially unchanged after fructose ingestion. Glucose, but not fructose, elicited increases in cardiac output (28%) and splanchnic blood flow (56%). Fructose, but not glucose, increased arterial blood temperature significantly. It is concluded that both fructose and glucose-induced thermogenesis occurs exclusively in extrasplanchnic tissues. Compared with glucose, fructose ingestion is accompanied by a more marked rise in CO2 production, possibly reflecting an increased extrasplanchnic oxidation of lactate and an accumulation of heat in the body.

Paradoxical hypotension following increased hematocrit and blood viscosity

2005 ◽  
Vol 289 (5) ◽  
pp. H2136-H2143 ◽  
Author(s):  
Judith Martini ◽  
Benoît Carpentier ◽  
Adolfo Chávez Negrete ◽  
John A. Frangos ◽  
Marcos Intaglietta
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Viscosity ◽  
Exchange Transfusion ◽  
Vessel Diameter ◽  
No Production ◽  
Packed Red Blood Cells ◽  
Arterial Blood ◽  
Nos Inhibitor ◽  
Window Chamber

Hematocrit (Hct) of awake hamsters and CD-1 mice was acutely increased by isovolemic exchange transfusion of packed red blood cells (RBCs) to assess the relation between Hct and blood pressure. Increasing Hct 7–13% of baseline decreased mean arterial blood pressure (MAP) by 13 mmHg. Increasing Hct above 19% reversed this trend and caused MAP to rise above baseline. This relationship is described by a parabolic function ( R2 = 0.57 and P < 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) and endothelial NOS-deficient mice showed no change in MAP when Hct was increased by <19%. Nitrate/nitrite plasma levels of Hct-augmented hamsters increased relative to control and l-NAME treated animals. The blood pressure effect was stable 2 h after exchange transfusion. These findings suggest that increasing Hct increases blood viscosity, shear stress, and NO production, leading to vasodilation and mild hypotension. This was corroborated by measuring A1 arteriolar diameters (55.0 ± 21.5 μm) and blood flow in the hamster window chamber preparation, which showed statistically significant increased vessel diameter (1.04 ± 0.1 relative to baseline) and microcirculatory blood flow (1.39 ± 0.68 relative to baseline) after exchange transfusion with packed RBCs. Larger increases of Hct (>19% of baseline) led blood viscosity to increase >50%, overwhelming the NO effect through a significant viscosity-dependent increase in vascular resistance, causing MAP to rise above baseline values.

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.

5. Blood pressure and blood flow

2016 ◽  
pp. 83-102
Author(s):  
Chris Cooper
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Driving Force ◽  
Beta Blockers ◽  
Venous Blood ◽  
The Body ◽  
Chronic Hypertension ◽  
Arterial Blood ◽  
Lifestyle Choices

The heart is the organ that pumps blood around the body. If the heart stops functioning, blood does not flow. The driving force for this flow is the pressure difference between the arterial blood leaving the heart and the returning venous blood. ‘Blood pressure and blood flow’ first considers how blood pressure is measured and how blood pressure can affect health. High blood pressure is called hypertension and low blood pressure hypotension. Chronic hypertension has serious long-term adverse health consequences, but can be treated with improved lifestyle choices and a range of medicines, including anti-hypertensive drugs, beta blockers, and ACE inhibitor drugs. The different molecules affecting blood flow are also considered.

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.

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