Experimentally induced variations in canine gastric blood flow and its distribution

1965 ◽  
Vol 208 (2) ◽  
pp. 353-358 ◽  
Author(s):  
John P. Delaney ◽  
Eugene Grim

Total gastric blood flow and its distribution between antrum and corpus, and to the mucosa, submucosa, and muscularis of the corpus were measured in dogs under the influence of several agents known to affect gastric secretion. Histamine, infused intravenously or administered chronically in beeswax intramuscularly, produced increases in cardiac output, the fraction of the output going to the stomach and, hence, gastric tissue perfusion Epinephrine infusions also caused significant increases in cardiac output and gastric perfusion. Norepinephrine was the only agent that raised gastric vascular resistance; despite an increase in cardiac output, blood flow to the stomach fell. Neither intravenous secretin nor inspired 10% CO2 affected gastric perfusion. All agents except histamine increased the antrum/corpus perfusion ratio. Only norepinephrine altered the distribution of flow to the several tissues of the corpus; it caused a shift of flow from mucosa to muscle. The results provide no support for the frequently stated conclusion that gastric blood flow and secretion are closely related.

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 918-921
Author(s):  
Frans J. Walther ◽  
Paul Y. K. Wu ◽  
Bijan Siassi

Phototherapy is known to increase peripheral blood flow in neonates, but information on the associated cardiovascular effects is not available. Using pulsed Doppler echocardiography we evaluated cardiac output and stroke volume in 12 preterm and 13 term neonates during and after phototherapy. We concomitantly measured arterial limb blood flow by strain gauge plethysmography and skin blood flow by photoplethysmography. Cardiac output decreased by 6% due to reduced stroke volume during phototherapy, whereas total limb blood flow and skin blood flow increased by 38% and 41%, respectively. Peripheral blood flow increments tended to be higher in the preterm than in the term infants. The reduced stroke volume during phototherapy may be an expression of reduced activity of the newborn during phototherapy. For healthy neonates the reduction in cardiac output is minimal, but for sick infants with reduced cardiac output, this reduction may further aggravate the decrease in tissue perfusion.


1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.


1998 ◽  
Vol 275 (2) ◽  
pp. H680-H688 ◽  
Author(s):  
Linda Keyes ◽  
David M. Rodman ◽  
Douglas Curran-Everett ◽  
Kenneth Morris ◽  
Lorna G. Moore

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the [Formula: see text]channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) ( n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that [Formula: see text] channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments[Formula: see text] channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased[Formula: see text] channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.


1975 ◽  
Vol 79 (2) ◽  
pp. 337-350 ◽  
Author(s):  
Per Olof Janson ◽  
Ivan Albrecht ◽  
Kurt Ahrén

ABSTRACT In the search for data supporting the hypothesis that the luteolytic effect of prostaglandins (PG) is initiated by a vascular mechanism, some haemodynamic parameters including ovarian blood flow and vascular resistance were measured in pseudopregnant anaesthetized rabbits before and after exogenous administration of PGF2α. The measurements were performed on days 5–10 of pseudopregnancy induced by 500 IU HCG iv. Infusion of 50 μg/kg PGF2α iv over a one-minute period caused significant falls in cardiac output, heart rate and blood pressure after 1–3 min. Blood pressure and cardiac output were normalized after 16–49 min. Blood flow in the ovarian vein (direct measurements) decreased and returned to initial values parallel to the blood pressure and no change in resistance in the vascular bed drained by the vein was noted. Total ovarian blood flow and resistance, as measured in surgically intact ovaries before and after PG infusion, using 35 or 15 μm 169Yb and 46Sc-labelled microspheres, changed and remained constant respectively, according to the same pattern as in the direct measurements. The distribution of blood flow between the corpora lutea and the interstitial tissue of the ovary measured by 15 μm radioactive microspheres. PGF2α caused an interstitial vasodilation whereas no significant change in luteal vascular resistance was noted. Since luteal blood flow represented a predominant part of total ovarian flow in the type of ovary studied, the interstitial vasodilatation caused only negligible changes in blood flow to the whole ovary. The present study does not support the hypothesis of a PG-induced luteal blood flow reduction preceding luteolysis. The possible significance of the interstitial vasodilatation for luteal function remains to be elucidated.


1963 ◽  
Vol 204 (6) ◽  
pp. 1013-1017 ◽  
Author(s):  
Eugene D. Jacobson

The vasoactive properties of three naturally occurring substances which influence gastric secretion were investigated in the gastric vascular bed. A constant flow perfusion of the canine stomach was employed and vascular pressures were recorded in response to a wide range of drug doses. Histamine was found to decrease vascular resistance appreciably in the concentration range 0.01–0.50 µg/ml blood perfusing the stomach. Gastric vascular resistance declined in response to acetylcholine infusion when the concentration exceeded 0.10 µg/ml blood. Norepinephrine increased resistance to blood flow appreciably when perfusion concentration was greater than 0.05 µg/ml blood. It was also found that the responses to histamine and norepinephrine were esssentially the same whether the agents were infused locally or systemically for calculated concentrations in the gastric perfusate. These findings substantiate the concept that gastric secretory stimulants dilate, and that gastric secretory inhibitors constrict the gastric vascular bed.


1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.


1966 ◽  
Vol 164 (1) ◽  
pp. 81-89 ◽  
Author(s):  
ERWIN DOMANIG ◽  
PAUL B. HAIINLOSER ◽  
WORTHINGTON G. SCHENK

Physiology ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 250-253 ◽  
Author(s):  
LB Rowell ◽  
DD Sheriff

Powerful pressure-raising chemoreflexes arise from active skeletal muscle when its blood flow is reduced and metabolites accumulate. Muscle chemoreflexes may be tonically active in moderate but not in mild exercise. When unopposed by baroreflexes, chemoreflexes can correct flow errors by 85 % by raising vascular resistance, cardiac output, and blood pressure.


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