Effects of Dopamine and Other Catecholamines on the Splanchnic Circulation

1972 ◽  
Vol 50 (6) ◽  
pp. 594-602 ◽  
Author(s):  
Linda L. Shanbour ◽  
Don Parker
Keyword(s):  
Blood Flow ◽  
Hepatic Artery ◽  
Mesenteric Artery ◽  
Splanchnic Circulation ◽  
Blood Flows ◽  
Vascular Bed ◽  
Competitive Action ◽  
Responses To Dopamine ◽  
Mesenteric Vascular Bed ◽  
Dose Levels

Studies were conducted to evaluate the effects of dopamine (3, 4-dihydroxyphenylethylamine) and other catecholamines on the mesenteric vascular bed in dogs. Mesenteric and hepatic artery blood flows were measured with electromagnetic blood flow transducers. Catecholamines were infused intra-arterially into a branch-of the mesenteric artery. Dopamine consistently decreased mesenteric and hepatic artery blood flows at all dose levels studied (5–100 mg/kg). Phenoxybenzamine (12.5 mg/kg) blocked the effects of norepinephrine (0.05–1.0 μg/kg) and reversed the responses to dopamine in the mesenteric bed to those of pure vasodilation (no transient constriction was observed) but failed to abolish the constrictor action of dopamine on the hepatic artery. Propranolol or haloperidol, when administered with the phenoxybenzamine, did not attenuate the mesenteric responses to dopamine. Haloperidol prevented the hepatic artery vasoconstriction produced by dopamine but did not alter isoproterenol-induced hepatic artery vasodilation. No competitive action was observed between dopamine and norepinephrine or isoproterenol. These results suggest that (1) dopamine produces selective vasodilation of the mesenteric bed which is not blocked by haloperidol, and (2) dopamine has a unique action on the hepatic vascular bed which is blocked by haloperidol.

Effects of prostaglandins E1, E2, and F2alpha on uterine blood flow in nonpregnant sheep

1978 ◽  
Vol 234 (5) ◽  
pp. H557-H561 ◽  
Author(s):  
R. Resnik ◽  
G. W. Brink
Keyword(s):  
Blood Flow ◽  
Base Line ◽  
Uterine Blood Flow ◽  
Electromagnetic Flow ◽  
Blood Flows ◽  
Vascular Bed ◽  
Uterine Contractile ◽  
Vasodilating Activity

The effects of prostaglandins E1, E2, and F2alpha (PGE1, PGE2, and PGE2alpha, respectively) on uterine blood flow were investigated in chronically catheterized, nonpregnant sheep equipped with electromagnetic flow probes. PGE1 was found to be a potent dilator of the uterine vascular bed and, at initial arterial concentratios of 1.5 micron (500 ng/ml), produced peak uterine blood flows similar to those achieved by a pulsed dose of 1 microgram 17beta-estradiol; PGE2 had less active vasodilating activity. Conversely, uterine intra-arterial PGF2alpha infusions, which produced initial concentrations of 0.1 micron (50 ng/ml), promptly reduced peak estrogen-stimulated uterine blood flow by 60%. All prostaglandin infusions stimulated increases in uterine contractile frequency and base-line tone. The findings demonstrate the sensitivity of the nonpregnant sheep uterine vasculature to prostaglandins.

Effects of Intraabdominanlly Insufflated Carbon Dioxide and Elevated Intraabdominal Pressure on Splanchnic Circulation 

1998 ◽  
Vol 89 (2) ◽  
pp. 475-482 ◽  
Author(s):  
Manfred Blobner ◽  
Ralph Bogdanski ◽  
Eberhard Kochs ◽  
Julia Henke ◽  
Alexander Findeis ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Splanchnic Circulation ◽  
Arterial Blood Flow ◽  
Intraabdominal Pressure ◽  
Arterial Blood ◽  
Baseline Values ◽  
Air Insufflation

Background Intraabdominally insufflated carbon dioxide (CO2) during laparoscopy may have a specific effect on splanchnic circulation that may be unrelated to the effects of increased intraabdominal pressure alone. Therefore, the influences of insufflation with CO2 versus air on splanchnic circulation were compared. Methods Pigs were chronically instrumented for continuous recording of mesenteric artery, portal venous, inferior vena cava, and pulmonary arterial blood flow and portal venous pressure. After induction of anesthesia, CO2 or air was insufflated in 14 and 10 pigs, respectively. With the pigs in the supine position, intraabdominal pressure was increased in steps of 4 mmHg up to 24 mmHg by graded gas insufflation. Results During air insufflation, mesenteric artery vascular resistance was unchanged, whereas mesenteric arterial blood flow decreased with increasing intraabdominal pressure. Shortly after CO2 insufflation to an intraabdominal pressure of 4 mmHg, mean arterial pressure, mesenteric arterial blood flow, and mesenteric arterial vascular resistance were increased by 21%, 12% and 9%, respectively. Subsequently, with the onset of CO2 resorption in the third minute, mean arterial pressure declined to baseline values and mesenteric arterial vascular resistance declined to 85% of baseline values, whereas mesenteric arterial blood flow continued to increase to a maximum of 24% higher than baseline values. At steady-state conditions during CO2 insufflation, mesenteric arterial blood flow was increased up to an intraabdominal pressure 16 mmHg but decreased at higher intraabdominal pressures. Conclusions In contrast to air insufflation, intraabdominal insufflation of CO2 resulted in a moderate splanchnic hyperemia at an intraabdominal pressure < or = 12 mmHg. At higher intraabdominal pressure values, pressure-induced changes became more important than the type of gas used.

Fasting and post-prandial splanchnic blood flow is reduced by a somatostatin analogue (octreotide) in man

1991 ◽  
Vol 81 (2) ◽  
pp. 169-175 ◽  
Author(s):  
A. M. Cooper ◽  
G. D. Braatvedt ◽  
M. I. Qamar ◽  
H. Brown ◽  
D. M. Thomas ◽  
...  
Keyword(s):  
Blood Flow ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Venous Blood ◽  
Splanchnic Blood Flow ◽  
Somatostatin Analogue ◽  
Venous Blood Flow ◽  
Blood Flows ◽  
Portal Venous Blood ◽  
Mesenteric Artery Blood Flow

1. The effects of the subcutaneous administration of a long-acting somatostatin analogue (octreotide) or of placebo on the splanchnic blood flow response to a mixed solid meal has been examined in eight normal subjects by using a transcutaneous Doppler ultrasound technique. Each subject was studied on two occasions more than 1 week apart. 2. On the control day, feeding had a pronounced effect on both superior mesenteric artery and portal venous blood flows, causing a peak rise of 82% in superior mesenteric artery blood flow at 15 min and of 75% in portal venous blood flow at 30 min post-prandially (P < 0.001). Blood flows remained elevated 2 h after the meal. Pulse and blood pressure showed no significant changes from baseline. 3. Octreotide reduced fasting superior mesenteric artery blood flow by 59% (P < 0.05) and portal venous blood flow by 49% (P < 0.01) and blunted the normal post-prandial rise. Pulse and blood pressure did not change in response to either the injection or the ingestion of the meal. 4. Octreotide suppressed the release of insulin, glucagon and pancreatic polypeptide in response to feeding and resulted in post-prandial hyperglycaemia. 5. The mechanism of action of octreotide on splanchnic blood flow is uncertain. It may be mediated via a direct vascular effect or it may act via suppression of vasoactive intestinal hormones.

Vasorelaxant effects of and receptors for atrial natriuretic peptides in the mesenteric artery and aorta of the rat

1988 ◽  
Vol 66 (7) ◽  
pp. 951-956 ◽  
Author(s):  
Jean St-Louis ◽  
Ernesto L. Schiffrin
Keyword(s):  
Natriuretic Peptides ◽  
Mesenteric Artery ◽  
Atrial Natriuretic Peptides ◽  
Binding Assays ◽  
Structural Requirements ◽  
Vascular Bed ◽  
Relaxation Experiments ◽  
Mesenteric Vascular Bed ◽  
Anp Receptors ◽  
Atrial Natriuretic

Vasorelaxant effects of different atrial natriuretic peptides (ANP) were measured on rat aortic strips and mesenteric artery rings. These results were compared with the potency of the same peptides to displace 125I-labelled ANP (101–126) on membrane preparations of aorta and of mesenteric vascular bed. In aortic strips and mesenteric artery rings precontracted with phenylephrine (3 × 10−8 and 10−6 M, respectively), the order of potency of ANP was as follows: ANP (99–126) > ANP (101–126) > ANP (103–126) = ANP(103–125) [Formula: see text] ANP (103–123). In the displacement binding assays, the order of potency of ANP peptides was similar to that of the relaxation experiments: ANP (99–126) = ANP (101–126) > ANP (103–126) = ANP (103–125) [Formula: see text] ANP (103–123). When the vessels were precontracted by a smaller concentration of phenylephrine (10−7 M in mesenteric artery and 10−8 M in aorta), the IC50 of ANP (101–126) was significantly lower than when the higher concentration of phenylephrine was used. These results show that ANP receptors in the mesenteric artery and in the aorta have similar structural requirements, according to the order of potency of different length ANP, both for binding and myotropic responses.

Effects of exercise, hypoxia and feeding on the gastrointestinal blood flow in the Atlantic cod Gadus morhua

1991 ◽  
Vol 158 (1) ◽  
pp. 181-198 ◽  
Author(s):  
M. Axelsson ◽  
R. Fritsche
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Control Mechanisms ◽  
Artery Blood Flow ◽  
Blood Flows ◽  
Mesenteric Artery Blood Flow

Cardiac output, ventral and dorsal aortic blood pressure, heart rate, and coeliac and mesenteric artery blood flow were recorded simultaneously in the Atlantic cod, Gadus morhua L., at rest, during exercise, during hypoxia and after feeding. In the resting unfed animals, coeliac artery blood flow was 4.1 +/− 0.8 ml min-1 kg-1 and mesenteric artery blood flow was 3.5 +/− 1.1 ml min-1 kg-1 (mean +/− S.E.M., N = 10); together, these flows represent approximately 40% of the cardiac output. Exercise or exposure to hypoxia resulted in increased visceral vascular resistance, leading to reductions in the coeliac and mesenteric artery blood flows. Coeliac and mesenteric blood flows were increased 24 h after feeding and the coeliac and systemic vascular resistances decreased in comparison with the prefeeding values. Phentolamine did not affect the gastrointestinal artery blood flow, but produced a significant decrease in the mesenteric and systemic vascular resistance. Treatment with bretylium and phentolamine revealed differences between the coeliac and the mesenteric vasculature regarding the control mechanisms during hypoxia and during exercise and feeding. During hypoxia, an adrenergic control of the gastrointestinal vasculature with both nervous and humoral components was found, whereas during exercise and after feeding an additional non-adrenergic mechanism controlling gut blood flow was demonstrated.

Effects of potassium and ouabain on the vascular reactivity to norepinephrine in the rat mesenteric artery

1979 ◽  
Vol 57 (8) ◽  
pp. 908-912 ◽  
Author(s):  
Kazuoki Kondo ◽  
Tetsuji Okuno ◽  
Konosuke Konishi ◽  
Takao Saruta ◽  
Eiichi Kato
Keyword(s):  
Prostaglandin E2 ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Potassium Concentration ◽  
Vascular Wall ◽  
Vascular Response ◽  
Vascular Bed ◽  
Rat Mesenteric Artery ◽  
Low Potassium ◽  
Mesenteric Vascular Bed

In the perfused rat mesenteric vascular bed, the effects of potassium and ouabain on the vascular response to norepinephrine were studied. Neither changing the concentration of potassium (1.9 to 7.9 mM) nor adding ouabain (8.6 × 10−7 to 2.2 × 10−4 M) to the perfusate changed the basal pressure. A slight increase in the potassium concentration in the perfusate attenuated the vascular response to norepinephrine, and a slight decrease in the potassium concentration potentiated this response. Ouabain in the perfusate potentiated the vascular response to norepinephrine in a dose-related manner. The effect of potassium on the vascular response was inhibited in the presence of ouabain. In preparations in which vascular reactivity had been abolished by indomethacin and then restored by prostaglandin E2, the effects of potassium and ouabain on the vascular reactivity to norepinephrine were similar to those found in the untreated preparations. These results indicate that a slight change in potassium concentration in the perfusate can affect the vascular response to norepinephrine by changing the activity of a Na+–K+-dependent ATPase. It is also suggested that the potentiating effect of low potassium concentration on the norepinephrine response is, at least in the rat mesenteric vascular bed, not mediated by the synthesis of prostaglandin E2 in the vascular wall.

Role of prostaglandins and nitric oxide in gastrointestinal hyperemia of diabetic rats

1996 ◽  
Vol 270 (4) ◽  
pp. G684-G690 ◽  
Author(s):  
E. Goldin ◽  
M. Casadevall ◽  
M. Mourelle ◽  
I. Cirera ◽  
J. I. Elizalde ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Gastric Mucosa ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Left Gastric Artery ◽  
Diabetic Rats ◽  
Gastric Artery ◽  
Blood Flows ◽  
And Control

The aim of the study was to characterize the gastric and mesenteric vascular changes induced by diabetes and the implication of endothelial [nitric oxide (NO) and prostaglandins] and humoral (glucagon) factors in such changes. Diabetes was induced in rats by a single streptozotocin injection. Four weeks later, gastric mucosa, left gastric artery, and superior mesenteric artery blood flows were measured using hydrogen gas clearance and perivascular ultrasonic flowmeter techniques, respectively, in anesthetized and fasted diabetic and control rats. Blood pressure, hematocrit, blood volume, and blood viscosity were also measured. Left gastric (41 +/- 6 vs. 25 +/- 4 ml.min-1.100 g-1) and superior mesenteric artery blood flows (83 +/- 8 vs. 65 +/- 4 ml.min-1.100 g-1) were significantly higher in diabetic than in control rats. The increased blood flow in the left gastric artery was distributed to a hypertrophic mucosa in diabetic rats; therefore, the blood flow per 100 g tissue in the gastric mucosa was not significantly different in diabetic compared with control rats. Pretreatment with indomethacin reduced both increase gastric and mesenteric flows of the diabetic rats to the same levels as in control rats. NG-nitro-L-arginine methyl ester decreased gastric blood flow in a dose-dependent manner and to a similar extent in diabetic and control rats. In contrast, an increased sensitivity to the higher doses of the NO inhibitor was observed in the mesenteric vascular bed of diabetic rats. Glucagon reduction achieved by somatostatin infusion did not influence either gastric or mesenteric blood flow in diabetic rats. In summary, the present study revealed an increase in gastric and mesenteric arterial blood flows in streptozotocin-induced diabetic rats. The gastrointestinal hyperemia seems to be due, at least in part, to the increased demand of a hypertrophic mucosa and is mediated primarily by endogenous prostaglandins. Increased vascular sensitivity to NO may also contribute to the mesenteric vasodilation.

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