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At least 19 recordsLinked to original sources
PubMed1990

Experimental studies on the interrelationship between organs mediated by peptide YY: effect on splanchnic circulation and exocrine pancreas in dogs.

Peptide YY (PYY) which is most likely to mediate colonic inhibition on digestive organs is also a potent vasoconstrictor. However, very little is known about the effect of circulating PYY on splanchnic blood flow. This study examined the effect of systemic administration of peptide YY on splanchnic circulation and exocrine pancreas in dogs. Under secretin stimulation, intravenous administration of PYY (0.1, 0.5, 1 and 2 micrograms/kg) significantly decreased pancreatic secretion volume and blood flows in the pancreatic tissue, the superior mesenteric artery and the celiac artery in a dose-related manner. At the same time, PYY increased mean blood pressure. Under secretin plus cholecystokinin stimulation, PYY (1 micrograms/kg) significantly inhibited pancreatic secretion volume and protein output. This study first shows that PYY potently reduces celiac arterial blood flow as well as intestinal blood flow at such doses that PYY inhibits exocrine pancreatic secretion.

Animals↗
PubMed1991

Effects of positive end-expiratory pressure on splanchnic circulation and function in experimental peritonitis.

Splanchnic and central hemodynamic effects of positive end-expiratory pressure (PEEP) were studied in anesthetized pigs using mechanical ventilatory assistance, with or without sepsis (fecal peritonitis). One hour after sepsis, PEEP (10 cm H2O) was applied (n = 6). Another group (n = 6) had sepsis without PEEP. In one group (n = 6) without sepsis, PEEP was applied after 1 hour, while a fourth group (n = 5), without sepsis or PEEP, served as a control. The group with PEEP and sepsis had reduced cardiac index, portal venous blood flow, and liver surface blood flow. The group with PEEP alone had reduced splanchnic circulation by increasing gastrointestinal vascular resistance, while the group with sepsis alone had increased portal vascular resistance. In a separate series with sepsis, intermittent PEEP, and vigorous fluid resuscitation, it was demonstrated that avoiding hypovolemia did not seem to protect from the PEEP effects on the splanchnic circulation. The combination of sepsis and PEEP was not additive on portal blood flow reduction but reduced bile production.

Animals↗
PubMed1979

Effects of enflurane on splanchnic circulation.

A brief summary of the anatomy and physiology of the splanchnic circulation is presented. The influence of 1 MAC enflurane anaesthesia on splanchnic circulation and oxygenation was studied in 10 dogs. Superior mesenteric arterial, portal venous and hepatic arterial blood flows decreased less than mean arterial blood pressure, due to reductions in superior mesenteric arterial, preportal vascular and hepatic arterial resistances. It is suggested that these reactions within the splanchnic circulation are mainly dependent on normal autoregulative responses elicited by the fall in blood pressure. Oxygen consumption of the preportal tissues and the liver was unchanged as a result of increased extraction of oxygen.

Anesthesia, Inhalation↗
PubMed1992

Regional effects and clearance of endothelin-1 across pulmonary and splanchnic circulation.

To determine the impact of i.v. endothelin-1 on systemic, pulmonary and splanchnic circulation, as well as the peptide's regional clearance, hepatic venous and right heart catheterization was performed in healthy volunteers. During the peptide's continuous i.v. administration (0.4 pmol x kg-1 x min-1, 60 min) its plasma concentration rose from 2.1 +/- 0.5 to 9.5 +/- 5.3 pmol/l (pulmonary artery), from 2.1 +/- 0.9 to 5.0 +/- 1.6 pmol/l (femoral artery), and from 1.5 +/- 0.6 to 2.9 +/- 1.2 pmol/l (hepatic vein). This was accompanied by an increase in mean systolic arterial pressure from 127 +/- 14 to 131 +/- 12 mmHg (P less than 0.05). Concomitantly, cardiac output and heart rate decreased from 7.0 +/- 1.1 to 5.8 +/- 1.0 l/min and from 63 +/- 6 to 56 +/- 5 beats/min, respectively, while total vascular resistance increased from 964 +/- 273 to 1204 +/- 338 dyn x cm x s-5 (P less than 0.01). No major changes in pulmonary circulation were observed, while splanchnic vascular resistance increased from 4472 +/- 1056 to 5361 +/- 1420 dyn x cm x s-5 (P less than 0.01) and estimated hepatic blood flow decreased from 1403 +/- 218 to 1218 +/- 219 ml min-1 (P less than 0.01). During endothelin-1 infusion the pulmonary vascular bed accounted for approximately 53% of the peptide's overall disposal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

A lumped parameter mathematical model of the splanchnic circulation.

A lumped parameter mathematical model to describe the propulsion of blood in the splanchnic circulation was developed by integrating the principles of mechanics and physiology. A set of governing equations by derived by specifically considering the contractility of the portal vein, hepatic vein, liver sinusoids, and of the draining lymphatics. These equations were then simulated on a computer. The present simulation results substantiate previous experimental observations that hepatic venous pressure leads to portal hypertension and increased liver interstitial fluid volume.

Blood Pressure↗
PubMed1989

Effects of hypocapnia and hypercapnia on splanchnic circulation and hepatic function in the beagle.

The effects of mild hypocapnia (PaCO2 22 mm Hg) and hypercapnia (PaCO2 59 mm Hg) on the splanchnic circulation and hepatic function were studied in six pentobarbital anesthetized, laparotomized, mechanically ventilated beagles. Tidal volume and respiratory frequency were held constant throughout the measurements. Hepatic artery blood flow (HABF) and portal vein blood flow (PVBF) were measured by electromagnetic flowmeters. Hepatic function was assessed by indocyanine green (ICG) elimination kinetic analysis after intravenous injection of the dye. Hypocapnia caused a decrease in HABF without affecting the systemic circulation. Hypercapnia, on the other hand, caused a significant increase in cardiac output without changing mean arterial pressure. There was a significant increase in PVBF and total hepatic blood flow (THBF = PVBF + HABF). Despite the increases in PVBF and THBF, the half-life of ICG was significantly longer during hypercapnia (9.09 +/- 0.79 min) than during hypocapnia (7.16 +/- 0.37 min), and plasma ICG clearance was smaller during hypercapnia (4.79 +/- 0.44 ml.min-1) than during hypocapnia (5.44 +/- 0.33 ml.min-1) or normocapnia (5.27 +/- 0.50 ml.min-1), indicating the depressed hepatic function during hypercapnia. We conclude that mild hypocapnia decreases HABF without affecting hepatic function and that mild hypercapnia is associated with a depression of hepatic function in spite of the increases in PVBF and THBF.

Animals↗
PubMed1992

Effects of inhibiting nitric oxide biosynthesis on the systemic and splanchnic circulation of rats with portal hypertension.

1. The effects of inhibiting endogenous nitric oxide (NO) synthesis with NG-monomethyl-L-arginine (L-NMMA) on the systemic and splanchnic circulation have been investigated in rats with experimental chronic portal hypertension, anaesthetized with ketamine. 2. Portal hypertension was induced by partial portal vein ligation, 2 weeks prior to study. This procedure induced a reduction in systemic arterial blood pressure (MAP), an increase in cardiac output as measured by radiolabelled microspheres, a reduction in peripheral and splanchnic vascular resistance and an increased portal venous inflow (PVI) and portal pressure, as compared to control non-ligated rats. 3. L-NMAA (6.25 and 50 mg kg-1, i.v.) dose-dependently increased MAP, reduced cardiac output and PVI, and increased peripheral and splanchnic vascular resistance. With L-NMMA (50 mg kg-1), PVI and the vascular resistances returned to values comparable to those determined in control non-ligated anaesthetized rats under resting conditions. 4. Porto-collateral resistance was also increased by these doses of L-NMMA, whereas portal pressure was unchanged. The increase in renal blood flow and decrease in renal vascular resistance also seen in portal-hypertensive rats was reversed by L-NMMA (50 mg kg-1). 5. These effects of L-NMMA (50 mg kg-1) were inhibited by prior administration of L-arginine (300 mg kg-1, i.v.). 6. These findings indicate that the chronic hyperdynamic circulatory characteristics following portal vein stenosis can be attenuated by L-NMMA. Thus, the excessive formation of endogenous NO may be implicated in the pathogenesis of the haemodynamic disturbances and splanchnic vasodilatation associated with chronic portal hypertension.

Animals↗
PubMed1990

Measurement of splanchnic circulation in dogs: changes induced by prostaglandin E1.

In seven anesthetized dogs the effects of intravenously administered prostaglandin E1 on mesenteric arterial and portal venous blood flows and pancreatic capillary blood flow were measured with a transit-time ultrasonic volume flowmeter and a laser Doppler flowmeter. Basal blood flow of the superior mesenteric artery and of the portal vein were 5.7 +/- 0.6 and 11.2 +/- 1.0 ml/min/kg, respectively. Prostaglandin E1 caused a dose-dependent increase in these blood flows. The maximal effect was observed at a dose of 1.0 microgram/kg, when the superior mesenteric arterial blood flow increased 117.9 +/- 3.2% and the portal venous blood flow increased 99.4 +/- 1.7%. Prostaglandin E1 produced an initial rapid increase, followed by a decrease in pancreatic capillary blood flow. The results indicate that the flowmeters used in the present study are widely available for the study of splanchnic circulation and may have a possibility for clinical application.

Alprostadil↗
PubMed1990

Effect of human epidermal growth factor (hEGF) on splanchnic circulation in dogs.

The effect of intravenous administration of human epidermal growth factor on the splanchnic blood flows was examined in anesthetized dogs, using an ultrasonic transit-time volume flow meter. Human epidermal growth factor (0.1, 0.5 and 1 microgram/kg) significantly increased blood flows in the portal vein (36.9 +/- 7.4% at 1 microgram/kg) and the superior mesenteric artery (49.0 +/- 16.8% at 1 microgram/kg). Systemic blood pressure monitored simultaneously was significantly decreased (8.4 +/- 1.2% at 1 microgram/kg). This study is the first to demonstrate that intravenous administration of epidermal growth factor increases the portal venous blood flow.

Animals↗
PubMed1990

Characterization of norepinephrine sensitivity in the maternal splanchnic circulation during pregnancy.

Vascular sensitivity to exogenous norepinephrine and transmural nerve stimulation was studied in the splanchnic bed of nonpregnant, early pregnant, and late pregnant rats. Resistance-size mesenteric arteries were removed from late pregnant (18 to 20 days), early pregnant (7 days), and nonpregnant cycling rats and mounted in a myograph system, which permits the precise setting of vessel circumference for the determination of norepinephrine sensitivity. Norepinephrine dose-response curves and frequency-response curves for transmural nerve stimulation were obtained in the presence and absence of cocaine, a specific inhibitor of neuronal reuptake. The mesenteric arteries of late pregnant rats were 1.5 times less sensitive to exogenous norepinephrine than arteries of both early pregnant and nonpregnant rats. Sensitivity to transmural nerve stimulation was decreased in both early and late pregnant rats compared with nonpregnant controls. Cocaine potentiated the response to both exogenous norepinephrine and transmural nerve stimulation in the pregnant rats so that responses between nonpregnant, early pregnant, and late pregnant rats were no longer different. This suggests a greater reuptake activity from pregnant rats. In conclusion, pregnancy is associated with a reduction in splanchnic norepinephrine sensitivity, which may be due partly to an increase in neuronal deactivation of norepinephrine. The maximum contractile response to norepinephrine also was decreased in late pregnancy, which suggests additional mechanisms for changes in norepinephrine vascular sensitivity.

Animals↗
PubMed1990

Nonocclusive mesenteric ischemia associated with propranolol overdose: implications regarding splanchnic circulation.

We describe a case of massive propranolol overdose in a healthy 19-year-old woman associated with isolated mesenteric ischemia following shock. We postulate that endogenous catecholamine release from shock combined with massive beta-adrenergic blockade led to severe splanchnic vasoconstriction from unopposed alpha-adrenergic activity. This case supports current thinking regarding the effect of vasoactive mediators on the gastrointestinal tract in humans and might be relevant to the mechanism of action of propranolol in the prophylaxis of variceal bleeding.

Adrenergic beta-Antagonists↗
PubMed1989

Effects of angiotensin blockade on the splanchnic circulation in normotensive humans.

The effects of angiotensin-converting enzyme inhibition (ACE-I) by enalapril on splanchnic (n = 10) and central hemodynamics (n = 9) were examined in moderately salt-depleted healthy volunteers, at rest and during 15-20 min of lower body negative pressure (LBNP), reducing mean arterial pressure by 10 mmHg. During LBNP before ACE-I, both splanchnic and total peripheral vascular resistances increased. During ACE-I, splanchnic and total peripheral vascular resistances decreased. After enalapril administration, splanchnic vascular resistance did not increase during LBNP. Total peripheral vascular resistance still increased but not to the same extent as during LBNP before ACE-I. The increases in heart rate and plasma norepinephrine during LBNP were attenuated after ACE-I compared with LBNP before ACE-I. The effectiveness of the ACE-I was clearly demonstrated by unchanged and low plasma angiotensin II levels during ACE-I. We conclude that, in normal sodium-depleted humans, acute ACE-I decreases splanchnic vascular resistance at rest and abolishes splanchnic vasoconstriction during LBNP. Furthermore, it may interfere with autonomic nervous system control of the circulation.

Adult↗
PubMed1992

Anatomy of the splanchnic circulation.

The blood supply to the intestines is a complex one, including branches of the three main splanchnic arteries as well as a vast collateral circulation. The variant anatomy and collateral pathways are described, based on anatomic dissections and angiographic studies, to focus attention on anatomically based explanations for clinical entities.

Humans↗
PubMed1975

Effects of anesthetics on splanchnic circulation and metabolism.

In the last 10 years intense interest in "halothane hepatitis" plus simpler and more reliable technology for measuring splanchnic blood flow have led to a fuller understanding of the splanchnic effects of anesthetics. For the first time, a rational choice of anesthetic technique can be made for the patient with splanchnic organ dysfunction.

Abdomen↗
PubMed1976

The effect of vasopressin and triglycyl lysine vasopressin (glypressin) on the splanchnic circulation in cirrhotic patients with portal hypertension.

In four cirrhotic patients with portal hypertension we have measured some hemodynamic parameters over 60-120 min; portal venous pressure, hepatic venous pressure, mean arterial blood pressure, hepatic blood flow, transsinusoidal vascular resistance and splanchnic oxygen uptake under treatment with Vasopressin (1 IU/min for 10 min) and glypressin (50 mug/kg body weight). The effect on the parameters was less pronounced with glypressin but of longer duration.

Abdomen↗
PubMed1978

The effect of intestinal hormones on splanchnic circulation.

The influence of acidification of the duodenal contents, of intravenous secretin, cholecystokinin and pancreozym injections on hepatic (HAF) and left gastric artery (GAF) and on portal vein blood flow (PVF), bile and pancreatic juice output was studied in dogs. Acid introduction into the duodenum increased HAF and PVF by 20 and 25 percent, respectively. GAF did not change significantly. Secretin and cholecystokinin also increased PVF by 25 percent but HAF changes were less than after acidification. Pancreozym increased significantly only HAF. There were also differences between the effects of duodenal acidification and of the individual hormones on bile and pancreatic juice excretion. It is concluded, that splanchnic circulatory changes observed following duodenal acidification are not produced by the action of a single intestinal hormone but are due to the interplay of several factors.

Animals↗