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At least 127 records · Page 7Linked to original sources
PubMed2003

Impulse-response function of splanchnic circulation with model-independent constraints: theory and experimental validation.

Modeling physiological processes using tracer kinetic methods requires knowledge of the time course of the tracer concentration in blood supplying the organ. For liver studies, however, inaccessibility of the portal vein makes direct measurement of the hepatic dual-input function impossible in humans. We want to develop a method to predict the portal venous time-activity curve from measurements of an arterial time-activity curve. An impulse-response function based on a continuous distribution of washout constants is developed and validated for the gut. Experiments with simultaneous blood sampling in aorta and portal vein were made in 13 anesthetized pigs following inhalation of intravascular [15O]CO or injections of diffusible 3-O-[11C]methylglucose (MG). The parameters of the impulse-response function have a physiological interpretation in terms of the distribution of washout constants and are mathematically equivalent to the mean transit time (T) and standard deviation of transit times. The results include estimates of mean transit times from the aorta to the portal vein in pigs: T = 0.35 +/- 0.05 min for CO and 1.7 +/- 0.1 min for MG. The prediction of the portal venous time-activity curve benefits from constraining the regression fits by parameters estimated independently. This is strong evidence for the physiological relevance of the impulse-response function, which includes asymptotically, and thereby justifies kinetically, a useful and simple power law. Similarity between our parameter estimates in pigs and parameter estimates in normal humans suggests that the proposed model can be adapted for use in humans.

3-O-Methylglucose↗
PubMed1993

Evaluation of the effects of dopexamine, a novel DA1 receptor and beta 2-adrenoceptor agonist, on cardiac function and splanchnic circulation in a canine model of hemorrhagic shock.

In the present studies, the efficacy of dopexamine hydrochloride, a novel DA1-receptor and beta 2-adrenoceptor agonist in preventing deterioration of cardiovascular function in a canine model of hemorrhagic shock was investigated. Pentobarbital-anesthetized dogs were allowed to bleed into a height-regulated reservoir and the hypotensive state (about 40 mmHg) was maintained for a period of 150 min. Subsequently, blood was reinfused and recoveries in various hemodynamic variables were monitored for an additional period of 120 min. Either aqueous solvent or dopexamine HCl was randomly selected for i.v. infusion beginning 30 min before reinfusion of the blood and until the termination of the experiment. In the solvent-treated control group, various cardiovascular variables such as cardiac output, stroke volume, celiac and superior mesenteric arterial blood flows progressively declined to 50% or less of the basal values; these changes were associated with sustained increases in the regional as well as systemic vascular resistances. Dopexamine infusion lowered vascular resistances and facilitated recoveries in various hemodynamic variables to 80% to 100% of the basal values after reinfusion of the shed blood. With the exception of a transient inotropic effect during reinfusion in the dopexamine treated group, there were no essential alterations in the myocardial contractility, during the hypotensive state and/or after reinfusion of the blood. Hence, the results indicate that the efficacy of dopexamine to reduce vascular resistance by actions at DA1-receptors and beta 2-adrenoceptors would account for its ability to improve myocardial performance (secondary to reductions in afterload) and restoration of mesenteric and celiac hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed2000

Sustained infection induces 2 distinct microvascular mechanisms in the splanchnic circulation.

BACKGROUND: Altered intestinal blood flow during systemic inflammation leads to organ dysfunction. Mucosal ischemia occurs during sepsis despite an increase in portal blood flow. We hypothesized that separate mechanisms are active in the large resistance and small mucosal microvessels to account for this dichotomy. METHODS: Chronic infection was induced in rats by bacterial inoculation (Escherichia coli and Bacteroides fragilis) of an implanted subcutaneous sponge. Separate groups were studied at 24 and 72 hours after a single inoculation of bacterium or 24 hours after a second inoculation (ie, 72 hours of sepsis). Time-matched controls were used for each group. Intravital microscopy of the terminal ileum was used to assess endothelial-dependent vasodilation to acetylcholine (10(-9) to 10(-5) mol/L) in resistance (A(1)) and premucosal (A(3)) arterioles. Threshold sensitivity (-log of 20% response dose) was calculated from dose response curves for each animal. RESULTS: Vasodilator sensitivity to acetylcholine in A(1) arterioles was significantly decreased at 24 hours, and these changes persisted up to 72 hours after a single bacterial inoculation. There was no change in the dilator sensitivity of A(3) arterioles after a single inoculation. When there was a challenge with a second bacterial inoculation, there was a reversal of the A(1) dilator response and an increase in A(3) sensitivity. CONCLUSIONS: An initial septic event results in a decrease in dilator reactivity in the resistance A1 arterioles that persists for at least 72 hours. A sustained septic challenge results in increased dilator reactivity in both A(1) and A(3) vessels. This enhanced sensitivity during sepsis suggests that more than 1 therapeutic approach to preservation of intestinal blood flow will be necessary.

Acetylcholine↗
PubMed1995

Thyroid, renal, and splanchnic circulation in horses at rest and during short-term exercise.

Using radionuclide-labeled 15-microm-diameter microspheres injected into the left ventricle, we examined blood flow to the thyroid gland, adrenal glands, kidneys, and various gastrointestinal tract tissues in 9 healthy horses while they were standing quietly (rest) and during exercise at 2 work intensities (8 and 1 m/s). Hemodynamic measurements were made during steady-state conditions, as judged by the stability of heart rate as well as aortic, pulmonary, and right atrial pressures. The similarity of blood flow values for the left and the right kidneys during each of the 3 conditions indicated adequate mixing of microspheres with blood. In standing horses, of all tissues examined, the thyroid gland had the highest blood flow (1,655.2 +/- 338.5 ml/min/100 g)--being about threefold that in the kidneys. Adrenal blood flow, by contrast, was only 25% of that in the kidneys (589.5 +/- 50.4 ml/min/100 g). Among the gastrointestinal tract tissues, glandular stomach and pancreas had the highest blood flows (214.3 +/- 21.6 and 197.6 +/- 23.4 ml/min/100 g, respectively). Small intestinal perfusion was not different from that in the ventral colon and cecum, but their values exceeded those for the dorsal and small colons. Exercise at 8 and 13 m/s caused significant increase in adrenal blood flow as vascular resistance decreased significantly. In the kidneys, blood flow was only insignificantly affected during exercise at 8 m/s, but at 13 m/s there was a profound reduction in renal blood flow as intense renal vasoconstriction occurred. Vasoconstriction also caused thyroid and pancreatic blood flow to decrease significantly at both levels of exertion. Significant vasoconstriction occurring in all gastrointestinal tract tissues at 8 and 13 m/s caused blood flow to be diverted away from these vascular beds. Thus, our data indicated that renal, adrenal, and splanchnic organ/tissue blood flow responses of strenuously exercising horses closely resemble those described for exercising ponies.

Adrenal Glands↗
PubMed1987

Blood acetaldehyde and the ethanol-induced increase in splanchnic circulation.

Acute oral administration of ethanol significantly increases (50-60%) portal blood flow to the liver. As earlier studies have indicated that this effect is maximal at concentrations of ethanol that saturate the alcohol dehydrogenase (ADH) system and is blocked by the ADH inhibitor 4-methylpyrazol, we investigated the possible role of acetaldehyde, a product in the ADH reaction, as a mediator of this effect. In the first series of experiments it was shown that, contrary to expectations, cyanamide administration prior to alcohol suppressed fully the effect of ethanol on portal blood flow without altering it in the absence of ethanol [ethanol = 69.5 +/- 5.6; ethanol + cyanamide 42.9 +/- 2.4; control = 43.0 +/- 3.0; cyanamide = 55.1 +/- 3.7 ml X min-1 X (kg body wt)-1]. Arterial blood concentrations of acetaldehyde were elevated from 3.6 +/- 0.3 microM in the presence of ethanol to 293 +/- 48 microM in the presence of ethanol + cyanamide. Infusion of acetaldehyde either into the left ventricle, resulting in arterial blood acetaldehyde levels of 227 +/- 77 microM, or into the portal circulation, resulting in arterial blood levels of 198 +/- 40 microM, did not modify portal blood flow or splanchnic hemodynamics, nor the effect of ethanol per se. The combination of cyanamide + ethanol significantly reduced total peripheral resistance (from 28 +/- 3 to 19 +/- 2 dyne X cm X sec-5), while neither ethanol or cyanamide per se, nor acetaldehyde affected total peripheral resistance. Data suggest that acetaldehyde is not involved in the ethanol-mediated increase in portal vein flow. Further studies indicate that the effects of cyanamide in suppressing the ethanol-induced increase in portal blood flow and increasing total peripheral resistance appear to be related to an ethanol-cyanamide interaction which is independent of the acetaldehyde levels in the circulation.

Acetaldehyde↗
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↗
PubMed1993

Effect on liver and splanchnic circulation of graded flow rates through portal-systemic bypass during acute portal occlusion.

Using graded flow rates through a passive portal-systemic bypass during 2-hr portal occlusion in dogs, splanchnic, hemodynamic, and metabolic changes and liver insults were evaluated to determine critical bypass flow. To exclude effects caused by reduced circulating blood volume, constant preocclusion levels of cardiac output were maintained throughout the study by increasing intravenous infusion rates. With the decrease in bypass flow rates during portal occlusion, portal pressure increased, superior mesenteric arterial flow decreased, and hepatic arterial flow rapidly increased and these parameters maintained their individual levels during occlusion. These hemodynamic parameters recovered to nearly normal levels 3 hr after release of the portal clamp. Metabolic acidosis progressed with decreasing bypass flow, but portal potassium and inorganic phosphorus levels showed a significant rise only when there was no bypass. Portal levels of creatine phosphokinase BB, beta-glucuronidase, and endotoxin did not show significant changes corresponding to bypass flow. The amounts of infusion required were 3 to 6 times the basal level (10 ml/kg/hr) during occlusion and 1.7 to 3 times after release in 30% or less bypass groups. Upon ceasing infusion 3 hr after release, dogs in the 10% or less bypass groups underwent circulatory insufficiency. Changes in total adenine nucleotide and energy charge ratio of the liver, postoperative changes in transaminase levels, and animal survival indicated that a 2-hr interruption of the portal flow, either sufficiently or insufficiently bypassed, caused only minimal insults of the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Temporary extracorporeal perfusion of the splanchnic circulation dependent on the Riolan anastomosis.

A thorough investigation of a hypertensive 25 year old male was undertaken due to the finding of an absent right radial pulse. This work-up revealed widespread, largely asymptomatic arterial disease characterised by a combination of multiple sites of stenosis and occlusion, aneurysmal dilatation and extensive vessel wall calcification. The findings included a right renal artery stenosis, an abdominal aortic aneurysm and a splanchnic vasculature completely supplied by the inferior mesenteric artery. Consequently it was thought that a prolonged clamping time during the aortic repair would possibly result in ischemic injury. Therefore, the splanchnic organs were perfused by a paediatric oxygenator and pump during the aortic cross-clamping. This case report discusses the etiology of the disease and the technical aspects of splanchnic perfusion.

Adult↗
PubMed1988

[Study on splanchnic circulation: measurement of the liver blood flow].

In anesthetized patients during abdominal surgery, hepatic artery and portal vein flows were measured simultaneously utilizing an ultrasonic transit-time volume flowmeter. The total hepatic blood flow was 994.6 +/- 52.4 ml/min. The hepatic artery flow and the portal vein flow were 260.0 +/- 23.8 ml/min and 730.8 +/- 41.3 ml/min, respectively. The ratio of hepatic artery flow to portal vein flow was 0.37 +/- 0.04. A significant increase in hepatic artery flow (p less than 0.01) followed portal vein occlusion, whereas no significant change was observed in portal vein flow after hepatic artery occlusion. Common hepatic artery occlusion resulted in a significant decrease in hepatic artery flow (p less than 0.05), but no significant change was observed in portal vein flow. The present study firstly demonstrated that ultrasonic transit-time volume flowmeter is a device to quantitatively assess hepatic artery and portal vein flows with good reproducibility and stability in human subjects. This easy and simple technique seemed to have wide clinical application to abdominal surgery and would have a promising in studying splanchnic blood flows in various situations such as in cases of hepatectomy and portal hypertension.

Adult↗
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↗