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At least 19 recordsLinked to original sources
PubMed1985

Physiology of the splanchnic circulation.

The splanchnic circulation is composed of gastric, small intestinal, colonic, pancreatic, hepatic, and splenic circulations, arranged in parallel with one another. The three major arteries that supply the splanchnic organs, cellac and superior and inferior mesenteric, give rise to smaller arteries that anastomose extensively. The circulation of some splanchnic organs is complicated by the existence of an intramural circulation. Redistribution of total blood flow between intramural vascular circuits may be as important as total blood flow. Numerous extrinsic and intrinsic factors influence the splanchnic circulation. Extrinsic factors include general hemodynamic conditions of the cardiovascular system, autonomic nervous system, and circulating neurohumoral agents. Intrinsic mechanisms include special properties of the vasculature, local metabolites, intrinsic nerves, paracrine substances, and local hormones. The existence of a multiplicity of regulatory mechanisms provides overlapping controls and restricts radical changes in tissue perfusion.

Colon↗
PubMed1995

Influence of central command and ergoreceptors on the splanchnic circulation during isometric exercise.

The splanchnic circulation can make a major contribution to blood flow changes. However, the role of the splanchnic circulation in the reflex adjustments to the blood pressure increased during isometric exercise is not well documented. The central command and the muscle chemoreflex are the two major mechanisms involved in the blood pressure response to isometric exercise. This study aimed to examine the behaviour of the superior mesenteric artery during isometric handgrip (IHG) at 30% maximal voluntary contraction (MVC). The pulsatility index (PI) of the blood velocity waveform of the superior mesenteric artery was taken as the study parameter. A total of ten healthy subjects [mean age, 21.1 (SEM 0.3) years] performed an IHG at 30% MVC for 90 s. At 5 s prior to the end of the exercise, muscle circulation was arrested for 90 s to study the effect of the muscle chemoreflex (post exercise arterial occlusion, PEAO). The IHG at 30% MVC caused a decrease in superior mesenteric artery PI, from 4.84 (SEM 1.57) at control level to 3.90 (SEM 1.07) (P = 0.015). The PI further decreased to 3.17 (SEM 0.70) (P = 0.01) during PEAO. Our results indicated that ergoreceptors may be involved in the superior mesenteric artery vasodilatation during isometric exercise.

Adult↗
PubMed1999

Role of the splanchnic circulation in acid-base balance during cardiopulmonary bypass.

OBJECTIVE: The role of the splanchnic circulation in the development of the metabolic acidosis of cardiopulmonary bypass (CPB) is not fully understood. New quantitative methods of acid-base balance now offer the ability to define this phenomenon more accurately. Accordingly, we studied acid-base changes across the splanchnic circulation during CPB and defined and quantified the factors that contributed to acid-base balance. DESIGN: Prospective cohort study. SETTING: Tertiary institution. PATIENTS: Ten patients undergoing CPB for coronary artery bypass surgery. INTERVENTIONS: Sampling of arterial and hepatic venous blood at four time intervals: postinduction, on CPB during cooling and rewarming, and at skin closure. MEASUREMENTS: Measurement of serum Na+, K+, Mg++, Ca++, Cl-, HCO3-, and phosphate concentrations, arterial and hepatic venous blood gases and serum albumin, and lactate and pyruvate concentrations at each collection point. Analysis of findings according to quantitative physicochemical principles. MAIN RESULTS: All patients developed a mild metabolic acidosis with a decrease in median serum bicarbonate concentration from 24.97 mEq/L after induction to 22.29 mEq/L at cooling and 22.23 mEq/L at rewarming (p < .05). Before CPB, the pH decreased by 0.0275 (p < .05) across the splanchnic circulation, representing an increase of 2.26 nmol/L of hydrogen ions. Nevertheless, the splanchnic circulation induced a metabolic alkalosis, with a median transsplanchnic increase in the base excess of 1.50 mEq/L (p < .05). This change was largely due to a decrease in serum chloride and lactate concentration across the splanchnic circulation (p < .05). The acidifying effect of the splanchnic circulation was therefore the result of cell respiration with a median increase in carbon dioxide tension of 5.75 mm Hg (p < .05), causing the strong ion difference effective to increase by 1.94 mEq/L (p < .05). There were no other anions or acids added to the circulation by splanchnic organs (no change in strong ion gap). During and after CPB the splanchnic metabolic alkalinizing effect continued and the respiratory acidifying effect was reduced. This caused the splanchnic circulation to be pH neutral at these times. CONCLUSIONS: Using quantitative biophysical methods it can be demonstrated that the splanchnic circulation does not contribute to the metabolic acidosis of CPB, and that it continues to have a metabolic alkalinizing effect involving significant lactate extraction. However, its respiratory acidifying effect continues, although at a reduced rate.

Acid-Base Equilibrium↗
PubMed1988

Splanchnic circulation following coeliac plexus block.

Both the capacitance vessels and the resistance vessels of the splanchnic area are innervated by the sympathetic nerve fibers. We investigated the effect of abdominal visceral sympathectomy on splanchnic circulation, and the effect of altered splanchnic circulation on systemic circulation in ten mongrel dogs. Abdominal visceral sympathectomy was induced by coeliac plexus block with 1 ml/kg (body weight) of 1% lidocaine infiltrated around the coeliac artery. Comparison was made with infiltration of physiologic saline of the same volume. The saline infiltration caused no significant changes in the hemodynamic parameters of systemic and splanchnic circulation. Mean arterial pressure decreased significantly from 18.2 +/- 2.0 to 14.4 +/- 1.9 kPa following the coeliac plexus block, with a concomitant decrease in the cardiac index from 2.63 +/- 0.46 to 2.30 +/- 0.54 l X min-1 X m-2, while systemic vascular resistance was unchanged. Portal vein blood flow, hepatic artery blood flow and, therefore, splanchnic blood flow decreased by 8 to 17%. Portal vascular and hepatic artery resistances were not affected by abdominal sympathectomy. It was concluded that the capacitance vessels in splanchnic circulation are dilated during abdominal sympathetic denervation, causing a blood shift from systemic to splanchnic circulation. On the other hand, the resistance vessels in splanchnic circulation are affected little by abdominal visceral sympathectomy.

Animals↗
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↗
PubMed2006

Role of NPY for vasoregulation in the splanchnic circulation during portal hypertension.

Vascular dysfunction in the splanchnic circulation during portal hypertension is characterized by enhanced NO-mediated vasorelaxation and vascular hyporeactivity to norepinephrine that lead to arterial vasodilation. NPY most likely counteracts both of these key features. Firstly, NPY appears to inhibit Ach- and PNS-induced vasorelaxation in mesenteric arteries. This effect is more pronounced in portal hypertensive rats as compared to control, and most likely reflects the inhibition of increased e- and nNOS-derived NO-synthesis during portal hypertensive conditions. Secondly, NPY sensitizes the mesenteric vasculature to alpha(1)-adrenergic vasoconstriction. Most importantly, in portal hypertensive rats but not in sham rats NPY markedly augments vascular contractility and thereby corrects vascular hyporeactivity. Both actions of NPY increase vascular tone and may well act synergistically in the splanchnic circulation during portal hypertension. Moreover, the vasoconstrictive effects of NPY are most pronounced at particularly high levels of alpha(1)-adrenergic activity. Therefore, it appears that NPY becomes increasingly important for optimizing adrenergic vasoconstriction at particularly high adrenergic drive and also for playing a predominant role for vascular homeostasis. Cirrhotic patients present with elevated circulating plasma levels of NPY, which appears to be independent from the severity of liver dysfunction and to correlate with portal pressure. This finding indicates enhanced NPY release during portal hypertension that may represent a compensatory mechanism aimed at counterbalancing arterial vasodilation by restoring the efficacy of endogenous catecholamines and inhibiting vasodilative drive in the splanchnic circulation.

Humans↗
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↗
PubMed2003

Effects of dopamine, norepinephrine, and epinephrine on the splanchnic circulation in septic shock: which is best?

OBJECTIVE: To assess the effects of different doses of dopamine, norepinephrine, and epinephrine on the splanchnic circulation in patients with septic shock. DESIGN: Prospective, randomized, open-label study. SETTING: A 31-bed, medicosurgical intensive care unit of a university hospital. PATIENTS: Convenience sample of 20 patients with septic shock, separated into two groups according to whether (moderate shock group, n = 10) or not (severe shock, n = 10) dopamine alone was able maintain mean arterial pressure >65 mm Hg. INTERVENTIONS: Dopamine was progressively withdrawn and replaced successively by norepinephrine and then epinephrine (the order of the two agents was randomly determined) to maintain mean arterial pressure constant (moderate shock) or to increase mean arterial pressure above 65 mm Hg (severe shock). MEASUREMENTS AND MAIN RESULTS: Systemic circulation (pulmonary artery catheter) and splanchnic circulation (indocyanine green dilution and hepatic vein catheter) and gastric mucosal Pco(2) (gas tonometry) were measured during dopamine (moderate shock only), norepinephrine, and epinephrine administration (both groups). Data were analyzed with nonparametric tests and are presented as median [percentiles 25-75]. In moderate shock, cardiac index was similar to dopamine and norepinephrine (3.1 [2.7-3.8] vs. 2.9 [2.7-4.1] L/min.m2, p = nonsignificant) but greater with epinephrine (4.1 [3.5-4.4] p <.01 vs. dopamine and norepinephrine). Splanchnic blood flow was similar with the three agents (732 [413-1483] vs. 746 [470-1401] vs. 653 [476-1832] mL/min.m, p = nonsignificant). The gradient between mixed-venous and hepatic venous oxygen saturations was lower with dopamine than with norepinephrine and epinephrine, but the Pco(2) gap was similar with the three agents. In severe shock, cardiac index was higher, but splanchnic blood flow was lower, with epinephrine than with norepinephrine (4.6 [3.7-5.3] vs. 3.4 [3.0-4.1] L/min.m2, p <.01 and 860 [684-1334] vs. 977 [806-1802] mL/min.m2, p <.05, respectively). Epinephrine increased the mixed-venous and hepatic venous oxygen saturation gradient but did not alter Pco(2) gap. CONCLUSIONS: Dopamine and norepinephrine have similar hemodynamic effects, but epinephrine can impair splanchnic circulation in severe septic shock.

Aged↗
PubMed1988

Vasoactive intestinal polypeptide potentiates the hypoxemia-induced decrease in splanchnic circulation in the rat.

The effects of acute infusion of vasoactive intestinal polypeptide (VIP) and hypoxemia on splanchnic circulation were examined in 35 awake Sprague-Dawley rats. Indwelling catheters were placed in the superior vena cava and the proximal aorta via the internal jugular vein and internal carotid artery, respectively, while the rats were under ether anesthesia. Four hours later, when the rats were awake and active, VIP (molecular lot 3226) was infused intraarterially for 30 minutes. The distribution of cardiac output was measured at the end of VIP infusion using 125I-labeled microspheres. VIP was administered at a low (1.5 ng/min) and a high infusion rate (44.1 ng/min) for 30 minutes. The effect of hypoxemia on circulatory response to VIP was examined only in the high VIP infusion group, by placing the rat in a 10% oxygen environment. Appropriate control experiments were performed with each group. The high-dose VIP resulted in a marked reduction in distribution of cardiac output to the splanchnic circulation. This effect was potentiated by hypoxemia, particularly in the distal ileum and colon. The metabolic clearance rate of VIP increased with the rate of VIP infusion and was decreased by hypoxemia. It was concluded that only in high concentration does VIP have any effect on splanchnic circulation. However, in the presence of hypoxemia, VIP may have an important role in cardiovascular compensatory response and may contribute to the development of ischemic bowel injury.

Animals↗
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↗
PubMedDate not supplied

Effects of synthetic kassinin on splanchnic circulation and exocrine pancreas in dogs.

Effects of intravenously administered synthetic kassinin on splanchnic circulation and exocrine pancreatic secretion were examined in six anesthetized dogs. Kassinin caused dose-related increases in the blood flow in superior mesenteric artery and portal vein, and produced an initial increase followed by a decrease in pancreatic blood flow, but did not affect the exocrine pancreatic secretion. This study demonstrates that kassinin affects splanchnic blood flow in dogs, and suggests that kassinin or a kassinin-like substance functions as a neuropeptide controlling the splanchnic circulation in mammalian species.

Animals↗
PubMed1993

[The effect of intravenous cimetidine and histamine on splanchnic circulation in the dogs].

We investigated the effect of cimetidine and histamine on splanchnic circulation in the dogs. Hepatic artery, superior mesenteric artery and portal vein were cannulated to measure each blood pressure. Each blood flow was evaluated utilizing electromagnetic blood flowmetry. And vascular resistances were calculated by measured blood pressure and blood flow. Cimetidine, histamine, 2-PEA (H1-agonist), dimaprit (H2-agonist) and mepyramine maleate (H1-antagonist) were given by intravenous bolus to the dogs. Histamine caused vasodilation of hepatic artery but vasoconstriction of superior mesenteric artery and these effects were similar to the effect of 2-PEA. These hemodynamic responses to histamine were inhibited by H1-antagonist but not inhibited by H2-antagonist. Cimetidine produced dilatation of hepatic artery but constriction of portal vein, superior mesenteric artery and reduced total hepatic blood flow. These effects were not inhibited by H1-antagonist. We concluded that cimetidine did not stimulated H1, H2-receptors rather than had the own effects and that H1-receptor was superior to H2-receptor on splanchnic circulation in the dogs.

Animals↗
PubMed1987

Changes of splanchnic circulation with progression of chronic liver disease studied by echo-Doppler flowmetry.

Changes that occurred in splanchnic circulation with the progression of chronic liver disease were investigated using an ultrasonic Doppler flowmeter in healthy adults and in patients with chronic active hepatitis and liver cirrhosis in the supine position after an overnight fast. Superior mesenteric venous flow, splenic venous flow, and portal venous flow were significantly increased in patients with liver cirrhosis but not in patients with chronic active hepatitis compared with normal subjects. Portal venous flow (control value 10.5 +/- 2.3 ml/min/kg body weight) minus the sum of superior mesenteric venous flow and splenic venous flow was 0.8 +/- 2.1 ml/min/kg body weight in the control, (0.1 +/- 1.9) in chronic active hepatitis, and (-2.2 +/- 4.3) in liver cirrhosis; the difference was significant between the control and cirrhosis groups. These results indicate that in patients with liver cirrhosis a hyperdynamic state occurs in the splanchnic circulation of the intestine and spleen and that some portion of splanchnic blood flow bypasses the liver into the systemic circulation.

Adult↗
PubMed1983

Splanchnic circulation in hypertension.

The effect of arterial hypertension on the splanchnic circulation is assessed. In human essential hypertension, splanchnic vascular resistance rises in proportion to the blood pressure, and the transvascular escape rate of plasma proteins is increased. The various animal models of hypertension show variable results, but in general support the concept that vascular resistance changes in the splanchnic organs are similar in direction and magnitude to pressure changes. This is especially true in longer-term chronic experiments. These resistance changes appear to result from increased responsiveness of the arterioles to a variety of constrictor influences, and they may result from either structural or functional changes. Hypertension appears to alter splanchnic arteriolar permeability via a pressure-dependent mechanism. These vessels may also undergo degenerative histological changes. Capillaries and small venules experience increased endothelial permeability via a pressure-independent mechanism that is not mediated by angiotensin II. In addition to the resistive and exchange alterations, the capacitance function of splanchnic veins is reduced, probably via a structural change. Much work remains to be done before the characterization is complete. Especially needed are studies of individual organs with respect to vascular resistance, exchange, and capacitance alterations in the various models of hypertension.

Animals↗