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PubMed1998

Duodenal meal stimulation leads to coeliac artery vasoconstriction and superior mesenteric artery vasodilatation: an intra-abdominal ultrasound study.

To evaluate the influence of duodenal feeding on splanchnic blood flow, 14 patients with normal coeliac and superior mesenteric arteries underwent intra-abdominal duplex scanning of the systemic and splanchnic circulation under standardised basal and meal-stimulated conditions. Doppler samples and diameter measurements were taken of the aorta, coeliac artery, common hepatic artery, splenic artery, superior mesenteric artery, and inferior mesenteric artery. Duodenal meal stimulation has no systemic effects (p > 0.4). However, duodenal meal stimulation results in coeliac artery vasoconstriction (p < 0.06) and superior mesenteric artery vasodilatation (p < 0.05). This study supports other reported results that gastrointestinal blood flow is dependent on the site of food stimulation.

Aged↗
PubMed1997

Pharmacological manipulation of human gastrointestinal blood flow.

The splanchnic circulation is one of the largest vascular regions in man. In the past, this has been difficult to study because of methodological problems. The adapting of noninvasive Doppler techniques has made it possible to develop reproducible measurements of coeliac and superior mesenteric artery blood flow, which are the main contributors to the gastrointestinal vasculature. This has resulted in the further understanding of neurogenic and humoral control of this region in a number of physiological and pathophysiological states, and has contributed towards the knowledge of its pharmacological control. These studies are of relevance to cardiovascular homeostasis and, in particular, systemic blood pressure control which depends upon various factors including responses in different vascular regions. In this review the key physiological factors which influence pharmacological studies on this circulation will be discussed. Examples will be provided, in subjects with cardiovascular and neurological disorders, of how administration of endogenous and exogenous substances, including drugs with specific pharmacological effects, alter human gastrointestinal blood flow. These will include insulin, alcohol, the somatostatin analogue octreotide, the central acting sympatholytic clonidine and the angiotensin II-converting inhibitor captopril. The relevance of these studies to subjects with postural hypotension due to sympathetic denervation and to primary hypertension, in particular, will be discussed.

Adrenergic alpha-Agonists↗
PubMed1988

Etiology and pathophysiology of portal hypertension.

Portal hypertension may result from increased resistance of the hepatic vascular bed ("backflow") and from a hyperdynamic splanchnic circulation ("forward flow" theory). Most likely, both mechanisms contribute to the formation of portal hypertension in man. The classical macroscopic terminology describes prehepatic, intrahepatic and posthepatic forms of portal hypertension. Increased splanchnic blood flow represents the predominant cause of some pre- and intrahepatic types of portal hypertension. Intrahepatic portal hypertension has been subclassified as presinusoidal, sinusoidal or postsinusoidal. However, one to one allotments of diseases to this classification may not be made. The relative contribution of each of these causes to the increased portal pressure of liver cirrhosis varies with the etiology of the disease. A new ultrastructural classification of the processes leading to portal hypertension differentiates primarily hepatocellular (e.g., increased hepatocellular size) from interstitional causes (e.g., sinusoidal capillarization). The role of the fenestrated sinusoidal endothelial cells in the regulation of intrahepatic resistance and, thus, for the generation of portal hypertension is poorly defined up to date. A thorough evaluation of the effects of prostanglandins, leukotrienes, catecholamines, serotonin and others on sinusoidal endothelial cells and hepatic microcirculation may provide the basis for new therapeutic avenues.

Humans↗
PubMed2001

Gut blood flow in fish during exercise and severe hypercapnia.

This paper reviews the effects of exercise and hypercapnia on blood flow to the splanchnic circulation. Brief struggling behaviours are known to decrease blood flow to the gut (GBF). Likewise, prolonged swimming in unfed fish has been shown to reduce GBF in proportion to the increased oxygen uptake. Therefore, the normal postprandial increase in GBF theoretically should be impaired whenever fish are active. However, indirect evidence suggests that GBF is spared to some degree when fed fish swim continuously but at a cost (10-15%) to their critical swimming speed. Severe respiratory acidosis can be created by the new intensive aquaculture settings that use oxygen injection into re-circulated water. The only study so far to examine the effects of severe hypercapnia on GBF and its regulation showed that routine GBF and alpha-adrenergic control of GBF remained normal in unfed white sturgeon (Acipenser transmontanus). However, severe hypercapnia produced a hyperactive state and increased sensitivity of GBF to struggling. As a result, routine GBF was maintained for a short period of time. Thus, environmental changes such as severe hypercapnia can indirectly impact GBF through altered struggling behaviour, but the implications of the overall reduction in GBF to food assimilation have yet to be established.

Animals↗
PubMed1991

The effect of low dose dopamine on gut hemodynamics during PEEP ventilation for acute lung injury.

Mechanical ventilation with positive end-expiratory pressure (PEEP) diminishes gut and hepatic blood flow and redistributes cardiac output away from the splanchnic circulation. This flow-limited environment can aggravate underlying hypoperfusion and ischemia in the postinjury setting. To examine the effects of low dose dopamine on a lung injury PEEP model of gut hypoperfusion, six anesthetized, splenectomized canines were instrumented with arterial, pulmonary artery, portal vein, and hepatic vein catheters. Electromagnetic flow probes were placed around the hepatic artery and portal vein for continuous flow measurements. Gut and hepatic blood flow, oxygen delivery, oxygen consumption, and extraction ratio were calculated at four time points: baseline, 1 hr after lung injury with oleic acid, 1 hr after ventilation with 10 cm H2O PEEP, and 1 hr after the continuous infusion of dopamine. Portal flow and gut oxygen delivery fell significantly with the infusion of PEEP. These values returned to near baseline levels with the addition of dopamine. Gut oxygen extraction increased from 16 +/- 2% to 35 +/- 3% with PEEP but returned to near baseline with dopamine (20 +/- 4%, P less than 0.01 compared to PEEP). We conclude that dopamine improves blood flow and oxygen delivery to the gut in this flow-limited model. This may preserve splanchnic physiology during PEEP ventilation for acute lung injury.

Animals↗
PubMed1989

Discrepancy between portal pressure and systemic hemodynamic changes after incremental doses of propranolol in awake portal hypertensive rats.

The effects of increasing doses of propranolol were studied in awake portal hypertensive rats in order to elucidate the relative effects of the beta-blocker on systemic and splanchnic circulation. Hemodynamic responses to 0.1, 0.2 and 0.4 mg per min infusions of propranolol were compared with placebo in awake rats with portal hypertension due to portal vein stenosis. Heart rate significantly and progressively decreased from 356 +/- 13 to 293 +/- 10 beats per min (mean +/- S.E.). Cardiac output significantly decreased from 54 +/- 3 to 42 +/- 3 ml per min per 100 gm body weight at the highest dose. Significant decrease in portal tributary blood flow from 27 +/- 1 to 18 +/- 1 ml per min, at 0.4 mg per min dose, was due not only to the decrease in cardiac output but also to a significant increase in portal tributary vascular resistance from 269 +/- 17 to 368 +/- 31 dyne per sec per cm5 x 10(3). However, portal pressure showed only an insignificant decrease from 14.9 +/- 1.1 to 14.1 +/- 1.4 mmHg. The reduction in portal pressure being minimal, in spite of a significant decrease in portal tributary blood flow, is explained by an increase in combined hepatic and collateral resistance from 44 +/- 2 to 66 +/- 4 dyne per sec per cm5 x 10(3), p less than 0.05, at 0.4 mg per min dose. We conclude that the systemic and splanchnic effects of propranolol show discrepancy at two levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of the biguanide metformin on splanchnic blood flow in rats: preferential and dose-dependent increase in islet blood flow.

The aim of the present study was to evaluate if metformin, a biguanide used in the treatment of noninsulin-dependent diabetes, induced any changes in splanchnic circulation. For this purpose, anesthetized rats were injected intraperitoneally with saline alone (1 ml/kg BW) or metformin (15 or 30 mg/kg BW) 30 min before blood flow measurements. No effects on blood glucose or serum insulin concentrations could be discerned after administration of metformin. Both duodenal, whole pancreatic and islet blood flow were approximately doubled by the lowest dose (15 mg/kg BW) metformin. However, the higher dose (30 mg/kg BW) did not affect duodenal or pancreatic blood flow, whereas islet blood flow was markedly increased also in this group of animals. It is concluded that the blood flow to the pancreatic islets can be specifically enhanced by metformin. To what extent this contributes to the antihyperglycemic action of the drug is presently unknown.

Animals↗
PubMed1987

Computer analysis of portal hemodynamics after small-diameter portacaval H-grafts: the theoretical basis for partial shunting.

We have previously reported on the clinical results of partial shunting using small-diameter portacaval H-grafts. In this study, we defined the theoretical basis for partial shunting using the Wheatstone bridge model of the splanchnic circulation. The model was modified to include a variable resistance for a portacaval shunt and was programmed as a computer simulation. We calculated portal flow as a function of shunt resistance to determine the resistance necessary to maintain prograde portal flow in patients with portal hypertension. The resistance of 8- and 10-mm portacaval H-grafts, as positioned clinically, was determined using a laboratory apparatus. The experimentally derived values for resistance were inserted into the graph of portal flow predicted by the computer program. Portacaval H-grafts 8 mm in diameter should produce prograde portal flow, 10-mm H-grafts should be borderline, and shunts larger than 10 mm should routinely result in reversed flow. These predictions were confirmed by clinical observations in 29 patients undergoing portacaval H-grafts.

Computer Simulation↗
PubMed2004

Measurement of the liver tissue oxygenation by near-infrared spectroscopy.

OBJECTIVE: To study the relation between the liver tissue oxygenation index (TOI), transcutaneously measured with spatially resolved spectroscopy (a new method of near-infrared spectroscopy or NIRS), the mixed venous oxygen saturation and the blood flow in the different parts of the splanchnic circulation in newborn piglets. DESIGN: Tissue oxygenation index of the liver was measured in six newborn piglets at 33 degrees C, 35 degrees C, 37 degrees C and after a decrease in arterial carbon dioxide pressure (PaCO(2)). MEASUREMENTS: Mixed venous oxygen saturation, blood gas analysis and peripheral oxygen saturation were measured at each step. Gastric, proximal jejunal, midgut, distal ileal, splenic and hepatic arterial blood flow were measured by injection of coloured microspheres into the left atrium. NIRS optodes were attached to the skin over the liver and TOI was calculated. RESULTS: No significant changes of TOI of the liver were seen during the increase in temperature or change in PaCO(2). TOI correlated well with mixed venous oxygen saturation (r=0.85), the mid-ileal blood flow (r=0.57) and the distal ileal blood flow (r=0.72). CONCLUSIONS: Measurement of the TOI of the liver might be a non-invasive way to measure the distal ileal blood flow.

Animals↗
PubMed2000

Systemic and splanchnic endothelin-1 plasma levels in liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS).

AIMS/BACKGROUND: Endothelin-1 (ET-1) may be a mediator for portal hypertension in liver cirrhosis. The aim of the present study was to determine the concentrations of ET-1 in the systemic and splanchnic circulation before and after reduction of portal hypertension by transjugular intrahepatic portosystemic shunt implantation (TIPS). METHODS: Plasma concentrations of immunoreactive ET-1 were measured in peripheral venous blood samples from 25 patients with liver cirrhosis before and at 1, 3, 9 and 15 months after TIPS. Furthermore, acute effects of TIPS on ET-1 were studied in plasma samples from the hepatic vein, the portal vein 30 minutes before and after TIPS and in the femoral artery (only after TIPS) in a subgroup of 15 patients. In addition, the portocaval pressure gradient was determined before and after TIPS. RESULTS: Before TIPS peripheral venous plasma ET-1 concentrations (n=25; median 4.2 pg/ml; range 1.9-14.7) were significantly increased in patients with refractory ascites (n=7; median 7.8, range 3.5 14.7) compared to patients with repetitive bleeding (n=18; median 3.4; range 1.9-7.1) (p=0.003). Furthermore, peripheral ET-1 concentrations correlated with the degree of liver dysfunction according to the Child-Pugh classification (Spearman's r=0.46; p=0.02). Following TIPS, peripheral ET-1 concentrations remained unchanged during a follow-up of 15 months. Before TIPS, a positive gradient of ET-1 concentrations from portalvenous to hepatovenous and peripheral venous levels was found (p<0.03). Immediately after TIPS, arterial ET-1 concentrations reached markedly increased levels in individual patients (88, 92 and 103 pg/ml). Severe systemic reactions to these high levels were not observed. Peripheral venous, hepatovenous and portalvenous ET-1 concentrations did not correlate with portocaval pressure gradients. CONCLUSION: Cirrhotic patients demonstrated unchanged peripheral venous ET-1 concentrations up to 15 months after TIPS. Portal congestion was associated with increased ET-1 levels in the prehepatic splanchnic area. The effect of portal decompression on splanchnic and systemic ET-1 levels deserves further investigation.

Adult↗
PubMed1996

Characteristics of contractile 5-HT receptors in isolated human omental arteries: presence of 5-HT1 and 5-HT2 receptors.

5-Hydroxytryptamine (5-HT) has a variety of biological effects, e.g. it induces and modulates vascular smooth muscle activity. The effects are mainly mediated via a hetergenous group of 5-HT receptor subtypes. In order to elucidate the 5-HT receptor mechanisms in the human splanchnic circulation, in vitro studies were carried out on omental arteries obtained from patients undergoing abdominal surgery. Four 5-HT receptor agonists with different selectivity all induced concentration-dependent contraction (potency and order of potency indicated): 5-HT (non-selective; 6.12 +/- 0.14)=sumatriptan (5-HT1; 6.32 +/- 0.07) > alpha-methyl-5-HT (5-HT2; 5.41 +/- 0.05) > 2-methyl-5-HT (5-HT3; < or =4.46+/-0.05). The 5-HT1/5-HT2 receptor antagonist methiothepin antagonised the contraction induced by 5-HT, sumatriptan, alpha-methyl-5-HT and 2-methyl-5-HT. The 5-HT2 receptor antagonist ketanserin antagonised the contraction induced by 5-HT, alpha-methyl-5-HT and 2-methyl-5-HT. The 5-HT3 receptor antagonist tropisetron did not antagonise the contraction elicited by 2-methyl-5-HT. The results suggest that 5-HT-induced conataction in human omental arteries involves both 5-HT1 and 5-HT2, but maybe not 5-HT3-receptors.

Adult↗
PubMed2002

Correlation between peri-operative serum lactate levels and outcome in pancreatic resection for pancreatic cancer, preliminary report.

This study was undertaken in order to verify if peri-operative serum lactate level changes, resulting from manipulation of the splanchnic circulation during pancreatectomy, reflected clinical outcome in twenty patients (9 males-11 females age 33 to 76) operated for pancreatic cancer. Lactate levels were evaluated at the beginning of the procedure (T0), after surgical manipulation before pancreatic resection (T1), after resection (T2), and 24 hours post-op. (T3). Furthermore, to highlight possible hemodynamic instability that could contribute to altered lactate clearance, mean arterial pressure (MAP) and central venous pressure (CVP) were continuously monitored during the study period. Peri-operative mortality within 60 days after surgery, Intensive Care Unit (ICU) length of stay, and peri-operative complications were the main indicators investigated in order to evaluate the impact of serial lactate levels in this patient population. Hyperlactatemia observed peri-operatively during pancreatic resection for cancer is significantly correlated with peri-operative mortality and also with longer ICU length of stay. Though, due to the relatively small number of the patients, more extensive investigation is needed in order to confirm such interesting preliminary data.

Adenocarcinoma↗
PubMed1986

Prostaglandins in diagnostic and therapeutic superior mesenteric artery pharmacoangiography.

The hemodynamic effects of prostaglandins PGA1, PGE1, PGE2, and PGF2 alpha on the splanchnic circulation were evaluated in five chronic dogs with portal hypertension, periportal fibrosis, and portosystemic venous shunting. The maximum effect was achieved with dosages of 2 micrograms/kg/min after bolus injection into the superior mesenteric artery. With this dosage a monophasic increase of portal blood flow and pressure was found with PGA1, PGE1, and PGE2, whereas PGF2 alpha caused a biphasic response: an initial decrease in portal blood flow and pressure was followed by an increase in these parameters. The average peak increase in portal blood flow and pressure was similar for PGE1 and PGF2 alpha, and significantly smaller for PGA1 and PGE2. Average peak iodine concentrations in the portal blood after superior mesenteric angiography were highest with PGF2 alpha, similar for PGE1 and tolazoline, and lowest in controls. The vasoconstrictor effect of PGF2 alpha is, overall, reduced and less reproducible when compared with vasopressin. This investigation suggests that both PGE1 and PGF2 alpha are effective for improved arterial portography, the latter agent appearing superior. On the other hand, PGF2 alpha cannot be recommended as a therapeutic agent for the treatment for gastrointestinal and particularly variceal bleeding.

Angiography↗
PubMed2003

The effect of vasopressin on gastric perfusion in catecholamine-dependent patients in septic shock.

OBJECTIVE: To study the effect of continuous infusion of vasopressin on the splanchnic circulation in patients with severe septic shock. DESIGN: Prospective clinical study. SETTING: ICU in a teaching hospital. PATIENTS: Eleven consecutive patients with documented septic shock who remained hypotensive despite norepinephrine infusion at a rate > or =0.2 microg/kg/min. INTERVENTIONS: Insertion of a gastric tonometry catheter, and continuous infusion of vasopressin 0.04 U/min during 4 h. MEASUREMENTS AND MAIN RESULTS: Difference between gastric and arterial CO(2) partial pressure (P[g-a]CO(2) gap), mean arterial pressure, and cardiac index were recorded at baseline and after 15 min, 30 min, 60 min, 120 min, and 240 min. RESULTS: The median P(g-a)CO(2) gap increased from 5 mm Hg at baseline to 19 mm Hg after 4 h (p = 0.022). Mean arterial pressure increased from 61 +/- 13 mm Hg at baseline to 68 +/- 9 mm Hg after 4 h (p = 0.055). No significant changes in cardiac index were noted. CONCLUSIONS: In norepinephrine-dependent patients in septic shock, continuous infusion of low-dose vasopressin results in a significant increase of the P(g-a)CO(2) gap compatible with GI hypoperfusion.

APACHE↗
PubMed1991

Evidence for release of endothelin-1 in pigs and humans.

The release and pharmacokinetics of endothelin-1 (ET-1) in plasma were studied in pigs and humans in vivo. Between 50-90% of plasma ET-1-like immunoreactivity (LI) was cleared by the pig and human kidney, splanchnic circulation, and skeletal muscle. The precursor big ET-1 was only cleared to a moderate extent (34%) by the kidney with progressive formation of ET-1-LI in the pig. The half-lives of circulating ET-1-LI and big ET-1-LI were about 1 and 10 min, respectively. The threshold vasoconstrictor effects for plasma ET-1-LI in the splanchnic and renal circulation in humans were around 30 pM. ET-1-LI in fetal umbilical arterial plasma was very high (15 pM before and 94 pM after establishment of breathing) compared with about 2 pM in maternal plasma. Bacterial endotoxin or sepsis increased ET-1-LI in plasma more than fivefold in both pigs and humans reaching levels close to threshold vasoconstriction. However, hemorrhagic shock or hypotension did not alter plasma ET-1-LI. It is concluded that ET-1 has a short half-life with very high regional plasma clearance, which limits detection of overflow into the systemic circulation. However, release of ET-1 reaching vasoconstrictor levels seems to occur both upon special physiological circulatory changes in the newborn and in septic shock.

Animals↗
PubMed2005

Hepatorenal syndrome: a dreaded complication of end-stage liver disease.

Hepatorenal syndrome is the dreaded complication of end-stage liver disease characterized by functional renal failure due to renal vasoconstriction in the absence of underlying kidney pathology. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. This underfilling triggers a compensatory response with activation of vasoconstrictor systems leading to intense renal vasoconstriction. The diagnosis is based on established diagnostic criteria aimed at excluding nonfunctional causes of renal failure. The prognosis of patients with hepatorenal syndrome is extremely poor especially in those who have a rapidly progressive course. Liver transplantation is the best option in suitable candidates, but it is not always applicable due to the short survival expectancy and donor shortage. Pharmacological therapies based on the use of vasoconstrictor drugs (terlipressin, midodrine, octreotide, or noradrenline) are the most promising in the aim of successfully offering a bridge to liver transplantation. Other treatments such as transjugular intrahepatic portosystemic shunts and albumin dialysis are effective but experience is very limited. Although there is limited information on the prevention of hepatorenal syndrome, intravenous albumin infusion in patients with spontaneous bacterial peritonitis and with oral pentoxifylline in patients with acute alcoholic hepatitis seems to effectively prevent hepatorenal syndrome in these two settings.

Hepatorenal Syndrome↗
PubMedDate not supplied

Hepatorenal syndrome.

Hepatorenal syndrome is complication of advanced cirrhosis characterized by renal failure, changes in systemic blood pressure, and increased activity of endogenous vasoactive systems. Renal failure is due to severe renal vasoconstriction developing in the late stages of cirrhosis. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. This underfilling triggers a compensatory response with activation of vasoconstrictor systems. The diagnosis of hepatorenal syndrome is based on established diagnostic criteria aimed at excluding nonfunctional causes of renal failure. The prognosis of patients with hepatorenal syndrome is very poor. Liver transplantation is the best option in selected patients, but it is not always applicable due to the short survival expectancy and donor shortage. Pharmacological therapies based on the use of vasoconstrictor drugs (terlipressin, midodrine, octreotide or noradrenline) are the most promising in aims of successfully offering a bridge to liver transplantation. Prevention of hepatorenal syndrome with albumin infusion is recommended in patients with spontaneous bacterial peritonitis and with pentoxifylline in patients with acute alcoholic hepatitis.

Hepatorenal Syndrome↗
PubMed1988

Effect of portacaval surgical anastomosis on systemic and splanchnic hemodynamics in portal hypertensive, cirrhotic rats.

The effect of surgical end-to-side portacaval anastomosis (PCSA) on systemic and splanchnic circulation has been studied in cirrhotic rats with portal hypertension (CCl4-phenobarbital method) and in control animals. Hemodynamics have been measured using the microsphere technique, with a reference sample for the systemic hemodynamic measurements, and intrasplenic injection for portal systemic shunting rate measurements. Compared with controls, sham-operated (SO) cirrhotic rats showed a hyperdynamic circulation with increased cardiac output (CO) and decreased mean arterial pressure and peripheral resistances. PCSA in control rats induced only a small change in systemic hemodynamics, with parallel decreases in arterial pressure and peripheral resistances, and a small, nonsignificant increase in CO. In cirrhotic rats, PCSA induced a decrease of CO to values similar to those of control rats, with an increase in total peripheral resistances. PCSA induced an increase in hepatic arterial blood flow in control and in cirrhotic rats, portal pressure becoming in this latter group not different from that of control rats. Blood flow to splanchnic organs was higher in SO cirrhotic than in SO control animals. Thus portal venous inflow was also increased in SO cirrhotic rats. PCSA induced an increase in portal venous inflow in control rats, which was only significant in cirrhotic rats when expressed as a percentage of CO. In SO control animals, a significant correlation was observed between total peripheral resistances and splanchnic arteriolar resistances and between CO and splanchnic blood flow. These correlations were not observed in cirrhotic rats. These results do not support the hypothesis that hyperdynamic circulation shown by cirrhotic rats is based on increases in splanchnic blood flow and (or) massive portal systemic shunting.

Animals↗