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At least 55 records · Page 3Linked to original sources
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↗
PubMedDate not supplied

CT findings of increased splanchnic circulation in a case of celiac sprue.

We report a diagnosis of celiac disease first suggested by the computed tomographic appearance, which included findings indicative of increased splanchnic circulation. Similar findings have been reported with angiography and ultrasound but, to our knowledge, have not been reported with computed tomography.

Celiac Disease↗
PubMed1983

Circulatory responses to midazolam anesthesia: emphasis on canine splanchnic circulation.

Experiments were performed on nine dogs instrumented with pulmonary artery Swan-Ganz catheters and catheters placed into the distal aorta and posterior caval vein. Electromagnetic flowmeter probes were placed around the portal vein and hepatic artery, and the portal vein was cannulated. A week later, systemic and splanchnic circulatory variables were studied before and after 10 mg/kg of midazolam given intravenously. Three minutes after injection, heart rate increased 26% (P less than 0.006), cardiac index decreased 15% (P less than 0.001), portal flow increased 19% (P greater than 0.05), and hepatic arterial flow decreased slightly (P less than 0.002). Later, portal blood flow decreased 17% below baseline values (P less than 0.006). The biphasic response of portal blood flow to midazolam is probably related to redistribution of blood within the splanchnic system (blood mobilization from spleen and intestine). It is suggested that because maintenance of cardiac output during midazolam anesthesia depends on compensatory mechanisms, failure to increase cardiac output with compensatory increases in heart rate, contractility, and blood volume mobilization from the splanchnic circulation could result in decreased cardiac output.

Anesthesia, Intravenous↗
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↗
PubMed1993

Modified Doppler flowmetry in the splanchnic circulation.

BACKGROUND: Absolute measurements of blood flow by Doppler ultrasonography are subject to substantial error. A simplified method of Doppler flowmetry using conventional duplex Doppler equipment was studied to establish its validity in determining short-term changes in flow in the splanchnic circulation in portal hypertension. METHODS: Two simple indices were measured: peak velocity averaged over two cardiac cycles and vessel diameter. The relationship between peak and mean velocity was studied using a Doppler phantom. The feasibility of studying relevant vessels and the constancy of regional flow was determined by performing Doppler flowmetry in a basal state twice within 2 hours. RESULTS: Constancy of relationship between peak and mean velocities was confirmed (r > 0.98). Examination was successful in the majority of 28 consecutive patients with portal hypertension for superior mesenteric, main portal, right portal, and paraumbilical (when patent) veins, but was successful in only 54% for the hepatic artery. Constancy of basal flow was found in 11 selected patients when group data were considered, but in individuals, substantial and unpredictable variance was found. CONCLUSIONS: Modified Doppler flowmetry appears valid in the assessment of short-term changes in splanchnic blood flow of patients with portal hypertension. Individual variance in baseline flow is identified as a potential problem and is further reason for caution in the interpretation of measurements of Doppler flow.

Hepatic Artery↗
PubMed2004

Changes in splanchnic circulation during an alveolar recruitment maneuver in healthy porcine lungs.

UNLABELLED: Recruitment maneuvers (RM) are advocated as a complement to mechanical ventilation during anesthesia and in acute lung injury. However, they produce high intrathoracic pressures and volumes that may compromise hemodynamics. Our aim was to analyze the effect of a RM on hemodynamics in 10 anesthetized pigs. We assessed carotid, pulmonary, femoral, and hepatic arterial pressures, hepatic and portal venous pressures, total splanchnic (celiac trunk + superior mesenteric artery), hepatic, splenic, renal, and carotid arterial flows, and portal venous flow. We recorded hemodynamics, respiratory mechanics and blood gases before and at 8 min after RM (sustained inflation to 40 cm H(2)O of airway pressure lasting 20 s). Hemodynamics were also measured during RM, and at 1, 3, and 5 min after RM. All flows (P = 0.030) and arterial pressures (P < or = 0.048) decreased during RM, whereas venous pressures increased (P = 0.030). Flows and pressures returned to 75%-109% of baseline immediately after RM. Total splanchnic, renal and portal flows remained decreased at 8 min after RM (P < or = 0.042). Oxygenation did not change, and respiratory mechanics improved after the RM. RM produced a marked, though transitory, impairment of blood flow in all studied vessels. Despite prompt partial recovery, total splanchnic circulation remained reduced at 8 min after RM. This residual decrease may present a risk in conditions with markedly compromised circulatory reserves. IMPLICATIONS: Recruitment maneuvers (RM) produce high intrathoracic pressures and volumes that may compromise hemodynamics. We found a marked transient impairment of hemodynamics during a RM in 10 anesthetized pigs. At 8 min after RM, blood flow remained reduced in the celiac trunk, superior mesenteric, and renal arteries, as well as in the portal vein. This residual decrease may present a risk in conditions with markedly compromised circulatory reserves.

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↗
PubMed2000

Heparin induces release of phospholipase A(2) into the splanchnic circulation.

UNLABELLED: Cardiopulmonary bypass results in increased plasma activity of phospholipase A(2) (PLA(2)) that appears to be caused by the administration of heparin. High PLA(2) activity may be responsible for increased production of eicosanoids and, thus, may be implicated in various pathophysiologic events associated with cardiac surgery. To investigate the site of PLA(2) secretion, blood samples were simultaneously collected from the radial artery, the pulmonary artery, and the hepatic vein at 2, 4, 6, and 20 min after systemic heparinization (350 U/kg). Within 2 min of the heparin injection, plasma activity of PLA(2) increased 4- to 9-fold and remained so for at least 20 min. Two minutes after the heparin injection, PLA(2) was significantly higher in the hepatic vein than in the radial artery (P: < 0.01). No such difference was detected between pulmonary and radial arteries. When heparin was added to blood samples in vitro (5-100 U/mL), plasma activity of PLA(2) did not increase, which suggests that the enzyme was not secreted by blood cells. IMPLICATIONS: Heparin, given in the dosage required for cardiopulmonary bypass, caused release of phospholipase A(2) into the splanchnic circulation.

Aged↗
PubMed1987

Effect of synthetic neuromedin U-8 and U-25, novel peptides identified in porcine spinal cord, on splanchnic circulation in dogs.

Two novel peptides which exert a potent stimulant effect on rat uterus smooth muscle have recently been identified in porcine spinal cord. These peptides designated neuromedin U-8 and U-25 have been reported to exert a hypertensive effect in rats. But further biological activities are not known. In the present study, the effect of these peptides on blood flow in portal vein, superior mesenteric artery and pancreatic tissue and on blood pressure were examined in dogs, utilizing recently developed ultrasonic transit time volume flow meter and laser Doppler flow meter. Neuromedin Us potently reduced blood flow in superior mesenteric artery. The minimum reductions could be observed even at very small doses of neuromedin U-25 (32 fmol/kg) and U-8 (90 fmol/kg), while the maximal reductions of 48.4 and 51.0% were attained at the doses of 320 pmol/kg (U-25) and 900 pmol/kg (U-8), respectively. These peptides also reduced portal vein blood flow, and the maximal reductions of 42.1 and 37.2% were attained at the doses of 32 pmol/kg (U-25) and 90 pmol/kg (U-8), respectively. On the other hand, blood flow in pancreatic tissue increased slightly with the maximal increases of 13.8% at 3.2 pmol/kg (U-25) and 11.8% at 9 pmol/kg (U-8), respectively. The maximal increases of blood pressure were 5.2% at 320 pmol/kg (U-25) and 4.3% at 90 pmol/kg (U-8). Furthermore, neither neuromedin U-25 nor U-8 influenced the axillary artery blood flow, suggesting their selective effect on splanchnic blood flow. Because of the potent and probably selective activity on splanchnic circulation, neuromedin U-25 and U-8 may well be recognized as physiologically significant novel neuropeptides or hormones.

Animals↗
PubMed1989

[Effects of celiac plexus block on splanchnic circulation--II: Changes in the systemic hemodynamics and the blood flow of the liver and kidney in dogs].

Effects of celiac plexus block (CPB) on systemic and splanchnic circulation, especially of liver and kidney, were investigated in twenty nine mongrel dogs. CPB was performed by an anterior approach through a catheter placed in a paraaortic compartment using 7 mg.kg-1 of 2% mepivacaine. Tissue blood flow measurement was performed by a hydrogen clearance method in eleven dogs, and vascular blood flow was measured in eighteen dogs by an electromagnetic flow meter. Swan-Ganz catheter was inserted to measure mean arterial pressure (ABP), heart rate (HR), central venous pressure (CVP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP) and cardiac output (CO). Then stroke volume (SV), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were calculated. Following CPB, ABP, HR, CVP and C.O. were significantly decreased at 7 to 9%. PAP decreased at 5%. PCWP, SV, SVR and PVR were unchanged. The hepatic arterial blood flow increased significantly, and portal venous blood flow decreased after CPB transiently, and then recovered to control value or to a higher level at 60min after CPB. The tissue blood flow of the liver tended to increase, but the change was not significant. In the kidney, both arterial and tissue blood flows increased significantly after CPB. The results suggest that following CPB, hepatic and renal tissue blood flows increased because of the increments of their arterial blood flows, unless a profound systemic hemodynamic depression occurred.

Animals↗
PubMed1986

Role of ethanol metabolism in the ethanol-induced increase in splanchnic circulation.

In this study we report the effect on splanchnic hemodynamics of acute oral ethanol at doses ranging from 0.25 to 4.0 g/kg body wt. Flows were determined by use of a radioactive microsphere technique. Ethanol was found to increase portal blood flow by 23-57%. In awake rats this increase reached a plateau at the 0.5 g/kg dose. In ketamine-anesthetized rats, the increase was observed only at doses of 3.0 g/kg or more, with the response at doses of 0.5, 1.0, and 2.0 g/kg being suppressed by ketamine. Inhibition of alcohol dehydrogenase by intra-arterial administration of 4-methylpyrazole resulted in suppression of the liver blood flow increase after ethanol was administered to awake animals. Ethanol in the range of doses studied did not result in changes in blood glucagon levels. Rats fed ethanol-containing diets for 4 wk and withdrawn for 18 h had the same response to acute oral ethanol as did naive rats. It is suggested that ethanol metabolism mediates the effects of ethanol on splanchnic blood flow. An increase in splanchnic blood flow when concurrent with an increase in liver O2 consumption induced by ethanol might protect the liver from hypoxic damage.

Animals↗
PubMed1985

Acute effect of propranolol on splanchnic circulation in normal and portal hypertensive rats.

Propranolol decreases portal venous pressure in patients with cirrhosis but no method is available in man to study the effect of this beta-blocker on splanchnic organ blood flow. Because in rats, the microsphere method allows evaluation of regional blood flow, the acute effect of propranolol on both splanchnic and systemic circulations was studied in normal rats and in rats with portal hypertension due to portal vein stenosis. Portal venous pressure significantly decreased during propranolol administration in normal (5.6 +/- 1.0-4.7 +/- 1.1 mm Hg; mean +/- SD) as well as in portal hypertensive rats (11.7 +/- 2.3-10.3 +/- 1.8 mm Hg). Propranolol slightly decreased cardiac output and arterial pressure in all rats. Portal tributary blood flow was significantly reduced by propranolol in normal rats (17.4 +/- 3.0-11.3 +/- 2.2 ml/min) and in portal hypertensive rats (23.7 +/- 5.0-16.6 +/- 3.3 ml/min). Accordingly vascular resistance of the different organs in the portal venous territory increased in these rats receiving propranolol. The percentage of the decrease in portal tributary blood flow was significantly more marked than the percentage of reduction in cardiac output in portal hypertensive rats but, in normal rats, these percentages were parallel. Hepatic arterial blood flow did not change or slightly increased and, consequently, hepatic arterial vascular resistance decreased. These findings further clarify the marked effects of propranolol on splanchnic circulation.

Animals↗