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Control of the splanchnic circulation.
The major regulatory factors in the mesenteric circulation include general hemodynamic forces, the autonomic nervous system, circulating vasoactive substances, tissue metabolites and intrinsic characteristics of vascular smooth muscle. During mesenteric ischemic states smooth muscle spasm elevates resistance to blood flow and aggravates intestinal tissue hypoxia leading to mucosal necrosis. Close intraarterial infusion of potent vasodilator drugs holds the promise of reversing intestinal ischemia and preserving viability of the gut.
[Collateral splanchnic circulation (author's transl)].
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Adaptations in control of blood flow with training: splanchnic and renal blood flows.
Acute exercise is associated with large increases in cardiac and active skeletal muscle blood flows and reduced blood flows to inactive muscle, skin, kidneys, and organs served by the splanchnic circulation. Splanchnic and renal blood flows are reduced in proportion to relative exercise intensity. Increased sympathetic nervous system outflow to splanchnic and renal vasculature appears to be the primary mediator of reduced blood flows in these circulations, but the vasoconstrictors angiotensin II and vasopressin also make important contributions. Human and animal studies have shown that splanchnic and renal blood flows are reduced less from resting levels during acute exercise after a period of endurance exercise training. Investigations of mechanisms involved in these adaptations suggest that reductions in sympathetic nervous system outflow, and plasma angiotensin II and vasopressin concentrations, are involved in lesser splanchnic and renal vasoconstriction exhibited by trained individuals. In addition, a reduced response to the sympathetic neurotransmitter norepinephrine in renal vasculature may contribute to greater blood flow to the kidney during acute exercise after training. Greater splanchnic and renal blood flows during acute exercise following training are potentially beneficial in that disturbance from homeostasis would be less in the trained state. Additionally, increased splanchnic blood flow in the trained state may confer benefits for glucose metabolism during prolonged exercise.
The effect of bucolome on the blood circulation of splanchnic organs in rats with and without pentobarbitone anesthesia.
Using carbonized microspheres, either 15 microns or 50 microns in diameter and labeled with 85Sr, 51Cr or 141Ce, the effect of bucolome (1-cyclohexyl-5-n-butyl-2-, 4, 6-trioxoperhydropyrimidine), a non-steroid anti-inflammatory agent and potent choleretic, on the splanchnic blood circulation was studied in rats with and without pentobarbitone sodium anesthesia. Pentobarbitone sodium caused a significant increase in the distribution of cardiac output in the major splanchnic organs, in particular in the small and large intestines. An i.p. injection of bucolome (20 mg/100 g) produced a significant increase in the cardiac output distribution in the small intestine, and a significant decrease in the pancreatic fraction in both rat groups with and without pentobarbitone anesthesia, in spite of the large increase in the base-line values caused by anesthesia.
Mechanisms of a clonidine-induced decrease in portal pressure in normal and cirrhotic conscious rats.
The effects of clonidine on portal pressure and splanchnic blood flow were studied in conscious rats with sinusoidal portal hypertension due to cirrhosis induced by bile duct ligation. In cirrhotic and sham-operated rats, clonidine (20 micrograms per kg body weight, intravenously) significantly reduced portal, pressure from 19.0 +/- 0.6 to 14.5 +/- 1.0 mmHg and from 9.8 +/- 0.9 to 7.3 +/- 0.5 mmHg, respectively. No significant change in systemic hemodynamics was observed. In cirrhotic rats, clonidine reduced portal pressure, probably by producing a significant increase in portal tributary vascular resistance leading to a 25% decrease in portal tributary blood flow (radioactive microsphere method). In sham-operated rats, clonidine reduced portal pressure presumably by decreasing hepatic portal vascular resistance, since no significant change in portal tributary blood flow was observed. In both groups, clonidine administration significantly decreased plasma noradrenaline concentration. Placebo administration produced neither significant hemodynamic nor significant plasma noradrenaline concentration change. These findings indicate that the sympathetic regulation of the splanchnic circulation is impaired in cirrhotic rats.
Circulatory actions of vasopressin in anaesthetized rats with portal hypertension subjected to haemorrhage.
To assess the influence of vasopressin on splanchnic and renal circulatory changes induced by haemorrhage in portal hypertension, we studied 4 groups of 7 rats with chronic portal vein stenosis. Two groups received saline (C and H) and two groups vasopressin, 0.01 IU/kg/min (VP and VP-H). Ten minutes after starting drug infusion, group H and VP-H animals were allowed to bleed from the superior mesenteric vein. Both haemorrhage and vasopressin alone, decreased portal venous tributary blood flow and pressure but their association was not additive (as reflected by comparable bleeding rate in groups H and VP-H). By contrast, vasopressin increased renal perfusion in bleeding and non-bleeding animals whereas haemorrhage alone decreased renal perfusion. These results indicate that the effects of vasopressin on the splanchnic circulation in bleeding anaesthetized animals differ from the effects observed when blood volume is normal. Therefore, in patients with cirrhosis the effects of vasopressin during bleeding might also differ from those observed in patients in stable condition.
Role of EDRF in splanchnic blood flow of normal and chronic portal hypertensive rats.
The role of endogenous endothelium-derived relaxing factor (EDRF) in splanchnic blood flow was assessed in normal and portal vein-stenosed rats (PSRs). Specific and maximal inhibition of EDRF was achieved by intravenous administration of NG-nitro-L-arginine (L-NOARG) as a 1.75 mumol/kg bolus, followed by constant infusion of 1.75 mumol/kg for 20 min. Pretreatment with L-arginine (175 mumol/kg iv) completely blocked both hypertension and the reduction in blood flow induced by L-NOARG. Pretreatment with D-arginine (175 mumol/kg iv) and prazosin (500 micrograms/kg iv) did not attenuate the pressor effect of L-NOARG. These results indicate that L-NOARG selectively blocks EDRF. The blood flow to the stomach, duodenum, jejunum, ileum, cecum, and colon in control rats was 81.1 +/- 8.7, 199.1 +/- 21.9, 153.3 +/- 20.0, 68.6 +/- 10.6, 79.4 +/- 11.8, and 59.3 +/- 7.8 ml.min-1.100 g-1, respectively, and in PSRs was 141.4 +/- 10.8, 244.0 +/- 10.4, 208.3 +/- 9.8, 126.8 +/- 13.0, 166.9 +/- 16.5, and 94.8 +/- 4.7 ml.min-1.100 g-1, respectively. Blood flow was measured using the radioactive microsphere method. L-NOARG significantly reduced blood flow to the stomach, duodenum, jejunum, ileum, cecum, and colon in control rats by 47, 44, 48, 55, 40, and 41%, respectively, and in PSRs by 30, 27, 36, 33, 28, and 23%, respectively. The magnitude of blood flow reduction in PSRs was lower than in normal rats. These results indicate that EDRF plays an important role in control of the splanchnic circulation, but its effect on the hyperdynamic circulation observed in PSRs is insignificant.
Regional vascular responses to prolonged lower body negative pressure in normal subjects.
The purpose of this study was to determine the effects of sustained unloading of baroreceptors in humans. The regional hemodynamic responses to lower body negative pressure (LBNP) were determined in 20 normal subjects. LBNP at -10 mmHg for 1 h decreased central venous pressure (CVP) without affecting blood pressure or heart rate, suggesting that only cardiopulmonary baroreceptors were unloaded. Forearm blood flow (FBF) and splanchnic blood flow (SBF) both decreased. Renal blood flow (RBF) did not change, but glomerular filtration rate (GFR) increased. Plasma renin activity rose slightly, whereas plasma norepinephrine levels did not change. Peak LBNP (either -20 or -40 mmHg for 1 h) caused a further decline in CVP and narrowed pulse pressure, thus unloading both arterial and cardiopulmonary baroreceptors. FBF returned to base-line values and SBF decreased further. RBF fell and the GFR remained increased. Plasma renin activity increased further, and plasma norepinephrine level rose. Thus the forearm and splanchnic circulations are sensitive to sustained unloading of cardiopulmonary baroreceptors; renal vasoconstriction occurs with additional unloading of arterial baroreceptors. Renin-angiotensin system activation during LBNP may be pertinent to the preservation of glomerular filtration.
Involvement of endogenous endothelin-1 in exercise-induced redistribution of tissue blood flow: an endothelin receptor antagonist reduces the redistribution.
BACKGROUND: Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide. Exercise results in a significant redistribution of tissue blood flow, which greatly increases blood flow in active muscles but decreases it in the splanchnic circulation. We reported that exercise causes an increase of ET-1 production in the internal organ and then hypothesized that ET-1 participates in the exercise-induced redistribution of tissue blood flow. We investigated the effects of acute endothelin-A (ETA)-receptor blockade on regional tissue blood flow during exercise in rats. METHODS AND RESULTS: Regional blood flow in the kidney, spleen, stomach, intestine, and muscles was measured using the microsphere technique before and during treadmill running of 30 minutes duration at 30 m/min after pretreatment with either an ETA-receptor antagonist (TA-0201; 0.5 mg/kg) or vehicle in rats. Blood flow in the kidney, spleen, stomach, and intestine was decreased by exercise, but the magnitude of the decrease after pretreatment with TA-0201 was significantly smaller than that after pretreatment with vehicle. Furthermore, the increase in blood flow to active muscles induced by exercise was significantly smaller in rats pretreated with TA-0201 than those pretreated with vehicle. CONCLUSIONS: The present study revealed that ET-1-mediated vasoconstriction participates in the decrease of blood flow in the internal organs of rats during exercise, and therefore, that these actions of endogenous ET-1 partly contribute to the increase of blood flow in active muscles during exercise. The data suggest that endogenous ET-1 participates in the exercise-induced redistribution of tissue blood flow.
Regional renal and splanchnic blood flows during nicotine infusion: effects of alpha and of combined alpha and beta adrenergic blockade.
Renal (cortex and medulla) and splanchnic (duodenum, liver, pancreas and spleen) blood flows were measured with 25-mu radioactive microspheres in anesthetized, open-chest dogs. The effects of nicotine (36 micrograms/kg/min i.v.) before and after selective alpha adrenergic blockade (phenoxybenzamine, 1 mg/kg i.v.) and before and after combined alpha and beta adrenergic blockade (phenoxybenzamine, 1 mg/kg i.v. and propranolol, 1 mg/kg i.v.) were evaluated. Before adrenergic blockade, nicotine increased arterial pressure (+82%) but had heterogeneous directional effects on regional blood flows: pancreas (-64%), duodenum (-33%), kidney cortex (-31%), kidney medulla (-17%), liver (+5%) and spleen (+71%). Vascular conductance was reduced in kidney cortex (-61%), kidney medulla (-57%), duodenum (-59%), liver (-46%) and pancreas (-79%) and was not altered in spleen. Selective alpha adrenergic blockade prevented the hypertensive response to nicotine, but heterogeneous changes in regional flows persisted: pancreas (-40%), spleen (-40%), kidney medulla (-35%), kidney cortex (-31%), liver (+50%) and duodenum (+74%). After combined alpha and beta adrenergic blockade, nicotine increased systemic arterial pressure (+75%) and decreased vascular conductance in all tissues. Results indicate: 1) a heterogeneous influence of nicotine in renal and splanchnic circulations associated with regional differences in activities of alpha and beta adrenergic receptors and 2) a potent nonadrenergic vasoconstrictor response in these circulations to nicotine after blockade of alpha and beta adrenergic receptors.
Duplex-Doppler evaluation of the effects of propranolol and isosorbide-5-mononitrate on portal flow and splanchnic arterial circulation in cirrhosis.
BACKGROUND: A decrease in portal flow is an important pharmacological effect of drugs used for the prophylaxis of variceal bleeding. AIM: To assess the acute and chronic effects of propranolol, and the effect of the acute addition of isosorbide-5-mononitrate, on splanchnic circulation. METHODS: Measurements of portal blood flow volume (PBFV) and of Doppler ultrasound pulsatility index of the superior mesenteric, femoral and interlobar renal arteries were performed in 10 cirrhotic patients with varices at baseline, 90 min after propranolol or placebo, after 30 days of chronic propranolol treatment and 45 min after the addition of isosorbide-5-mononitrate. RESULTS: The mean PBFV was significantly lower at all times than at baseline, with the greatest mean percentage decrease achieved after the addition of isosorbide-5-mononitrate (> or = 20% in all patients). Acute changes, however, did not predict the chronic effects in many patients. Isosorbide-5-mononitrate significantly increased the mesenteric and femoral pulsatility indices, whereas no significant change was observed in the kidney. CONCLUSIONS: Propranolol significantly decreases PBFV, but chronic effects cannot be reliably predicted by the acute change. All patients achieved a decrease in PBFV of > or = 20% after the acute addition of isosorbide-5-mononitrate to chronic propranolol treatment.
[Splanchnic portal circulation (enhancement of radiologic image intensity and of visibility of collateral branches with prostaglandin E1)].
The authors present the results of a comparative study of mesenterico-portographies with and without the use of Prostaglandin E1 (PGE1) injected intrarterially into the superior mesenteric artery as an adjunct to the radiographic procedure. Twenty eight patients, with varied hepatic and biliopancreatic ailments, referred to the Radiologic Department for angiographic appraisal of the splanchnic circulation were studied. Two series of radiographies were realized after catheterization of the superior mesenteric artery: a first after the injection of the contrast only and a second after the injection of 50 micrograms of PGE1 as a bolus prior the contrast means. The difference in opacification of the various segments of the portal system and the lapse of time necessary to attain the maximum radiographic density were appraised. They observed that, with the use of PGE1 was attained a regular, intense and swift opacification of the superior mesenteric vein, portal vein and intrahepatic branches in all patients that had those segments previous and/or hepatotropic circulation. There was a significative reduction in the lapse of time necessary to attain the maximum opacification. Also they observed, with the use of the PGE1, the opacification of collateral branches of the portal system in more patients and intensification in those that were previously opacified. Because of the good results attained with the use of the PGE1, its transitory pharmacologic action and absence of collateral reactions with the dose used, they recommend its regular use when this investigation is performed.
Effects of ACE-inhibition on regional circulation in congestive heart failure.
During development of heart failure there are marked changes in the peripheral circulation. The renal and splanchnic circulations are reduced early. The cerebral circulation is maintained by autoregulation. Skeletal muscle blood flow is reduced in relation to the decrease of cardiac output. There are also important metabolic changes in these muscles with reduced mechanical efficiency. Treatment with arterial vasodilators increase cardiac output. However, most of this increase is usually shunted, probably in the splanchnic circulation. If any, only small increases in muscle blood flow have been reported. ACE-inhibition has been shown to have beneficial acute effects on the renal, cerebral and skeletal muscle blood flow with improved flow in these areas. This treatment seems to be the most beneficial vasodilatory alternative available so far.
Mean transit times and the sites of synthesis and catabolism of tissue plasminogen activator and plasminogen activator inhibitor type 1 in young subjects.
Using an invasive technique, we studied the mean transit time, the net quantitative turnover rate, and the sites of synthesis and catabolism of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) in healthy young volunteers in the fasting, steady state. Blood was sampled simultaneously from a large hepatic vein, an artery and the inferior caval vein, while measuring the splanchnic plasma flow rate and the plasma volume. We found that the catabolism of active t-PA and t-PA antigen took place in the splanchnic circulation with net rates of 7.2 and 6.3 pmol/min, respectively. The extraction fraction and the mean transit time in the splanchnic circulation were, respectively, 0.63 and 5.6 min for active t-PA and 0.17 and 21 min for t-PA antigen. Active PAI-1 was synthesized in the splanchnic circulation at a rate of 890 IU/min and had a mean transit time of about 9.8 min. No net extraction of PAI-1 antigen took place in the splanchnic circulation. In conclusion, we demonstrated that active t-PA and t-PA antigen are catabolized and active PAI-1 produced in the splanchnic circulation in young healthy subjects during steady state. Furthermore, our data show that active t-PA was also eliminated outside the splanchnic region with a catabolism rate of about 8.4 pmol/min. No net complex formation could be demonstrated in the peripheral circulation. We therefore suggest that active t-PA is eliminated by a re-uptake in the endothelium in the peripheral vessels or in the lung circulation.
[Physiology and pathophysiology of intestinal circulation].
Splanchnic blood flow is regulated by cardiovascular factors, the autonomic nervous system, circulating vasoactive agents and local mechanical factors. Typical physiologic phenomena such as "autoregulation", "autoregulatory escape" and "countercurrent exchange" are discussed. Aspects of therapy especially for acute mesenteric infarction, are elucidated with reference to the circulating vasoactive agents, the effects of bowel distension on intestinal blood flow and reperfusion injuries.
Effect of acute hemodilution on intestinal perfusion and intramucosal pH after shock.
BACKGROUND: Restoration of oxygen delivery, especially to the splanchnic bed, is of critical importance during trauma resuscitation. Acute normovolemic hemodilution (ANH) has been used to reduce blood transfusion requirement during elective surgery. The effect of hemodilution on the splanchnic circulation during hemorrhagic shock (HS) is not well defined. METHODS: Swine were instrumented to measure systemic and splanchnic circulation effects of ANH after HS. The adequacy of the splanchnic circulation was assessed by changes in measured mucosal blood flow, mucosal tonometry, as well as by portal venous blood O2 saturation, portal venous CO2 saturation, and lactate. RESULTS: ANH after HS resulted in a final hematocrit of 18+/-2%. Superior mesenteric artery blood flow was returned to baseline levels; however, mucosal blood flow was still only 64% of baseline levels. However, at the same time mucosal PCO2 and intramucosal pH as well as portal venous O2 and CO2 saturation had normalized. CONCLUSION: As long as an adequate intravascular volume is maintained, hemodilution is well tolerated by the gut after HS. Concern about the adequacy of gut perfusion should not be a transfusion trigger after HS.
The renin-angiotensin system in swine during hypovolaemic shock combined with low-flow ischaemia of the sigmoid colon.
Colonic ischaemia is a serious complication after aortic surgery, and is most frequent after repair of ruptured aortic aneurysms. It was felt that the increased risk of colonic ischaemia during shock might be the result of a local effect of the renin-angiotensin system in the splanchnic circulation, which is exacerbated by poor perfusion. In order to evaluate the activity of the renin-angiotensin system in the colonic circulation, a subtotal occlusion of the distal aorta was induced in nine pigs. A colonic flow reduction of 70% was created for 4 hours. In the experimental group (n = 6), induce hypovolaemic shock, 20 cm3/kg blood was sampled at 45 min before resuscitation was performed with 20 cm3/kg haemaccel. The sham group (n = 3) did not have hypovolaemic shock induced. Blood samples were taken for determinations of angiotensin II, haemoglobin and lactate. Blood gas was obtained from the pulmonary artery and the caudal mesenteric vein for blood gas analysis and lactate determinations. ANOVA and the Wilcoxon sum rank test were used for statistical analysis. There was a significant increase in angiotensin II after induction of ischaemia in both groups. The increase in angiotensin II in the splanchnic circulation was more prominent than the increase in the systemic circulation (P < 0.01). In the experimental group, there was a sustained increase in angiotensin II levels in the splanchnic circulation following shock and reperfusion (P < 0/01). The increase in lactate concentrations, which was significantly higher in the experimental group (P < 0.05), was evidence of intestinal ischaemia. There was a significant decline in cardiac output and blood pressure during the period of shock (P < 0.05). The combination of colonic ischaemia and hypovolaemic shock followed by reperfusion leads to an increase in angiotensin II activity. The increase of the local activity of the renin-angiotensin system in the splanchnic circulation is more prominent after ischaemia and reperfusion. This is probably caused by a selective response of the splanchnic vasculature to shock, ischaemia and reperfusion.