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Role of glucagon in the splanchnic and systemic hemodynamic changes induced by portal-systemic blood shunting.

Portal-systemic blood shunting is often accompanied by hyperglucagonemia and hemodynamic changes. To determine this causal relation, splanchnic and systemic hemodynamics (radioactive microspheres) and plasma glucagon levels (radioimmunoassay) were assessed in conditions of total portal-systemic shunting in portacaval-shunted (PCS) rats and in sham-operated (SO) normal rats. To compare these results, another hemodynamic study was undertaken basally and during glucagon infusion in nonoperated normal rats. PCS rats showed a threefold greater plasma glucagon concentration than SO animals (924 +/- 134 vs. 309 +/- 18 pg/ml, p less than 0.01), and they developed a hyperdynamic splanchnic circulation with higher portal venous inflow than SO rats (8.29 +/- 1.1 vs. 5.09 +/- 0.4 ml/min/100 g, p less than 0.05). Infusion of a pharmacological dose of glucagon in normal rats increased portal venous inflow (from 4.92 +/- 0.33 to 6.24 +/- 0.48 ml/min/100 g, p less than 0.05) so as to imply this hormone in the development of the hyperdynamic splanchnic circulation in conditions of portal-systemic shunting. However, the discrepancies in systemic hemodynamics between PCS and glucagon-infused rats may be a result of the different plasma glucagon levels reached in the two groups.

Animals↗

Splanchnic and total body oxygen consumption differences in septic and injured patients.

The splanchnic and total body oxygen exchange and flow dynamics for injured patients (n = 7) and patients with sepsis and stable vital signs (n = 12) were studied. All patients were judged to be in the hyperdynamic phase of the stress response. In both patient groups 27% to 28% of the cardiac index was directed to the splanchnic circulation. However, in sepsis the splanchnic region consumed a significantly larger fraction (p less than 0.05) of the total body oxygen (43.8%) compared with that consumed in injury (30.2%). After injury, the regional splanchnic flow and oxygen consumption appeared to be well matched whereas in sepsis, a disproportionately higher oxygen consumption is found, which must be supplied by increasing blood oxygen extraction. This regional hypermetabolism of the splanchnic area probably results from the increased metabolic demand imposed by the various synthetic processes of this region. In addition, it is proposed that excessive discrepancy between splanchnic flow and oxygen demand may precipitate regional ischemia.

Aged↗

Usefulness of Doppler ultrasound in the evaluation of patients with active Crohn's disease.

OBJECTIVES: To assess the usefulness of Doppler ultrasound in the evaluation of the vascular changes in the splanchnic circulation and bowel wall described in patients with active Crohn's disease (ACD). DESIGN: We analyzed prospectively with Doppler ultrasound the mean velocity of portal flow, the resistive index (RI) of the superior mesentery artery (SMA) and we looked for vessels within the bowel wall. PATIENTS: 50 patients with ACD and 30 normal individuals. RESULTS: In comparison with normal individuals, patients with ACD showed a statistically significant difference (p < 0.001) in the mean velocity of the portal flow and in the RI of the SMA. In all patients with ACD, vessels could be seen within the bowel wall using the color Doppler ultrasound. CONCLUSION: Doppler ultrasound can be used as a non-invasive method to evaluate the vascular changes which develop in the splanchnic circulation and bowel wall of patients with ACD.

Adult↗

Peritoneal ventilation in rabbits: augmentation of gas exchange with cisapride.

BACKGROUND: Peritoneal ventilation has been shown to be effective in achieving extrapulmonary oxygenation and carbon dioxide elimination in an animal model of severe adult respiratory distress syndrome (ARDS). Cisapride is a "prokinetic" agent (increases gastric emptying), that may increase the splanchnic circulation and thus favourably affect gas exchange in peritoneal ventilation. METHODS: Using Doppler ultrasound the effect of cisapride on the portal venous circulation was examined in eight spontaneously breathing rabbits and the effect of cisapride on gas exchange in five rabbits spontaneously breathing room air was compared with that of a control group who did not receive cisapride. Its effect on gas exchange in five rabbits with ARDS being treated with mechanical lung and peritoneal ventilation was compared with that of a control group, and its effect on gas exchange in five rabbits with ARDS treated with conventional ventilation was also compared with that of a control group. RESULTS: Enteral administration of cisapride increased portal venous blood velocity, as measured ultrasonographically, by a mean of 188% one hour after receiving the drug. In rabbits with ARDS being treated with both peritoneal ventilation and mechanical ventilation to the lungs, those receiving cisapride had arterial oxygen tensions 1.5-3 times that of controls. Cisapride had no effect on arterial blood gas tensions in rabbits who were spontaneously breathing room air, nor in rabbits with ARDS who received only conventional mechanical lung ventilation. CONCLUSIONS: Cisapride increases arterial oxygenation in rabbits with severe ARDS treated with peritoneal ventilation, probably due to its ability to increase splanchnic circulation. It should be considered as an adjuvant medication to peritoneal ventilation.

Animals↗

Mesenteric blood flow response to feeding after systemic-to-pulmonary arterial shunt palliation.

BACKGROUND: We hypothesized that the splanchnic circulation protects against diastolic steal through a systemic-to-pulmonary arterial shunt by reducing its resistance. To test the hypothesis we compared the basal and postprandial mesenteric blood flow velocities and vascular resistance in infants after shunt palliation for their underlying cyanotic heart disease with those in nonshunted infants. METHODS: The basal and postprandial superior mesenteric arterial (SMA) time-average flow velocity (TAMV), end-diastolic flow velocity (EDFV), and relative resistance were assessed in 23 infants with congenital heart disease. The findings in the 9 shunted infants (group I) were compared with those in 14 nonshunted ones (group II). RESULTS: In group II, TAMV (0.25 +/- 0.07 versus 0.33 +/- 0.09 m/s, p < 0.001) and EDFV (0.08 +/- 0.04 versus 0.11 +/- 0.04 m/s, p = 0.003) increased, while SMA relative resistance decreased (297 +/- 121 versus 198 +/- 73 mm Hg/ms(-1), p < 0.001) postprandially. Similarly, in group I, TAMV (0.35 +/- 0.13 versus 0.48 +/- 0.19 m/s, p = 0.008) increased, while SMA relative resistance decreased (182 +/- 61 versus 116 +/- 38 mm Hg/ms(-1), p = 0.005) after feeding. However, whereas basal and postprandial diastolic flow was antegrade in group II, absent or retrograde diastolic flow was characteristic of group I (preprandial, -0.10 +/- 0.07 m/s; postprandial, -0.13 +/- 0.06 m/s). Furthermore, group I had significantly lower SMA relative resistance both before (p = 0.02) and after (p = 0.006) feeding. CONCLUSIONS: Profound disturbance of splanchnic perfusion occurs in infants palliated with a systemic-to-pulmonary arterial shunt. Their basal and postprandial SMA diastolic blood flow is either absent or reversed. The lowering of basal and postprandial resistance of the splanchnic circulation probably represents an adaptive mechanism to counteract such diastolic steal.

Blood Flow Velocity↗

Color duplex ultrasonography of the superior mesenteric artery after placement of endografts with suprarenal stents.

After endovascular repair of abdominal aortic aneurysm with endografts with suprarenal stents, the proximal uncovered stent may cross the origin of the superior mesenteric artery. Effects on splanchnic circulation are unknown and may include development of stenosis at the vicinity of the stent. The criteria of high-grade superior mesenteric artery stenosis using color duplex ultrasonography have been previously reported. The purpose of this study is to examine the incidence of high-grade superior mesenteric artery stenosis in patients with endografts with suprarenal stents using color duplex ultrasonography. Candidates for the study were patients who had placement of an aortic endograft with a suprarenal stent and were able to undergo ultrasonography of the superior mesenteric artery. After reviewing computed tomography scans, patients who had the origin of the superior mesenteric artery crossed by the suprarenal stent underwent color duplex ultrasonography of this vessel. Presence of turbulence or narrowing of the superior mesenteric artery, or a peak systolic velocity greater than 2.75 m/sec, or an end-diastolic velocity greater than 0.45 m/sec were considered significant for the presence of high-grade superior mesenteric artery stenosis. There were 24 patients (21 males, three females), median age 71 years (range, 59-83). The suprarenal stent was crossing the superior mesenteric artery in 17 of 24 patients (71%). Color duplex ultrasound was technically successful in 13 of 17 (76%). The test was performed after a median follow-up of 9 months (range, 3 days to 34 months). No patient had evidence of turbulence or narrowing of the superior mesenteric artery during ultrasonography. The median peak systolic velocity was 0.92 m/sec (range, 0.53-1.21 m/sec). No patient had peak systolic velocity greater than 2.75 m/sec. The median end-diastolic velocity was 0.10 m/sec (range, 0.09-0.14 m/sec). No patient had end-diastolic velocity greater than 0.45 m/sec. Color duplex ultrasonography did not demonstrate the presence of high-grade superior mesenteric artery stenosis during early follow-up of patients with endografts with suprarenal stents. Longer follow-up of larger series of patients is needed to determine the long-term effects of suprarenal stents on splanchnic circulation.

Aged↗

Effect of vasopressin on esophageal varices blood flow in patients with cirrhosis: comparisons with the effects on portal vein and superior mesenteric artery blood flow.

BACKGROUND/AIMS: Vasopressin reduces portal pressure which may be due to decreased portal inflow. However, it remains unclear whether vasopressin is able to selectively reduce esophageal varices blood flow. The aim of this study was to address this question. METHODS: Fifteen patients with cirrhosis and esophageal varices were included in this prospective study. Portal vein and superior mesenteric artery flow velocity were measured with a percutaneous echo-Doppler. Esophageal varices flow velocity was measured using a transesophageal echo-Doppler technique. Mean arterial pressure and heart rate were also recorded. These measurements were performed at baseline condition and 15 min after observer blind drug administration. In this study, two groups, six patients receiving placebo and nine patients receiving 0.3 U/min of vasopressin, were randomized according to the coded number. RESULTS: Placebo administration had no effect on systemic and splanchnic circulation. In contrast, vasopressin administration increased mean arterial pressure (p < 0.05) associated with a bradycardia (p < 0.01). In splanchnic circulation, vasopressin decreased portal vein (-32 +/- 3%, p < 0.01), superior mesenteric artery (-30 +/- 2%, p < 0.01), and esophageal varices flow velocity (-48 +/- 5%, p < 0.01). When the magnitude of these reductions was compared, ANOVA showed a significant difference (p < 0.01). Furthermore, the reduction in esophageal varices flow velocity was significantly higher than that in portal vein flow velocity (p < 0.01) and that in superior mesenteric artery flow velocity (p < 0.01). CONCLUSIONS: These data support the view that vasopressin is able to selectively reduce esophageal varices blood flow. This effect, in addition to its well-established portal pressure reducing action, may play a role in its therapeutic efficacy in the treatment of variceal bleeding.

Aged↗

The effects of vasopressin on systemic and splanchnic hemodynamics and metabolism in endotoxin shock.

UNLABELLED: We compared the effects of vasopressin and norepinephrine on systemic and splanchnic circulation and metabolism in endotoxin shock in pigs. Twenty-one pigs were randomized to endotoxin shock (Escherichia coli endotoxin infusion) (n = 6), endotoxin and vasopressin (VASO; n = 6), endotoxin and norepinephrine (NE; n = 6), and controls (n = 3). Endotoxin infusion was increased to induce hypotension, after which vasopressin or norepinephrine was started to keep systemic mean arterial blood pressure >70 mm Hg. Regional blood flows and arterial and regional lactate concentrations were measured. Tonometers with microdialysis capillaries were inserted into the stomach, jejunum, and colon. Systemic mean arterial blood pressure >70 mm Hg was achieved in the VASO and NE groups. Vasopressin decreased cardiac output, superior mesenteric artery, and portal vein blood flow, whereas hepatic arterial blood flow increased. Arterial lactate concentration increased from 2.0 mM (1.6-2.1 mM) to 4.7 mM (4.7-4.9 mM) (P = 0.007). Systemic and mesenteric oxygen delivery and consumption decreased and oxygen extraction increased in the VASO group. Vasopressin increased mucosal-arterial PCO(2) gradients in all three locations, whereas luminal lactate release occurred only in the jejunum. Animals in the NE group remained stable. Vasopressin reversed hypotension but decreased systemic and gut blood flow. This was associated with hyperlactatemia, signs of visceral dysoxia, and jejunal luminal lactate release. IMPLICATIONS: Although vasopressin induces vasoconstriction in visceral region, its effects on splanchnic circulation and metabolism during septic-endotoxin shock are still poorly characterized. We evaluated the metabolic and hemodynamic effects of vasopressin and norepinephrine within the splanchnic area in porcine endotoxin shock.

Animals↗

Blockade of spinal pathways decreases pre- and postganglionic discharge differentially.

Although discharge of many sympathetic nerves decreases substantially on transection of the spinal cord in cats, firing of splenic and mesenteric postganglionic nerves continues unabated (R. L. Meckler and L. C. Weaver, Brain Res. 338: 123-135, 1985; R. D. Stein and L. C. Weaver. J. Physiol. Lond. 396: 155-172, 1988). Therefore, ongoing sympathetic outflow directed to the splanchnic circulation was proposed to be less dependent on supraspinal excitatory drive than that directed to other vascular beds. Blockade or transection of cervical spinal pathways in chloralose-anesthetized cats significantly decreased firing of gastric, hepatic, adrenal, and lumbar chain sympathetic nerves. Discharge of gastric and hepatic nerves decreased as much as that of adrenal and lumbar chain nerves; therefore, sustained discharge in the absence of bulbospinal excitation is not a characteristic of all sympathetic nerves innervating the splanchnic circulation. In contrast, discharge of the preganglionic greater splanchnic nerves was not decreased after spinal transection, although it changed from a rhythmic to an asynchronous pattern. This provocative finding suggests that rhythmicity of preganglionic discharge may be important for effective synaptic transmission to some postganglionic neurons, since postganglionic gastric, hepatic, and adrenal nerve firing decreased in the presence of sustained but asynchronous preganglionic input.

Animals↗

The effect of increased inferior vena cava pressure on hepatic circulation in the dog.

Inferior v. cava pressure (IVCP) was raised in the dog by a baloon catheter introduced via the jugular vein. Hepatic artery flow (HAF) and portal venous flow (PVF) were measured with the electromagnetic flow meter. The increase of IVCP reduced uniformly HAF and PVF, the relative contribution of the two vessels to the HBF did not change. The relationship between IVCP increase and HAF reduction and between the decrease of AP-IVCP and the reduction of HAF was linear. There was no sign of autoregulation or vasomotor regulation of HAF. The changes in IVCP are only partially transmitted to the portal venous pressure (PVP). There was no change in intrahepatic portal resistance with increased IVCP. The increase in PVP did not lead to resistance changes in the splanchnic circulation. As a sign of the autoregulation of splanchnic circulation of the AP-PVP versus PVF curve was concave to the pressure axis. It is concluded that as a result of opposing autoregulatory and vasomotor influences in the intact animal the hepatic circulation appears to react passively to the increased outflow pressure.

Animals↗

Sex hormone binding globulin in arterial, and in peripheral, hepatic, renal and spermatic venous blood of children and adults.

Human sex hormone binding globulin (SHBG) was measured in arterial serum and in serum obtained from different venous territories. In 6 children, SHBG ranged from 44.4 +/- 4.8 (mean +/- SD) in arterial blood to 55.3 +/- 5.3 in the hepatic vein (P less than 0.01), while it did not change significantly in renal or peripheral tissue venous blood. In 6 male adults, no significant arteriovenous differences were found either in the peripheral tissues or in the splanchnic circulation. In the spermatic vein of 8 subjects, SHGB was significantly lower (17.1 +/- 5.7) than in the arterial blood (22.8 +/- 7.5), P less than 0.025. The arterio-venous difference found in the splanchnic circulation of children supports the hepatic origin of SHBG, and also suggests extra-hepatic clearance of the binding globulin. Testicular uptake of SHBG might be necessary to regulate delivery of androgens to Sertoli cells in the seminiferous tubules.

Adult↗

Early effects of catecholamine therapy on mucosal integrity, intestinal blood flow, and oxygen metabolism in porcine endotoxin shock.

OBJECTIVE: To determine the early effects of therapy of endotoxin (ET) shock with epinephrine, norepinephrine, or dopexamine on splanchnic circulation, oxygen metabolism, sigmoid mucosal pHi, bacterial translocation, and morphologic integrity of the ileal, colonic, and sigmoid mucosa. SUMMARY BACKGROUND DATA: Conflicting concepts exist concerning the catecholamine therapy of septic shock, but little is known about the effects of catecholamine treatment on splanchnic circulation and mucosal integrity. METHODS: ET shock was induced in pigs by ET infusion over 30 minutes, and animals were studied for 4 hours. All animals were resuscitated with fluid. To mimic the treatment of septic shock in humans, mean arterial pressure was maintained in two groups at >70 mm Hg with the administration of epinephrine or norepinephrine. A third group of animals received dopexamine at 7 microg/kg per minute. Systemic and splanchnic blood flow and oxygen metabolism were studied, sigmoid colon mucosal pHi was obtained tonometrically, and bacterial translocation was determined by culture of portal venous blood, mesenteric lymph nodes, liver, spleen, and lung specimens. Histologic sections of ileal, colonic, and sigmoid mucosa were morphometrically examined for therapy effects. RESULTS: All investigated catecholamines increased cardiac output and systemic oxygen delivery, whereas intestinal blood flow and oxygen delivery remained unchanged. Sigmoid mucosal pHi decreased in all study animals, but the decrease was most pronounced in the epinephrine group. Pigs receiving epinephrine also showed >40% damage of the mucosa of the ileum and colon, whereas animals receiving ET alone, norepinephrine, or dopexamine showed only moderate lesions with signs of restitution. No animal showed bacterial translocation. CONCLUSIONS: Systemic hemodynamics and oxygen metabolism data do not reflect intestinal perfusion. Norepinephrine or dopexamine administration in ET shock causes no additional impairment of intestinal integrity. Epinephrine therapy, in contrast, is associated with a significant reduction of mucosal pHi and considerable early mucosal damage. Its application in septic shock is hazardous.

Animals↗

The effect of inhibition of renin-angiotensin system by valsartan during hypovolemic shock and low flow sigmoideal ischaemia in pigs.

The aim of this experiment was to study the effect of Renin-Angiotensin System (RAS) blockade by means of valsartan on the colonic and systemic circulation in pigs during low flow sigmoideal ischemia in combination with hypovolemic shock. This condition resembles the situation that occurs in patients suffering from a ruptured aneurysm and a compromised colonic circulation. An experimental study in pigs was performed : 6 pigs with low flow sigmoideal ischemia and hypovolemic shock were treated with valsartan and a control group of 5 pigs with low flow sigmoideal ischemia and hypovolemic shock without medical treatment.Valsartan, 3 mg/kg, was administered intravenously. The operation was performed via left sided lumbotomy. The distal aorta was partially occluded to a flow reduction of 30% of the initial value. Hypovolemic shock was induced by withdrawing 20 ml/kg blood in 45 min. Resuscitation with 30 ml/kg haemaccel was iniated after 2 h of shock. The following parameters were measured: blood pressure, cardiac output; hemoglobin, lactate, angiotensin II in mixed venous blood (obtained from pulmonary artery) and in splanchnic blood (obtained from caudal mesenteric vein); and endoluminal pulse oximetry of the sigmoideal mucosa. Statistical analysis was performed by ANOVA and Wilcoxon signed rank test. There was a significant increase of lactate levels both in systemic and splanchnic circulation (P<0.05) in both groups. In the control group, the mean angiotensin II concentrations in the systemic circulation increased, after induction of ischaemia and shock. In the experimental group, the increase in angiotensin concentrations after resuscitation was significantly more prominent. In the colonic circulation, in both groups, there was a significant increase in angiotensin II levels in the splanchnic circulation following ischaemia and reperfusion (P<0.05), but there was no significant difference between the groups. There were no detectable mucosal signals measured by pulse oximetry after induction of shock throughout the experiment, whereas in the experimental group, median mucosal oxygen saturations of 81, 74.5 and 85% were achieved after resuscitation and declamping (P<0.01).In conclusion, angiotensin II inhibition during hypovolemic shock improves the colonic circulation, measured by pulse oximetry. However, other parameters of tissue ischaemia did not improve.

Angiotensin Receptor Antagonists↗

Haemodynamic and neurohumoral effects of caffeine in elderly patients with symptomatic postprandial hypotension: a double-blind, randomized, placebo-controlled study.

1. The aim of this study was to determine the effects of caffeine on haemodynamic and neurohumoral responses to meal ingestion in elderly patients with a history of symptomatic postprandial hypotension. 2. Postprandial hypotension is a common disorder of blood pressure regulation in the elderly, associated with falls and syncope. The pathophysiological mechanism is thought to be related to impaired vascular compensation for splanchnic blood pooling after a meal. Since caffeine inhibits vasodilatory adenosine receptors in the splanchnic circulation, we postulated that caffeine would reduce splanchnic blood pooling and prevent the development of postprandial hypotension. 3. We conducted a randomized, double-blind, placebo-controlled, cross-over study in nine elderly patients [age 76 +/- 9 (SD) years] with histories of symptomatic postprandial hypotension. Standardized 1674kJ liquid meals with 250 mg of caffeine or placebo were given on two occasions, at least 1 week apart. Blood pressure, heart rate, forearm vascular resistance (by venous occlusion plethysmography), and plasma caffeine and catecholamine levels were measured. Cardiac and splanchnic blood volume were determined by radionuclide scans. 4. By 30 min after both caffeine and placebo meal studies, supine mean arterial blood pressure fell significantly (P = 0.006) by 31 +/- 7 and 19 +/- 6 mmHg, respectively (mean +/- SEM, between group difference was not significant). Heart rate, cardiac output and splanchnic blood volume increased significantly, but to a similar extent, after caffeine and placebo. Forearm vascular resistance was unchanged after both meals. 5. Oral caffeine given with a meal does not reduce splanchnic blood pooling nor prevent postprandial hypotension in symptomatic elderly patients.

Aged↗

Anatomic arterial-venous shunting in endotoxic and septic shock in dogs.

Shunting of radionuclide labeled 9 micron diameter microspheres by the systemic circulation, and 6 body regions was measured in two dog shock models: endotoxic shock (1 mg/kg E. Coli endotoxin intravenously) and sepsis and septic shock (5 days after cecal ligation). Mean systemic arterial blood pressure was significantly lower than control in both the endotoxic and septic shock groups. Mean systemic shunting was 7.7% in the control group and 7.3% and 4.3% respectively in the endotoxic and septic shock groups. Regional shunting of the head, heart, and skeletal muscle were not significantly different in the three groups. However, mean shunting in the splanchnic circulation was 36.5% in the septic shock group as compared to 18.6% in the control group (p less than 0.05). Mean kidney shunting in the endotoxic group was 15.1% compared to 4% in the control group (p less than 0.05). During resuscitation with crystalloid, mannitol, blood, and cortiocosteroids mean aterial blood pressure and cardiac index increased but systemic arterial-venous shunting was 3.8 and 4.3% in endotoxic and septic shock respectively. These data show that systemic anatomic arterial-venous shunting is small and not different from control in both dog shock models, and regional arterial-venous shunting is increased only in the splanchnic circulation in the septic model and in the kidney in the endotoxin model.

Animals↗

A preclinical model of hepatocyte gene transfer: the in vivo, in situ perfused rat liver.

Delivering retroviruses targeted to hepatocytes in vivo involves the injection of retroviruses directly into the portal vein. The aim of this work was to establish a clinically relevant system for retrovirus-mediated gene transfer in a new model of in vivo, in situ perfused rat liver and to study the transgene expression. At 24 h after partial hepatectomy, the liver was completely excluded from the splanchnic circulation using an extracorporeal shunt. Two independent normothermal, oxygenated perfusion systems were used. First, liver perfusion was carried out with a recirculating system (1 h). Culture supernatant containing retroviruses (1.5 x 10(8) ffu/ml, beta-galactosidase gene) was used as perfusate. Then the liver perfusion was maintained for more 30 min in a single liver passage system using culture medium without retroviruses as perfusate. High hepatocyte transduction rates (up to 34.4%) were obtained. PCR analysis showed no provirus in extrahepatic organs. Viral titrations performed simultaneously (inflow and outflow liver lines) showed that after 1 h of perfusion (up to 30 successive liver passages) retroviruses were still detected in the liver outflow perfusate (up to 2.0 x 10(7) ffu/ml). Washing the liver for 30 min dramatically decreased the leakage of retroviruses in the outflow. In order to be of clinical use, the injection of retroviruses targeted to hepatocytes in vivo should be done while the liver is completely excluded from the splanchnic circulation to avoid any extrahepatic retrovirus diffusion.

Animals↗

[Calculated gastric intramucosal pH changes in the early phase of acute pancreatitis].

Based on the literature dysfunction of splanchnic circulation may be assumeol in the development of severe acute pancreatitis. Abnormal gut functions investigated by routinely used clinical examination is not available. Gastric tonometry indirectly gives information about gut function. Authors followed prospectively 12 patients who suffered from acute pancreatitis. Four patients recovered without complications, 4 patients had different complications and 4 patients died. Gastric intramucosal pH (pHi) was measured by TRIP NGS catheter and Tonocap monitor. Measurements were started at the time of hospitalisation and repeated every six hours on the first 3 days. Intramucosal acidosis (pHi < 7.3) could be measured independently from aetiology. Gastric pHi showed strong correlation with Acute Physiology and Chronic Health Evaluation II. (APACHE II) score (p = 0.02). APACHE II scores were significantly higher in-group pHi < 7.2 (13.9 +/- 1.7) compared to group pHi > 7.2 (7.33 +/- 1.06) (p = 0.002). 24-hour changes in APACHE II scores were significantly greater in the cases of pHi < 7.2 (3.3 +/- 1.47) versus pHi > 7.2 (-0.6 +/- 0.97) (p = 0.03). Changes of pHi in the early phase of acute pancreatitis indicate that splanchnic circulation is already involved and the pHi may have a prognostic value.

Acute Disease↗

Time course of renal responses to greater splanchnic nerve stimulation.

The objective of the present study was to describe the time courses of renal responses during renal sympathetic stimulation and to determine whether the kidney can provide a sustained response to sympathetic stimulation for 3 h. In four pentobarbital sodium-anesthetized dogs, stimulation (3.3 Hz) of a greater splanchnic nerve (GSN) on one side caused reductions in renal blood flow (RBF) and sodium excretion (UNaV) of both stimulated and contralateral-denervated kidneys, plus an increase in plasma renin activity (PRA). During continued stimulation, RBF partially recovered, but UNaV fell to less than 5% of control and PRA rose and remained at least eight times above control. In nine dogs, a single GSN was stimulated after ipsilateral adrenal medullectomy and ligation of the splanchnic circulation. The acute response to GSN stimulation was now confined to the ipsilateral kidney. Ipsilateral RBF fell by 32 +/- 10% but returned to 85 +/- 5% of control values by the end of the stimulation period. Contralateral RBF fell slowly by approximately 10%. Ipsilateral and contralateral UNaV fell to 34 +/- 10 and 43 +/- 11% of control values, respectively. PRA increased rapidly at the onset of GSN stimulation and remained at least 2.8 times control levels. After stimulation, RBF, UNaV, and PRA returned toward control levels. These results confirm the findings of others that the response of the renal vasculature to sympathetic stimulation is mainly transient. However, they additionally demonstrate a strong and sustained decrease in UNaV lasting for the total 3-h period of sympathetic stimulation.

Adrenal Medulla↗