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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although hepatic blood flow increases significantly during early sepsis [as produced by cecal ligation and puncture (CLP)], it is not known whether this is due to the increase in portal or hepatic arterial blood flows. To study this, rats were subjected to CLP, after which they and sham-operated rats received either 3 or 6 ml normal saline/100 g body wt subcutaneously (i.e., all rats received crystalloid therapy). Blood flow in various organs was determined by using a radioactive microsphere technique at 5 and 20 h after CLP or sham operation. Portal blood flow was calculated as the sum of blood flows to the spleen, pancreas, gastrointestinal tract, and mesentery. Total hepatic blood flow was the sum of portal blood flow and hepatic arterial blood flow. A significant increase in portal blood flow and in total hepatic blood flow was observed at 5 h after CLP (i.e., early sepsis), and this was not altered by doubling the volume of crystalloid resuscitation after the induction of sepsis. In contrast, hepatic arterial blood flow during early sepsis was found to be similar to control; however, it was significantly reduced in late sepsis (i.e., 20 h after CLP). Cardiac output was significantly higher than the control in early sepsis. However, even in late sepsis, cardiac output and total hepatic blood flow were not significantly different from controls. These results indicate that the increased total hepatic blood flow during early hyperdynamic sepsis is solely due to the increased portal blood flow.
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PMID:Increase in hepatic blood flow during early sepsis is due to increased portal blood flow. 175 May 74

Glucose dyshomeostasis and insulin resistance are well-documented characteristics of sepsis. The insulin resistance could be manifested in a decreased peripheral glucose uptake and/or an increased hepatic glucose output. To investigate the hepatic and peripheral responses to insulin in a three-day model of sepsis, 14 mongrel dogs were studied. Animals were randomly assigned to a SEPTIC (n = 5), SHAM (n = 4), or CONTROL (n = 5) group. Sepsis was induced in anesthetized dogs via a midline laparotomy with subsequent placement of a fecal-soaked gauze sponge around intestines. SHAM and CONTROL dogs were pair-fed with the SEPTIC dogs. On the third day, animals were anesthetized, intubated, and ventilated. Via a left-side laparotomy, electromagnetic flow probes were placed to measure hepatic arterial and portal venous blood flows. Cannulas were placed in femoral, portal, and hepatic veins and femoral artery to measure hepatic outputs of glucose, lactate, and oxygen during hyperinsulinemic-euglycemic clamps ranging from 0.4 to 4,000 mU insulin/min. Portal venous insulin concentrations in SEPTIC animals were significantly increased compared to CONTROL animals during 0.4 and 4 mU insulin/min infusions. An insulin infusion rate of 40 mU/min significantly decreased net hepatic glucose output (NHGO) in CONTROL animals but did not affect NHGO in SHAM or SEPTIC animals. An insulin infusion rate of 4,000 mU/min significantly decreased NHGO in all groups. An attempt to analyze the ED50 of the three dose-response curves was inconclusive. Glucose infusion rates (GIR) increased during insulin infusion but the GIR were not different between groups at any insulin infusion rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic insulin resistance during canine sepsis. 206 41

Fluoxetine (PROZAC) is a recently marketed straight chain antidepressant unrelated to the cyclic anti-depressants. There is only limited information on fluoxetine and a single case report on overdose (benign outcome) in the literature. In response to this we performed a 1y retrospective chart review at 2 AAPCC certified poison centers. Forty-four exposures to fluoxetine were reviewed from 1988; 31 cases were treated in a HCF, 2 cases were followed at home by phone and 11 cases were lost to follow up. Thirteen cases with follow up (FU) reported no coingestants; 3 cases reported increased anxiety without cardiovascular (CV) changes, 2 cases presented confused with out CV changes, and 8 cases were asymptomatic. Eight cases with FU had ETOH and/or benzodiazepines as a coingestant and experienced only a decreased level of consciousness that could be explained by the coingestant. Five cases remained asymptomatic with reported coingestants of APAP #3, lorazepam, haloperidol, molindone, alprazolam, propranolol, phenobarbital (level 18.2). Four cases were excluded from the evaluation due to the coingestants involved. No seizures were recorded in this series. Three possible drug reactions occurred; 2 cases had reactions with tranylcypromine (PARNATE), and 1 case with a diagnosis of septicemia had a severe hyperthermic reaction with therapeutic coingestants of mephytoin, verapamil, digoxin and indocin. We believe overdose with fluoxetine present minimal risk of serious cardiovascular or neurological complications.
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PMID:Fluoxetine ingestion: a one year retrospective study. 232 65

The intestinal metabolism of glucose and glutamine was studied in rats made septic by cecal ligation and puncture technique. Sepsis resulted in negative nitrogen balance and produced increases in the concentrations of blood pyruvate, lactate, alanine, and glutamine, and decreases in those of 3-hydroxybutyrate and acetoacetate. Both plasma insulin and glucagon concentrations were increased by 2.2- and 3.2-fold in septic rats, respectively. Portal-drained visceral blood flow increased in septic rats, and was accompanied by a decrease in the rates of utilization of glutamine and production of lactate, glutamate, and ammonia compared with those rates in sham-operated animals. Enterocytes isolated from septic rats showed decreased rates of glucose and glutamine utilization compared with cells isolated from corresponding controls. The maximal activities of hexokinase, 6-phosphofructokinase, pyruvate kinase, and glutaminase were decreased in intestinal mucosal scrapings of septic rats. It is concluded that a moderate form of sepsis decreases the rates of glucose and glutamine utilization (both in vivo and in vitro) by the epithelial cells of the small intestine. This may be caused by changes in the maximal activities of key enzymes in the pathways of glucose and glutamine metabolism in these cells as a metabolic adaptation to spare glucose and glutamine for use by other tissues.
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PMID:Glucose and glutamine metabolism in the small intestine of septic rats. 236 28

Portal venous thrombosis in hepatic transplant candidates is considered a relative contraindication to transplantation. In addition to thrombectomy, which is often technically impossible, donor portal venous arterialization or extra-anatomic venous bypass have been described. Two patients who underwent portal venous resection and subsequent anatomic reconstruction are presented herein. In the first patient, a graft with donor common iliac vein was interposed, and in the second, the donor portal vein was long enough to be anastomosed to the mesentericosplenic venous confluens. One patient is well 12 months after transplantation with patent portal vein and the other died of fungal sepsis after rejection treatment (the portal vein being open and unobstructed at autopsy).
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PMID:Management of portal venous thrombosis in hepatic transplant recipients. 238 18

Among 69 patients with PVT, 338 variceal bleeding episodes occurred. Only two patients died from bleeding, and both lived in remote communities and were inaccessible to medical care. Fifty-three children underwent 164 operations for the management of PVT. Once operative management was undertaken, subsequent operations frequently were necessary. Nonoperative measures controlled acute variceal hemorrhage in most instances during the past 10 years. Almost all patients who underwent splenectomy alone, variceal ligation, gastric division, splenic transposition, or makeshift shunts subsequently rebled. These operations are rarely indicated in the current management of children with PVT. Portal venography is essential to define the portal venous circulation before a shunt operation is attempted. Cavomesenteric or central splenorenal shunts prevented further bleeding in eight of 15 patients and are the most reliable operations to control bleeding in patients with PVT. Emergency operation is rarely necessary to control bleeding. Sixteen patients (average age 14.6 years) with PVT did not undergo any operations, and are alive. Each of the six patients with PVT who died from complications of portal hypertension did so within nine months of an operation. Four of these patients had previous splenectomy and died with sepsis as one of the major factors. Bleeding episodes became less frequent as the patients increased in age. Patients who underwent shunts under unfavorable circumstances or who received various other operations to treat portal hypertension appeared to have a higher risk of morbidity and mortality than those managed nonoperatively.
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PMID:Management of extrahepatic portal hypertension in children. 447 92

Nitrogen flux across the splanchnic bed is altered following operation, injury, and sepsis, but the individual contributions of gut and liver and their interrelationships remain undefined. Since more than 60% of whole blood amino acid nitrogen is transported as glutamine and alanine, we determined the flux of these amino acids across the gastrointestinal tract and liver in splenectomized, awake dogs during a control period and a 2 and 4 days following a standard laparotomy. Blood flow was measured in all studies and substrate flux calculated from flow and arteriovenous and portovenous concentration differences. Portal blood flow decreased by 25% following operation from a control value of 26 +/- 2 ml/kg body weight . min to 19 +/- 2 (P less than 0.05). Total hepatic blood flow did not change significantly after operation, but the individual contributions of the hepatic artery and portal vein were altered; hepatic artery flow increased from a control value of 10 +/- 1 ml/kg . min to 23 +/- 3 (P less than 0.001). Glutamine uptake by teh gastrointestinal tract nearly doubled from a control value of 0.75 +/- 0.16 microM/kg . min to 1.31 +/- 0.13 (P less than 0.05) on postoperative day 2. This increase in flux occurred despite a diminished arterial concentration and a reduced portal blood flow, indicating that extraction of glutamine by the gastrointestinal tract was not primarily dependent on increased arterial concentration. Alanine, on the other hand, was released by the gut at a rate of 1.97 +/- 0.37 microM/kg . min in controls and decreased to 0.81 +/- 0.13 microM/kg . min (P less than 0.05) in dogs that had operation. Glutamine was released by the liver in control dogs at a rate of 1.59 +/- 0.59 microM/kg . min but switched to an organ of slight glutamine uptake (0.31 +/- 0.31, P less than 0.01) on postoperative day 2. Alanine uptake by the liver doubled from 2.94 +/- 0.29 to 5.46 +/- 0.63 microM/kg . min (P less than 0.05) following surgical stress. The gastrointestinal tract plays an active metabolic role in the processing of amino acids following operation and may be a key regulatory of interorgan substrate flux following injury and infection.
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PMID:Postoperative alteration of arteriovenous exchange of amino acids across the gastrointestinal tract. 687 48

The reactions in the series-coupled vascular sections of the small intestine and the changes in aortic blood flow, systemic arterial, and pulmonary arterial blood pressure were followed continuously in cats made septic by IV infusion of live E coli bacteria for 2 hours. Peripheral venous infusion initially induced systemic hypotension, pulmonary hypertension, and increased aortic blood flow, but decreased intestinal blood flow. These changes were normalized within 5-10 minutes. During the next 110 minutes systemic arterial blood pressure, aortic blood flow, and intestinal blood flow decreased continuously while intestinal blood flow resistance remained in the control range. Portal venous infusion induced a significantly less pronounced initial pulmonary arterial blood pressure increase. No initial intestinal vasoconstriction was noticed and intestinal blood flow resistance decreased during the bacterial infusion. In both series only small and insignificant changes of intestinal tissue volume were seen. The data suggest that the route of infusion is important to the response in experimentally-induced sepsis. The constant intestinal tissue volume argues against intestinal pooling as being of importance to the development of low blood pressure in septic shock.
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PMID:Hemodynamic effects of systemic or portal IV infusion of live E coli bacteria in the cat. A preliminary report. 703 61

The central hemodynamic responses were studied in experimental sepsis in cats, following various routes of infusion of live E. coli bacteria. The aortic blood flow (ABF) was electromagnetically recorded. The pulmonary artery was cannulate for pressure recording. Platelet and white blood cell concentrations, PO2, PCO2, pH and oxygen saturation were measured at intervals. I.v. infusion of bacteria induced initially decreased ABF, systemic hypotension, pulmonary hypertension. Portal infusion evoked, on the other hand, increased ABF, but induced no significant change in systemic or pulmonary arterial blood pressures. Aortal infusion induced responses in between. The initial hemodynamic changes were followed by relative normalization after 5-10 min. Then, in all series, a progressive fall in ABF and systemic blood pressure were noticed. Within 5 min following bacterial infusion the platelet and white blood cell concentrations fell to 65 and 50%, respectively. In all series a moderate metabolic acidosis developed. Thus, the initial hemodynamic response following infusion of live E. coli was dependent on the route of infusion; intraportal infusion induced initially a more hyperdynamic state. The different initial central hemodynamic responses did not influence the subsequent development of a hypotensive shock state.
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PMID:Central hemodynamic responses to venous, aortal or portal infusion of live E. coli bacteria in the cat. 704 28

The responses of the series-coupled vascular sections in the feline small intestine were studied in experimental sepsis induced following various routes of infusion of live E. coli bacteria. The intestinal hemodynamics were followed by means of plethysmography combined with direct recording of the intestinal venous outflow. After 2 hours of bacterial infusion the experiments were terminated. Infusion of E. coli in the inferior caval vein induced initially hypotension, decreased intestinal blood flow (Q) and increased intestinal vascular resistance (R). Portal venous infusion induced, on the other hand, an initial arterial blood pressure increase, an increase of Q and a decrease of R. Aortal infusion evoked only minor initial changes. The early response was in all series followed by a progressive hypotension during which Q decreased and R increased gradually. There were no changes in intestinal tissue volume, indicating that there was no pooling of blood or extravasation of fluid, during the experiments. Intestinal mucosal lesions were equally distributed in the three series. Thus, depending on the route of infusion live E. coli induced intestinal vasoconstriction or vasodilatation. Regardless the route, there was no intestinal pooling of blood or fluid. Hypotension developed in most cats after 120 min, regardless the site of infusion and the initial vascular response.
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PMID:Intestinal hemodynamic effects of varying the route of infusion of live E. coli bacteria in the cat. 704 29


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