Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small bowel cutaneous fistula appearing after laparotomy was treated with the tetradecapeptide somatostatin in six patients to reduce the volume and enzyme content of the intestinal secretion. Continuous intravenous infusion of somatostatin diminished output from the fistula in all cases. Spontaneous fistula closure occurred after 11 to 33 days of treatment in four patients. There were no complications such as sepsis, peritonitis, or wound or skin problems from the contact with intestinal secretion. The hospital stay ranged from 19 to 50 days and bowel function was restored to normal. These preliminary results indicated that somatostatin can promote healing of small bowel fistula by inhibiting intestinal secretions.
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PMID:Small bowel fistulas treated with somatostatin: preliminary results. 287 6

Because of its wide distribution in the organism, natural somatostatin (SRIF) demonstrates an ample spectrum of actions, involving mainly the central neuroendocrine system and the enteropancreatic area. In the former, this peptide may find its field of application in conditions characterized by excessive GH, TSH or ACTH secretion, depending on the central or peripheral cause of the inappropriate hormone control. The inhibitory effect of SRIF on gastrointestinal and pancreatic hormones may be useful in the management of tumors originating in this system and also in the treatment of inflammatory processes such as pancreatitis, in malignant diarrhea, and in gastrointestinal bleeding. A complex action of SRIF and its derivative on insulin release and glucose homeostasis may offer some advantages in the control of unstable diabetes. Dampening of organic functions in the upper digestive tract may also render SRIF and its analogues useful in the exploration of the gallbladder, gastric and pancreatic functions. The effect of such peptides on tissue growth and on the regulation of blood pressure are the subject of present investigations. Cytoprotection, an interesting aspect of SRIF application, is discussed elsewhere in this compendium. Finally, some comments on the possible use of SRIF as an additive to the conventional treatment of burns and sepsis close this review.
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PMID:Clinical applications of somatostatin. 290 Feb 4

We have assessed the role of glucagon and sympathetic nervous system (SNS) activity on glucose and palmitate kinetics and oxidation in the conscious dog infused with live Escherichia coli bacteria by means of the simultaneous primed constant infusion of [1,2-13C]palmitate and [U-14C]-glucose. The basal rate of glucose production in septic dogs and controls was similar. However, when the glucagon concentration was selectively decreased in the septic animals by the appropriate infusion of somatostatin (S), insulin (I), and glucagon (G), the rate of glucose production decreased significantly, whereas in control animals S + I + G infusion had no effect on glucose kinetics. When alpha- and beta-adrenergic blockade was added to the infusion, the rate of glucose production decreased further and hypoglycemia developed in the septic dogs, whereas in the controls both glucose production and concentration increased. The basal rate of appearance of palmitate was increased in the septic dogs (P less than 0.01). S + I + G had no effect on palmitate appearance in either group, and sympathetic blockade caused a significant decrease in palmitate appearance in both groups of dogs. The rates of oxidation of both glucose and palmitate was related directly to their availability in plasma. Thus, in sepsis, glucagon and SNS activity play important roles in the mobilization of glucose and palmitate into the plasma and therefore in the overall state of energy metabolism.
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PMID:Glucose and FFA kinetics in sepsis: role of glucagon and sympathetic nervous system activity. 388 89

The effect of gram-negative sepsis on the kinetics and oxidation of very low-density lipoprotein (VLDL) fatty acids was assessed in conscious dogs in the normal state and 24 h after infusion of live Escherichia coli. VLDL, labeled with [2-3H]glycerol and [1-14C]palmitic acid, was used to trace VLDL kinetics and oxidation, and [1-13C]palmitic acid bound to albumin was infused simultaneously to quantify kinetics and oxidation of free fatty acid (FFA) in plasma. Sepsis caused a fivefold increase in the rate of VLDL production (RaVLDL). In the control dogs, the direct oxidation of VLDL-fatty acids was not an important contributor to their overall energy metabolism, but in dogs with sepsis, 17% of the total rate of CO2 production could be accounted for by VLDL-fatty acid oxidation. When glucose was infused into dogs with insulin and glucagon levels clamped at basal levels (by means of infusion of somatostatin and replacement of the hormones), RaVLDL increased significantly in the control dogs, but it did not increase further in dogs with sepsis. We conclude that the increase in triglyceride concentration in fasting dogs with gram-negative sepsis is the result of an increase in VLDL production and that the fatty acids in VLDL can serve as an important source of energy in sepsis.
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PMID:Effect of sepsis on VLDL kinetics: responses in basal state and during glucose infusion. 389 May 59

We have investigated the response of glucose and free fatty acid (FFA) kinetics and oxidation to betahydroxybutyrate (BOHB) infusion (30 mumol/kg X min) in both normal and Escherichia coli septicemic conscious dogs. In both the septic and control groups, experiments were performed in which hormone levels were allowed to change in response to the BOHB infusion, and in which the infusion of somatostatin, insulin, and glucagon were used to hold those hormone levels constant and sympathetic activity was blocked by the infusion of propranolol and phentolamine. In the nonseptic groups, the infusion of BOHB decreased both glucose production and FFA appearance (RaFFA) independent of the hormonal status. Glucose oxidation decreased in proportion to the decrease in production and uptake. FFA oxidation decreased only when hormones were controlled. In contrast, the infusion of BOHB in septic dogs did not suppress either glucose production or RaFFa, irrespective of the hormonal status. Substrate oxidation again corresponded to the rate of appearance of the substrate. We conclude that in normal dogs, ketones act directly as metabolic regulators to decrease the appearance of both glucose and FFA in the plasma, but do not directly affect the ability of the animal to oxidize these substrates. In sepsis, the normal regulatory actions of ketones appear to be lost.
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PMID:Energy and substrate kinetics and oxidation during ketone infusion in septic dogs: role of changes in insulin and glucagon. 614 25

The present study examines the effect of acute liver failure induced by a single intraperitoneal (i.p.) injection of D-galactosamine-HCl (3 g/kg) on somatostatin (SS) binding and levels in the rat frontoparietal cortex and hippocampus. Neurobehavioural changes were evaluated by the method of Zieve et al. [(1984) J. Lab. Clin. Med., 104:655-664]. The rats were decapitated as soon as they reached neurobehavioural stage I or II. In stage I, rats had lethargy and in stage II they showed mild ataxia, mainly in the hind limbs. The administration of D-galactosamine elevated serum transaminase levels (mean peak level 2,242 IU/1) but hypoglycemia, gross cerebral edema, or signs of sepsis were not detected in any of the animals studied. In addition, D-galactosamine did not affect somatostatin-like immunoreactivity (SSLI) levels in either brain area in any of the experimental groups as compared to the control groups. The rats sacrificed in stage I showed no change in the number or affinity of specific 125I-Tyr11-somatostatin (125I-Tyr11-SS) receptors in synaptosomes from the frontoparietal cortex and hippocampus. The rats sacrificed in stage II showed a decrease in the number of specific 125I-Tyr11-SS receptors in synaptosomes from both brain areas, with no change in receptor affinity. Binding studies were also conducted on synaptosomes from the frontoparietal cortex and hippocampus of rats that received D-galactosamine but did not develop acute liver failure and consequently did not develop neurobehavioural changes. The SS receptors in these synaptosomes did not change in comparison with controls, indicating that the D-galactosamine was not directly responsible for the changes in the cerebral SS receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain somatostatin receptors in a rat model of acute liver failure. 757 Mar 44

Cytokines seem to act predominantly in a paracrine manner when producing their deleterious effects during sepsis. Therefore, local TNF alpha release by pulmonary macrophages would have a central role in the pathogenesis of the adult respiratory distress syndrome (ARDS). By contrast, pentoxiphylline (PTXF) can reduce lung damage in septic animal models, and somatostatin (SS-14) has been shown to down-regulate TNF alpha-receptor expression in monocytes, suggesting an immunomodulatory action for this hormone. The aim of this work was to study the effect of PTXF and SS-14 on lipopolysaccharide (LPS)-induced TNF alpha release by human pulmonary macrophages. Macrophages were obtained from multiple organ donor lungs. Donors with either a recent history of tobacco smoking, more than 72 hr of mechanical ventilation, or any radiological pulmonary infiltrate were not included in this study. After 1 hr of culture, LPS stimulated TNF alpha release in a dose-dependent manner (2.34 +/- 0.20 and 11.32 +/- 1.38 pg/microgram protein, P < 0.01, in response to 2.5 and 10 micrograms/ml LPS, respectively). This response was significantly inhibited by both PTXF, 100 micrograms/ml (0.24 +/- 0.07 vs. 2.43 +/- 0.20, P < 0.01, and 1.30 +/- 0.08 vs. 11.32 +/- 1.38, P < 0.01, pg/micrograms protein, 2.5 and 10 micrograms/ml LPS, respectively) and SS-14, 0.4 ng/ml (0.26 +/- 0.07 vs. 2.43 +/- 0.20, P < 0.01, and 0.60 +/- 0.19 vs. 11.32 +/- 1.38, P < 0.01, pg/micrograms protein, 2.5 and 10 micrograms/ml LPS, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of pentoxifylline and somatostatin on tumour necrosis factor production by human pulmonary macrophages. 783 20

This study examined the acute role of glucagon in sustaining the increased hepatic gluconeogenesis observed in the conscious infected dog. After a basal sampling period, arterial glucagon levels were selectively decreased for 180 min by a peripheral infusion of somatostatin and basal intraportal infusion of insulin (GGN deficient; n = 6). In a separate protocol (GGN replaced; n = 5) glucagon was also infused intraportally to maintain the glucagon level at that seen during sepsis. Tracer and arteriovenous difference techniques were used to assess hepatic glucose metabolism and gluconeogenesis. In the GGN-deficient group the arterial plasma glucagon level fell from 416 +/- 49 to 88 +/- 21 pg/ml, whereas in the GGN-replaced group it remained elevated throughout (321 +/- 48 to 248 +/- 22 pg/ml). When glucagon was reduced, endogenous glucose production decreased by 1.6 +/- 0.3 mg.kg-1.min-1, and an exogenous glucose infusion was required to maintain euglycemia. Glucose metabolism remained unaltered when glucagon was replaced. When glucagon was deleted, net hepatic gluconeogenic precursor uptake was not altered. In contrast, the efficiency of gluconeogenesis was decreased by 33% compared with the GGN-replaced group. Liver biopsies taken at the end of the experiment indicated that a diversion of gluconeogenic carbon to glycogen accounted for 50% of the fall in gluconeogenic efficiency. In summary, the basal hyperglucagonemia seen during an infection helps sustain glucose production both through its effects on hepatic glycogen metabolism and on gluconeogenic efficiency.
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PMID:Effect of acute glucagon removal on metabolic response to infection in conscious dog. 784 Jan 88

Spontaneous splenic rupture as a complication of infectious mononucleosis was diagnosed in a 19-year-old woman. Sonographic and MRI investigations revealed subcapsular hematoma of the spleen without overt rupture. The patient was managed conservatively. Somatostatin treatment was initiated in order to reduce splanchnic blood flow. Further clinical course of the patient was favourable. Seven days after the diagnosis of splenic rupture the patient was discharged from hospital. Non-operative management should be considered in patients with subcapsular splenic rupture to avoid complications of splenectomy (e.g. post-splenectomy sepsis).
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PMID:Non-operative management in a case of spontaneous splenic rupture in infectious mononucleosis. 788 80

Major pancreatic resection is still accompanied by considerable morbidity and even mortality. Complications which occur after pancreatic surgery are chiefly associated with exocrine pancreatic secretion, hence, the inhibition of exocrine pancreatic secretion perioperatively is a promising concept in the prevention of complications. The hormone somatostatin and its synthetic analogue octreotide have been shown to profoundly inhibit exocrine pancreatic secretion, particularly the secretion of proteases. In a randomized, placebo-controlled, multicenter double-blind trial we analyzed the potential role of octreotide in the prevention of postoperative complications after major pancreatic surgery. A significant reduction in complications such as fistula, abscess, fluid collection, sepsis, pulmonary insufficiency, and postoperative acute pancreatitis could be demonstrated in patients who received octreotide at 3 x 100 micrograms/day subcutaneously. Octreotide was particularly effective in patients undergoing Whipple resection for cancer.
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PMID:Prevention of postoperative complications following pancreatic surgery. 810 13


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