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)

The hemodynamic response to a dopamine HCl infusion (10 microgram/kg per min) was measured in 25 adult patients with severe sepsis: there were 6 patients with circulatory hyperdynamic states, 9 patients with myocardial failure, and 10 with hypovolemia. Each patient also had acute respiratory failure. Changes of intrapulmonary shunt fraction (Qs/Qt), arterial and mixed venous oxygen tension (PaO2 and PvO2), oxygen transport, and oxygen consumption (VO2) were evaluated before and after dopamine infusion. Dopamine infusion produced clinical improvement and increased cardiac output. The hemodynamic response seemed to differ slightly according to the pattern of circulatory failure: chronotropic effect appeared to be predominant in hyperdynamic states, whereas inotropic effect appeared to be predominant in myocardial failure or hypovolemia. Moreover, in hypovolemic patients we noted a rise in pulmonary capillary wedge pressure suggesting an additional increase in venous return. During this treatment, we also noted a worsening of the Qs/Qt despite the increase in pulmonary blood flow; this worsening did not prevent significant improvements in VO2, but the improvement in PVO2 was offset by increased Qs/Qt and PaO2 remained unchanged.
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PMID:Effect of dopamine on intrapulmonary shunt fraction and oxygen transport in severe sepsis with circulatory and respiratory failure. 44 60

Dogs were subjected to tracheostomy and intubation with low pressure cuffed tracheostomy tubes. Various mixtures of bile, gastric secretion and 0-1 N Hydrochloric acid were injected into the trachea via a small catheter attached to the main tracheostomy cannula to simulate the effect of aspirated gastric contents. Bronchoscopic observations were made during the study to investigate the local effects of secretions pooling above the cuff, in contact with the tracheal wall. Gross pathological changes were observed when the animals were sacrificed at the end of the study. The constituents of a mixture of bile and gastric juice increased the severity of tracheal damage due to mechanical trauma and sepsis. Healing was delayed and the reparative process was abnormal. This experimental study indicates that the combination of bile and acid pepsin reaching the tracheal wall may also be a major factor which predisposes to the development of early and late tracheal injury.
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PMID:Tracheal damage associated with cuffed tracheostomy tubes. Aspiration of gastric content as a cause of local damage in tracheotomised dogs. 90 Apr 35

We retrospectively analyzed the gastrointestinal complications observed in 119 patients who had ingested corrosive agents. Hydrochloric acid and sodium hydroxide were the agents involved in 62% of patients. Women predominated over men (p less than 0.001); mean age was 36 for males and 29 for women (p less than 0.05). Endoscopy was performed in 55% of patients and revealed acute lesions in 69%. Complications were observed in 18% of patients requiring surgery in 12 (10%). Main complications included sepsis of abdominal or mediastinal origin and gastrointestinal bleeding. Mortality among these patients was 73%.
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PMID:[Early complications of caustic injuries of the digestive tract]. 251 64

Effects of lidocaine on organ localization of neutrophils and bacteria and on hemodynamic and metabolic variables were determined during septic shock in dogs. Twelve anesthetized dogs were infused with 10(10) Escherichia coli/kg of body weight through a portal vein catheter over a 1-hour period. Six of these 12 dogs were treated with 2 mg of lidocaine HCl/kg (6 mg/kg/h) 15 minutes after the bacterial infusion had begun. Six dogs not given E coli (surgical controls) were given saline solution at the same rate as the bacterial and lidocaine infusions. Over 4 hours, nontreated dogs with septicemia developed systemic hypotension, decreased cardiac output, increased portal pressure, increased serum alanine transaminase activity, increased liver extravascular water, increased liver glycogen depletion, and decreased PaO2, compared with control dogs. Accumulations of polymorphonuclear leukocytes and E coli were found in the liver and lungs of dogs with septicemia. Lidocaine treatment did not alter the hemodynamic measurements and resulted in metabolic acidosis and hypoalbuminemia. Decreased numbers of E coli were recovered from the liver of lidocaine-treated dogs, whereas increased numbers of organisms were recovered from the blood. Neutrophil sequestration was increased in the liver, but not the lungs of lidocaine-treated dogs.
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PMID:Lidocaine treatment of dogs with Escherichia coli septicemia. 328 25

The protein B of group B streptococci can bind in a nonimmune reaction to Ig of the IgG and IgM classes of various mammalian species (i.e., human, mouse, rabbit, and bovine). Protein B binding involves the Fc parts of both IgG and IgM molecules. Monoclonal or polyclonal IgG or IgM and the IgM-FC5 mu fragment of human myeloma protein combined with the protein B thereby inhibiting protein B-induced hemolysis in the CAMP reaction. The protein B/Ig complex can be dissociated with 1% Triton or guanidine-HCl (6 M). Mice infected intraperitoneally with sublethal doses of group B streptococci (GBS) and that received seven repeated intravenous injections of highly purified protein B during the first 9 h of infection developed fatal septicemia within 24 h with colony counts of up to 10(8) CFU/ml in the blood. Animals treated in the same way with either PBS or trypsinized protein B recovered. The protein B itself was not pathogenic when injected into healthy mice. Tissue sections of liver or spleen from mice infected with a lethal dose of GBS revealed the presence of protein B together with large numbers of cocci when stained by the peroxidase method using specific antibodies raised against purified protein B in the rabbit.
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PMID:Unspecific binding of group B streptococcal cocytolysin (CAMP factor) to immunoglobulins and its possible role in pathogenicity. 354 80

Live Escherichia coli were infused into anesthetized cats given 0.6 ml bile/kg and 80 mM HCl into the stomach. Systemic and pulmonary arterial blood pressures, cardiac output, and gastric blood flow were monitored. Gastrointestinal total wall and mucosal blood flow were measured by microspheres. The microscopic mucosal damage was graded 0-4 (stomach) or 0-5 (intestine). One group of cats (N = 8) received 5 mg yeast CuZn superoxide dismutase (SOD) as a bolus before bacteria followed by infusion 50 mg/3 hr. Four of these cats were also given catalase in the same dose. Controls (N = 8) had no treatment. After 3 hr gastric ulceration (grades 2-4) was found in controls but only in 50% of treated cats (P less than 0.1). About 50% and 25% of the cats in both groups developed significant small intestinal and colonic mucosal damage, respectively. SOD or SOD/catalase had no effect on late systemic hypotension, decrease in cardiac output, or transient increase in pulmonary pressure. Total gastric blood flow did not change, while at late sepsis gastric mucosal flow was decreased in the treated group. Small intestinal mucosal flow decreased in both series. It is concluded that free oxygen radicals may be of partial importance in the development of sepsis-induced gastric, but not intestinal, mucosal damage.
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PMID:Role of free oxygen radicals in the development of gastrointestinal mucosal damage in Escherichia coli sepsis. 391 36

An experimental model was used which includes intragastric instillation of 80 mM HCl and 0.6 ml bile/kg followed by intravenous infusion of live E coli in cats for up to three hours. This procedure regularly induces gastric mucosal ulcerations. Mucosal blood flow was measured by microspheres before, early, and late in sepsis. Total gastric blood flow was recorded electromagnetically. Mucosal regeneration capacity as reflected by the RNA/DNA ratio was measured. Misoprostol (a PGE1 analogue) was infused iv (5 micrograms/kg X h) or given locally in the stomach (10 micrograms/kg) before bacteriemia. Misoprostol did not influence the haemodynamic response to bacteria. The gastric mucosal damage was assessed either as an index representative for the entire corpus-fundus region or as the number of areas with intact surface epithelium within the series. Misoprostol iv protected the mucosa from ulceration compared with untreated septic controls while misoprostol intragastrically significantly reduced the number of damaged areas only. Topical misoprostol increased total gastric and mucosal blood flows early in sepsis compared to iv or no pretreatment while no difference was seen during late sepsis. The protective effect of misoprostol was thus not dependent on increased gastric mucosal blood flow. Nor was it mediated through effects on mucosal nucleic acid concentrations or ratio.
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PMID:Gastric mucosal damage in sepsis--effects of pretreatment with a synthetic prostaglandin E1 analogue. 393 38

Intravenous infusion of live. E. coli bacteria in cats did not induce microscopic damage to the gastric mucosa within 3 hours. However, if the cats before the induction of bacteremia were given 80 mM HCl and 0.6 ml gallbladder bile/kg b.w. microscopic mucosal damage developed regularly in the corpus-fundus area of the stomach. The gastric mucosal damage was not associated with significant decrease of total gastric blood flow as measured continuously electromagnetically or decreased gastric mucosal blood flow measured early and late during sepsis using radioactively labelled microspheres. Neither was the development of gastric mucosal damage associated with reduced gastric wall collagen concentration nor in RNA, DNA concentrations or RNA/DNA ratio in the gastric mucosa.
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PMID:Acute gastric mucosal ulceration in septic shock. An experimental study on pathogenic mechanisms. 608 89

We investigated the effects of ketamine HCl on endotoxin-induced pulmonary injury in 20 chronically instrumented sheep with lung lymph fistulas. The caudal mediastinal lymph node was cannulated in 20 ewes (45-55 kg). The catheter was externalized and the lymph allowed to drain freely. Pulmonary injury was induced by an intravenous infusion of Escherichia coli endotoxin (1.0-1.5 micrograms/kg body wt) over a 5-min period in 11 animals. The injury was characterized by an increase in pulmonary arterial pressure, pulmonary arterial wedge pressure, and lung lymph flow. There was no change in mean systemic arterial pressure. These changes were significantly attenuated by intravenous administration of ketamine HCl (5 mg/kg) following endotoxin injury in 9 other animals. When ketamine was given, the pulmonary arterial pressure decreased 32%, lung lymph flow decreased 27%, and systemic blood pressure increased 22%. Potential mechanisms for the hemodynamic effects of ketamine HCl in sepsis are discussed with particular reference to the pulmonary microvasculature.
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PMID:The effect of ketamine on endotoxin-induced lung injury. 633 61

Strain differences have been postulated to explain the observation that group B Streptococcus type III (GBS III) late-onset disease occurs in only a fraction of colonized infants. To determine the distribution of type-specific polysaccharide antigen (Ag) in GBS III, Ag was measured by rocket immunoelectrophoresis in both supernatant fluids and EDTA extracts and by radial immunodiffusion in multiple HCl extracts of the pellet from cultures of 10 strains of GBS III. Capsular Ag was defined as the sum of Ag in EDTA extracts + Ag in multiple HCl extracts. Both Ag in EDTA extracts and Ag in supernatant fluids correlated with capsular Ag (r = 0.94). GBS III strains were obtained from the blood of 19 infants with late-onset sepsis, from the cerebrospinal fluid or blood of 22 infants with late-onset meningitis, and from mucosal surfaces of both 18 infants and 12 mothers of infants with low levels of type-specific antibody and asymptomatic colonization. Mean values of Ag in supernatant fluids in strains from infants with late-onset sepsis (1.50 +/- 0.08 micrograms/ml) and late-onset meningitis (1.67 +/- 0.09 micrograms/ml) were significantly greater than those in asymptomatic colonization strains (1.14 +/- 0.05 micrograms/ml; P less than 0.001). The number of organisms required for a 50% lethal dose in the chick embryo, determined in 29 strains, was inversely related to Ag in supernatant fluids (r = -0.60). The demonstration that the quantity of capsular Ag produced by GBS III strains is related to their virulence in chick embryos and to their invasiveness in susceptible infants supports the hypothesis that Ag is a virulence factor in humans.
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PMID:Type-specific capsular antigen is associated with virulence in late-onset group B Streptococcal type III disease. 642 40


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