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)

One hundred fifty of 490 patients undergoing open heart surgery had renal failure attributable to cardiopulmonary bypass. In 69, serum creatinine concentrations did not exceed 2 mg/dl and returned to normal by the fourth postoperative day. In 60 patients, serum creatinine attained levels between 2 and 5 mg/dl, oliguria did not develop, and recovery of renal function occurred within 4 to 37 days. Serum creatinine increased to levels exceeding 5 mg/dl in 21 patients, 11 of whom were oliguric. Despite dialysis, 14 of these patients died from cardiac causes or sepsis. Prolonged cardiopulmonary bypass time, hypotension, oliguria, low output syndrome, and hemoglobinemia during open heart surgery correlated with the development of renal failure postoperatively. Although severe renal failure was an uncommon complication after open heart surgery, its occurrence carried a grave prognosis.
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PMID:Renal failure after open heart surgery. 93 79

Thrombocytopenia is characteristically associated with septicemia and hemolytic uremic syndrome (HUS), a subset of which has been shown to be associated with endotoxemia and shigellosis. An experimental model that closely resembles these clinical conditions is the generalized Shwartzman reaction modified with a continuous intravenous infusion of endotoxin for 5 hr in rabbits. In addition to exhibiting the triad of HUS (thrombocytopenia, hemolytic anemia, and azotemia), these animals also had circulating platelet aggregates, leukocytosis, lipidemia, hemoglobinemia, hyperfibrinogenemia, and prolonged partial thromboplastin time. Platelets that remained in circulation were chemically exhausted in serotonin content and functionally impaired in aggregation activities. Plasma from animals during thrombocytopenia and platelet functional deficiency had no effect of the aggregation responses of normal platelets. Although the single triggering event of endotoxin infusion was stopped at hour 5, recovery from abnormalities was only partial on day 2 and within normal limits by day 3. In vitro studies supported platelet exhaustion as a mechanism for decreased platelet function after endotoxin infusion. The presence of circulating platelet aggregates and exhausted platelets suggested that the process of platelet activation took place at as long as 24 hr after the cessation of LPS infusion. Endotoxin and other mechanism(s) are likely to be operative in the pathogenesis leading to platelet activation. Further studies to reveal the mechanism of platelet exhaustion in the experimental model may help our understanding of corresponding events in clinical endotoxic injury and HUS associated with endotoxemia.
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PMID:Impaired and exhausted platelets in modified generalized Shwartzman reaction: an analogue of hemolytic uremic syndrome associated with endotoxemia. 664 55

Experimental models of lethal endotoxemia in rodents are widely used to delineate pathogenic mechanisms of inflammation, sepsis, and septic shock. One long-standing but poorly understood observation is that removal of the pituitary gland (hypophysectomy) renders experimental animals 1,000-fold more sensitive to the lethal sequelae of lipopolysaccharide (LPS). Previous explanations for this phenomenon focused on hypophysectomy-induced deficiencies of corticosteroids, because glucocorticoids effectively suppress the synthesis of tumor necrosis factor (TNF), which is a primary mediator of LPS lethality. We measured LPS-stimulated macrophage TNF release in the presence of serum from hypophysectomized rats to detect the appearance of an inducible 65 kDa protein that enhances TNF release. Surprisingly, the N-terminal amino acid sequence analysis of the isolated, purified protein revealed its identity as hemoglobin. Hypophysectomy significantly increases serum hemoglobin levels (control hemoglobin = 103+/-18 microg/mL versus hypophysectomized serum hemoglobin = 279+/-13 microg/mL; p < .05). Purified hemoglobin enhances TNF synthesis in LPS-stimulated macrophages by at least 1,000-fold, which is specifically inhibited by antihemoglobin antibodies. Thus, hemoglobin mediates increased TNF synthesis in endotoxemic, hypophysectomized rats. This mechanism of increased TNF release has potential implications for patients with hemoglobinemia following blood transfusion, surgery, injury, infection, or other conditions that can be associated with endotoxemia and sepsis.
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PMID:Hypophysectomy, high tumor necrosis factor levels, and hemoglobinemia in lethal endotoxemic shock. 987 77