Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Septic shock is a life-threatening condition that results from exposure to bacterial endotoxin. It is mediated by the release of cytokines. Some of these cytokines cause the release of vasoactive substances. We report the case of a 62-year-old male patient who received redo operation for replacement of the degenerative porcine aortic and mitral prostheses. High cardiac output shock developed on the seventh postoperative day with severe metabolic acidosis and oliguria. Systemic vascular resistance and mean arterial pressure elevated within 5 min and stabilized 60 min after the start of a single dose of intravenous administration of NG-monomethyl-L-arginine (50 mg), a potent and selective inhibitor of nitric oxide synthesis. These findings indicate that nitric oxide overproduction is an important contributor to refractory hypotension in high cardiac output septic shock. Our findings suggested the utilization of nitric oxide synthase inhibitor in the treatment of septic shock in humans.
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PMID:Reversal of refractory hypotension in septic shock by inhibitor of nitric oxide synthase. 753 33

Asymmetric dimethylarginine (ADMA) represents an endogenous inhibitor of nitric oxide (NO) production. The production of ADMA has been shown to increase during cellular stress, e.g., hypoxia. Furthermore, ADMA has recently been reported to accumulate in plasma during terminal renal failure as a consequence of diminished urinary excretion. Since tissue hypoxia and oliguria are both characteristics of severe hemorrhagic shock, this study was performed in order to establish whether plasma concentrations of ADMA increase during hemorrhagic shock. Six pigs were subjected to graded hemorrhage (20% and 40% of the calculated blood volume), resulting in significant (P < 0.05) reductions in blood pressure and cardiac output (from 98 +/- 4 to 36 +/- 5 mm Hg and from 3.0 +/- 0.2 to 1.4 +/- 0.2 L/min, respectively). Plasma ADMA concentrations as determined by high-performance liquid chromatography (HPLC) increased from a pre-hemorrhage value of 3.4 +/- 0.3 microM to 3.9 +/- 0.4 microM (ns) and 5.2 +/- 0.4 microM (P < 0.05), respectively. The present study demonstrates that plasma ADMA concentrations increase significantly during hemorrhagic shock. Thus, inhibition of the arginine-nitric oxide pathway as a result of ADMA accumulation, may represent an additional physiological mechanism to maintain systemic blood pressure in response to acute hypovolemia.
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PMID:Accumulation of an endogenous inhibitor of nitric oxide synthase during graded hemorrhagic shock. 754 18