Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves. Because BK production increases in myocardial ischemia, endogenous BK could foster NE release and associated arrhythmias. We tested this hypothesis in guinea pig and human myocardial ischemia models. BK administration (100 nM) markedly enhanced exocytotic and carrier-mediated NE overflow from guinea pig hearts subjected to 10- and 20-min ischemia/reperfusion, respectively. Ventricular fibrillation invariably occurred after 20-min global ischemia; BK prolonged its duration 3-fold. The BK B2 receptor antagonist HOE140 (30 nM) blocked the effects of BK, whereas the B1 receptor antagonist des-Arg9-Leu8-BK (1 microM; i.e., 2.5 x pA2) did not. When serine proteinase inhibitors (500 KIU/ml aprotinin and 100 microg/ml soybean trypsin inhibitor) were used to prevent the formation of endogenous BK, NE overflow and reperfusion arrhythmias were diminished. In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced. B2 receptor blockade abolished these effects but was ineffective if kininases were not inhibited. B2 receptor stimulation, by either exogenous or endogenous BK, also markedly enhanced carrier-mediated NE release in the human myocardial ischemia model; conversely, inhibition of BK biosynthesis diminished ischemic NE release. Because atherosclerotic heart disease impairs endothelial BK production, in myocardial ischemia BK could accumulate at sympathetic nerve endings, thus augmenting exocytotic and carrier-mediated NE release and favoring coronary vasoconstriction and arrhythmias.
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PMID:Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts. 1002 27

Endoscopic ultrasound-guided celiac plexus neurolysis (EUS-CPN) is a well-established intervention to palliate malignant pain. We report a patient who developed hepatic and splenic infarction and bowel ischemia following EUS-CPN. A 69-year-old man with known lung cancer and pancreatic metastasis was transferred for debilitating, significant epigastric pain for several months. The patient underwent EUS-CPN to palliate the pain. After the procedure, the patient complained continuously of abdominal pain, nausea, and vomiting; hematemesis and hematochezia were newly developed. Abdominal computed tomography revealed infarction of the liver and spleen and ischemia of the stomach and proximal small bowel. On esophagogastroduodenoscopy, hemorrhagic gastroduodenitis, and multiple gastric ulcers were noted without active bleeding. The patient expired on postoperative day 27 despite the best supportive care.
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PMID:Hepatic and splenic infarction and bowel ischemia following endoscopic ultrasound-guided celiac plexus neurolysis. 2376 46