Gene/Protein Disease Symptom Drug Enzyme Compound
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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GTN were evaluated histologically in reference to biologic behavior and response to chemotherapy. GTN requiring more intensive, multiple drug chemotherapy usually exhibited increased mitotic activity, nuclear atypias, compact growth of cytotrophoblast, and little maturation, as compared to lesions that responded more favorably. Fibrinoid at the interface of tumor and host tissues was associated with a favorable response to drug therapy. Patients requiring more intensive chemotherapy were more likely to present with distant metastases and high levels of hCG prior to treatment and to reach remission only after many courses of treatment. The clinical and morphologic features of fatal cases suggest that these represented the extreme of a biologic continuum, with collapse of defense mechanisms despite chemotherapy. The early recognition by the pathologist of those lesions that may be resistant to chemotherapy is important to the clinician in selection of an optimal treatment protocol.
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PMID:Gestational trophoblastic neoplasms: morphologic correlates of therapeutic response. 20 34

The literature on isolated right ventricular infarction is reviewed and local experience is reported. Chronic lung disease is an important risk factor. Chest pain and breathlessness are common. Syncope and sudden collapse can also occur. Rhythm disorders include sinus bradycardia, atrial fibrillation and ventricular tachycardia or fibrillation. Atrioventricular block is rare. Hypotension and a right-sided fourth heart sound are common. Cautious use of slow-release nitroglycerin is not hazardous in the absence of hypotension. High doses of steroids and anticoagulants can be helpful. The prognosis is usually good, although sudden collapse can occur due to ventricular fibrillation, rupture of the right ventricular free wall or massive pulmonary embolism.
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PMID:Isolated right ventricular infarction. 151 57

Nitroglycerin induced a paradoxical disappearance of a stenosed coronary artery in a 57-year-old man with non-Q wave myocardial infarction. On the coronary angiogram, the left anterior descending coronary artery (with a 95% stenosis) became completely invisible 2 min after 0.3 mg sublingual nitroglycerin. Three minutes later, the artery was opacified again. This transient occlusion may have resulted from a passive collapse of the distal portion of the artery, due to insufficient access of nitroglycerin across the stenotic region.
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PMID:Nitroglycerin-induced transient coronary artery occlusion. 195 19

Five patients developed coronary artery spasm during open heart surgery in our institute between 1984 and 1988. One patient was undergoing coronary artery bypass grafting and the other four valvular surgery or surgery for congenital heart disease. In one of the patients undergoing non-coronary surgery, the preoperative induction of right coronary artery spasm by ergonovine had been documented angiographically while the remaining three patients did not possess organic or functional coronary disease. All five patients exhibited a sudden onset of hemodynamic collapse with ventricular tachyarrhythmias or ST elevation during the early period of reperfusion, the time to onset being 89.2 +/- 84.8 minutes after unclamping of the aorta. In addition, contraction of the right ventricular free wall was severely impaired. Although one patient died due to left ventricular rupture caused by direct cardiac massage, the early mortality thus being 20 per cent, the other four were successfully treated with the intravenous administration of nitroglycerin and diltiazem. Three patients required the assistance of intraaortic balloon pumping for severe cardiac failure. Thus, during open heart surgery, coronary artery spasm can occur even in patients without organic coronary lesions and the possible mechanisms of this condition are discussed herein.
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PMID:A new aspect of coronary artery spasm induced by cardiac surgery. 196 Aug 98

Coronary vasomotion plays an important role in the regulation of coronary perfusion at rest and during exercise. Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vasorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. Various vasoactive drugs, such as nitroglycerin and calcium antagonists, prevent exercise-induced stenosis vasoconstriction. An additive effect on coronary vasodilation of the stenotic vessel segment was observed after combination of nitroglycerin with diltiazem. Thus, exercise-induced stenosis narrowing plays an important role in the pathophysiology of myocardial ischaemia during dynamic exercise. The antianginal effect of vasoactive substances can be explained--besides the effect on pre- and afterload--by a direct action on coronary stenosis vasomotion.
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PMID:Potential role of coronary vasoconstriction in ischaemic heart disease: effect of exercise. 211 91

Septic shock is a life-threatening condition that results from exposure to bacterial endotoxin. It is manifested by cardiovascular collapse and mediated by the release of cytokines such as tumor necrosis factor. Some of these cytokines cause the release of vasoactive substances. In the present study, administration of 40 microgram/kg of bacterial endotoxin to dogs caused a 33% decrease in peripheral vascular resistance and a 54% fall in mean arterial blood pressure within 30 to 90 minutes. Vascular resistance and systemic arterial pressure returned to normal within 1.5 minutes after intravenous administration of NG-methyl-L-arginine (20 mg/kg), a potent and selective inhibitor of nitric oxide synthesis. L-Arginine reversed the effect of L-NMA and restored the endotoxin-induced hypotension. Although NG-methyl-L-arginine injection increased blood pressure in control dogs, the hypertensive effect was much greater in endotoxemic dogs (24.8 +/- 2.7 mmHg vs 47.8 +/- 6.8 mmHg, p = 0.01, n = 4). NG-Methyl-L-arginine caused only a modest increase in blood pressure in dogs made hypotensive by continuous intravenous infusion of nitroglycerin (17.1 +/- 5.0 mm Hg, n = 3). These findings suggest that nitric oxide overproduction is an important contributor to endotoxic shock. Moreover, our findings demonstrate for the first time, the utility of nitric oxide synthesis inhibitors in endotoxic shock and suggest that such inhibitors may be of therapeutic value in the treatment of septic shock.
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PMID:Reversal of endotoxin-mediated shock by NG-methyl-L-arginine, an inhibitor of nitric oxide synthesis. 224 97

Clinical assessment of the activity of tumor necrosis factor (TNF) against human cancer has been limited by a dose-dependent cardiovascular toxicity, most frequently hypotension. TNF is also thought to mediate the vascular collapse resulting from bacterial endotoxin. The present studies address the mechanism by which TNF causes hypotension and provide evidence for elevated production of nitric oxide, a potent vasodilator initially characterized as endothelium-derived relaxing factor. Nitric oxide is synthesized by several cell types, including endothelial cells and macrophages, from the guanidino nitrogen of L-arginine; the enzymatic pathway is competitively inhibited by NG-methyl-L-arginine. We found that hypotension induced in pentobarbital-anesthetized dogs by TNF (10 micrograms/kg, i.v., resulting in a fall in mean systemic arterial pressure from 124.7 +/- 7 to 62.0 +/- 22.9 mmHg; 1 mmHg = 133 Pa) was completely reversed within 2 min following administration of NG-methyl-L-arginine (4.4 mg/kg, i.v.). In contrast, NG-methyl-L-arginine failed to reverse the hypotensive response to an equivalent depressor dose of nitroglycerin, a compound that acts by forming nitric oxide by a nonenzymatic, arginine-independent mechanism. The effect of NG-methyl-L-arginine on TNF-induced hypotension was antagonized, and the hypotension restored, by administration of excess L-arginine (100 mg/kg, i.v.). Our findings suggest that excessive nitric oxide production mediates the hypotensive effect of TNF.
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PMID:NG-methyl-L-arginine inhibits tumor necrosis factor-induced hypotension: implications for the involvement of nitric oxide. 233 6

The effect of transient cerebral ischaemia connected with acute orthostatic hypotension on plasma adrenaline and noradrenaline levels was studied in seven healthy male volunteers during tilt. Sublingual administration of 1 mg nitroglycerin was used to block peripheral vascular reflexes and thus to provoke orthostatic intolerance. A consistent increase in plasma adrenaline concentrations (from 19.2 to 104.3 pg/ml on average, P less than 0.01) was found in six subjects who developed clinical signs of collapse after tilting. Plasma adrenaline never changed after tilting without collapse. Posturally stimulated plasma noradrenaline increases were similar yet irrespective of the presence of collapse.
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PMID:Venous plasma adrenaline response to orthostatic syncope during tilting in healthy men. 308 88

Using quantitative biplane coronary arteriography, coronary vasomotion of normal and stenotic coronary artery segments was studied at rest and during supine bicycle exercise in 37 patients with coronary artery disease. Normal coronary arteries showed vasodilation during exercise, whereas stenotic arteries exhibited vasoconstriction. The occurrence of coronary stenosis narrowing during exercise can be explained either by a collapse of the free vessel wall due to an increase in coronary blood flow velocity (Venturi mechanism) or by insufficient production of the endothelium-derived vasorelaxing factor (endogenous nitrate). To explore further the nature of exercise-induced vasoconstriction of stenotic coronary arteries, intracoronary nitroglycerin, diltiazem or propranolol was given to a subgroup of patients prior to the exercise test. Administration of intracoronary nitroglycerin or diltiazem prevented exercise-induced vasoconstriction, probably due to the direct vasorelaxing effect of the drug on the smooth vasculature. Intracoronary administration of propranolol also prevented exercise-induced vasoconstriction, either due to a reduction in trans-stenotic pressure gradient (local beta blockade with a decrease in local coronary blood flow or an increase in distal arteriolar tone due to unopposed alpha-constrictor tone) or because of a local anesthetic effect of propranolol with a decrease in calcium influx into the smooth vasculature.
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PMID:[Coronary vasomotor activity; its significance for the therapy of angina pectoris]. 313 74

Between 1982 and 1983, we experienced four cases of hemodynamic collapse accompanied by an ST-segment depression in the ECG lead II, shortly after the cessation of cardiopulmonary bypass. The bypass graft flows monitored in these patients during the hemodynamic collapse episodes were remarkably low. In three cases, nitroglycerin (0.5-1 mg) was injected directly into the vein graft, which increased the graft flow suddenly, returned the ST-segment to the baseline, and improved the circulatory condition. Since 1984, however, diltiazem has been used in the cardioplegic solution and postoperative drip infusion. Due to the introduction of this drug, coronary artery spasm has not been seen in any of our patients since. These findings show that the monitoring of ST-segment changes and bypass graft flows are useful in the early diagnosis of coronary artery spasm after myocardial revascularization. Direct infusion of nitroglycerin into the vein graft is effective for the treatment of spasm, while diltiazem is useful in the prevention of coronary artery spasm incidental to myocardial revascularization.
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PMID:Coronary artery spasm during coronary artery bypass surgery: its diagnosis, treatment and prevention. 315 18


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