Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitroglycerin improves perfusion to ischemic myocardial regions and therefore has theoretical advantages over sodium nitroprusside to treat hypertension (mean arterial pressure [MAP] greater than 95 mm Hg) following coronary bypass operation. Thirty-three hypertensive patients were randomized to an initial infusion of either nitroglycerin or nitroprusside in a crossover trial designed to reduce MAP to 85 mm Hg. Thermodilution cardiac output measurements permitted calculation of left ventricular stroke work index (LVSWI), and nuclear ventriculograms permitted estimation of left ventricular ejection fraction, left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI). Coronary sinus blood flow was measured by the continuous thermodilution technique, and arterial and coronary sinus lactate measurements permitted calculation of myocardial lactate flux (MVL). Both nitroglycerin and nitroprusside reduced MAP (-25 +/- 12 mm Hg and -20 +/- 10 mm Hg, respectively; not significant [NS]). Nitroglycerin reduced LVSWI more than did nitroprusside (-15 +/- 13 gm-m/m2 and -7 +/- 9 gm-m/m2, respectively; p less than 0.01). Both agents increased left ventricular ejection fraction (nitroglycerin, +8 +/- 8%, and nitroprusside, +10 +/- 7%; NS), and decreased LVEDVI (-20 +/- 22 ml/m2 and -11 +/- 17 ml/m2, respectively; NS) and LVESVI (-13 +/- 14 ml/m2 and -10 +/- 12 ml/m2, respectively; NS). Coronary sinus blood flow decreased with both drugs (NS), but MVL increased with nitroglycerin (+0.02 +/- 0.14 mmol/min) and decreased with nitroprusside (-0.02 +/- 0.02 mmol/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of nitroglycerin and nitroprusside: I. Treatment of postoperative hypertension. 391 59

The present study was performed to compare hemodynamic effect of intravenous Nitroglycerin (TNT i.v.) in 14 patients developing acute hypertension (Group I) and in 7 non hypertensives after open heart surgery (Group II). In all patients, m.a. 56.6 yrs, (10 mitral and/or aortic prosthetic valve replacements, 9 aorto-coronary bypass, 1 open mitral commissurotomy, 1 closure of atrial septal defect) TNT was infused at doses of 0.5, 1, 2 microgram X kg X min. and subsequently at 2 microgram X kg X min. after volume administration (2 + V.A.) to maintain right and left atrial pressure the same as control (P = N.S.). Mean arterial, right and left atrial pressures (MAP, RAP, LAP), cardiac frequency and index (CF, CI and systemic vascular resistance index (SVRI) were monitorized. TNT i.v. resulted in hypertensive patients (Group I) in reduction vs. control of: a) RAP (--20.17%) and LAP (--20.58%) at 0.5 microgram X kg X min. b) RAP (--26.13%), LAP (--27.50%), MAP (--19.94%) and CI (--12.98%) at 1 microgram X kg X X min. c) RAP (--22.47%), LAP (--26.89%), MAP (--24.68%), CI (--12.6%) and SVRI (--17.34%) at 2 microgram X kg X min. When RAP and LAP was maintained by volume administration TNT i.v. (2 microgram X kg X min.) resulted in an even greater increase in CI and a greater decrease in MAP and SVRI ((--22.04% and --24.88% respectively). No significant hemodynamic modification (P less than or equal to 0.05) were observed in non hypertensive patients (Group II) at all doses of TNT i.v. The results confirm a predominant venodilator effect of TNT at low doses and a good effect on arterial resistances at high doses in hypertensive patients. In view of previous reports of differing effects on ischemia TNT i.v. may be preferable to other vasodilator drugs for control of acute post-ECG hypertension, only on condition to maintain an adequate left ventricular filling pressure to prevent a fall of cardiac index. Moreover the absence of significant (P less than or equal to 0.05) hemodynamic modifications in non hypertensive patients may be a further advantage in the treatment of myocardial ischemia with i.v. TNT.
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PMID:[Effect of intravenous nytroglicerin in hypertensive patients during and after open heart surgery (author's transl)]. 678 Apr 1

Hypertensive emergencies are uncommon and physiologically diverse. Consequently, it is difficult for most physicians to develop a familiarity with all the different hypertensive crises and with all drugs available for treating them (Table 4). Clinicians should not agonize over which is the perfect therapeutic agent for a particular emergency, but instead, they should focus on scrupulous monitoring and familiarize themselves with a few agents that will serve in most situations. Generally, these agents will be sodium nitroprusside and nitroglycerin. Vigilant neurologic monitoring is mandatory in all hypertensive emergencies. The early symptoms and signs of cerebral hypoperfusion can be vague and subtle, but if recognized, serious complications of therapy can be avoided. Remember, the patient may still be hypertensive. Avoid acute (during the first hour) reductions in MAP of more than 20% whenever possible; subsequent reductions should be gradual. In patients known to have markedly elevated ICP and who need acute reductions in their BP, serious consideration should be given to direct monitoring of the ICP so that CPP can be maintained within safe limits. In general, oral agents should not be used for the treatment of hypertensive emergencies. Intravenous Labetalol and intravenous nicardipine are not suitable for general use in hypertensive emergencies. In special situations (e.g., perioperative hypertension and subarachnoid hemorrhage), however, they may be employed. Their role may expand with further study. Trimethaphan may be superior to nitroprusside for hypertension complicated by elevated ICP or cerebral dysfunction. Realistically, most physicians will continue to use nitroprusside. Intense neurologic monitoring is more important than the specific agent used. Nitroglycerin is the agent of choice for acute ischemic heart disease complicated by severe hypertension; if it fails, use nitroprusside. For aortic dissection, the combination of nitroprusside and IV propranolol is the therapy of choice; beta-blockade must be achieved rapidly or the dissection may worsen. Trimethaphan is also an agent for first-line therapy. Esmolol is an alternative to IV propranolol for the treatment of aortic dissection, if prolonged beta-blockade might seriously jeopardize the patient. For eclampsia, unless an expert in hypertension during pregnancy has established an alternative, the therapy of choice is hydralazine and magnesium. The treatment of subarachnoid hemorrhage is in flux; calcium channel blockers are used to prevent spasm, not to lower BP. If the BP must be lowered immediately, use nitroprusside.
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PMID:Hypertensive emergencies. 758 98

Combretastatin A-4 phosphate (CA4P) is a novel and promising anti-neoplastic agent. However, it is associated with transient hypertension in both animal and human models. In this study, we examined the potential cardiac toxicity and hypertensive effects of CA4P, and defined the most effective pharmacological inhibition of CA4P-induced hypertension in rats. There was a significant, concentration dependent increase in mean arterial blood pressure with a maximum increase of about 60% of the baseline MAP at 30 mg/kg of CA4P compared to the saline control. However, there was no significant increase in the cardiac troponin I level after CA4P injection. Nitroglycerin and the calcium channel blocker diltiazem effectively blocked the hypertensive effects of CA4P while the beta blocker metoprolol was ineffective. Furthermore, sublingual nitroglycerin administration demonstrated an additional anti-hypertensive effect in a setting of a low dose diltiazem infusion (10 microg/kg/min). We conclude that CA4P treatment resulted in a concentration dependent increase in blood pressure without significant myocardial damage in healthy rats. The hypertensive effect of CA4P was effectively blocked by both nitroglycerin and diltiazem, but not metoprolol.
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PMID:Pharmacological inhibition of the hypertensive response to combretastatin A-4 phosphate in rats. 1973 29