Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that apressin in doses of 0.5 and 1 mg/kg intravenously prevented a drop of the amplitude of the left ventricular pressure, pressure, maximal speed of its rise and relaxation which developed in control experiments on dogs after ligation of the coronary artery. Apressin increased the volumetrical rate of the collateral coronary blood flow, diminished peripheral vascular resistance in the zone of myocardial ischemia and reduced the ST segment of the heart epicardial electrogram. The drug lowered glucose consumption, lactate content, and "excess' lactate in blood samples collected from the ischemic zone. At succinate and glutamate oxidation, it decreased oxygen consumption by mitochondria from the myocardial ischemic zone in the acceptor-free system, and increased the respiration stimulation coefficient, the respiratory control alccording to Change being improved at glutamate oxidation.
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PMID:[Effect of apressin on the contractility, blood supply and bioenergetics of the ischemic myocardium]. 48 18

Vasodilator and inotropic drugs work through independent mechanisms in augmenting left ventricular pump function in patients with heart failure. The selection between these two classes of pharmacologic agents for an individual patient may be based on the control blood pressure as well as the underlying disease. Although vasodilator drugs are easiest and safest to employ in patients with normal or high arterial presure levels, even in relatively hypotensive subjects (systolic arterial pressure less than 105 mm Hg), a salutary hemodynamic effect can be achieved without an undue decrease in pressure. Inotropic drugs may be safest to administer to patients without coronary artery disease, but the oxygen-consuming effect of these drugs need not necessarily have an adverse effect on patients with ischemic heart disease. Combined vasodilator and inotropic drug therapy is the most potent pharmacologic means of restoring pump function in patients with severe heart failure. The long-term use of vasodilator and inotropic drugs in the treatment of heart failure is dependent on the availability of agents that will produce a sustained hemodynamic effect. Hydralazine, nitrates and prazosin have been employed alone or in combination and provide a promising approach to vasodilator treatment of heart failure. Better and more selective oral inotropic agents are needed to allow this therapeutic modality to be employed optimally.
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PMID:Selection of vasodilator, inotropic or combined therapy for the management of heart failure. 68 92

Increased peripheral vascular resistance is the cause of elevated systemic blood pressure in most patients with long standing hypertension. The desired haemodynamic effect in antihypertensive therapy is dilation of the constricted arterioles by a drug that acts directly on the vascular smooth muscle while not affecting the heart or the venous return. Hydralazine, diazoxide and minoxidil act directly on vascular smooth muscle to produce vasodilatation and have been used with variable degrees of success in the long term treatment of hypertension. Their cellular mechanism of dilation is not understood fully, but the ability to chelate certain trace metals required for smooth muscle contraction has been proposed as a possible mechanism of action for these drugs. The calcium antagonists (calcium entry blocking drugs) are a distinct group of compounds that interfere with the normal transmembrane flux of extracellular calcium ions on which vascular tissue depends for contraction or impulse generation. Thus, calcium anti-agonists can reduce the contractile activity of the heart, and promote coronary and systemic vasodilatation. These effects provide the clinical rationale for the use of calcium antagonists in the management of ischaemic heart disease and hypertrophic cardiomyopathy. Since systemic vasodilatation can be expected to reduce elevated arterial blood pressure, interest has focused recently on calcium antagonists in the medical management of systemic hypertension. All the calcium antagonists are able, in low concentrations, to relax the smooth muscle vasculature from coronary, cerebral, mesenteric, and renal arteries. The effects on the myocardium, cardiac impulse tissue, and vascular smooth muscle are different in magnitude, however, depending on the individual agent that is used. Clinical experience in the treatment of hypertension with this class of agents is confined to verapamil, nifedipine, and diltiazem. In this article, the scientific rationale for using calcium antagonists in the treatment of arterial hypertension is explored and the clinical experiences with the different calcium antagonists used in hypertension are reviewed.
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PMID:Calcium antagonists. Clinical use in the treatment of systemic hypertension. 633 98

Hypertensive emergency is a condition in which there is elevation of both systolic and diastolic blood pressure with the presence of acute target organ disease. Hypertensive urgency is a condition where the blood pressure is elevated (diastolic > 120 mmHg) with the absence of acute target organ disease. Hypertensive emergencies are best managed with parenteral drugs and careful intraarterial blood pressure monitoring. Hydralazine has been widely used in treatment of hypertension in eclampsia and preeclampsia, and its safety has been demonstrated in these patients. Sodium nitroprusside (SNP) has the most reliable antihypertensive activity, which begins immediately after its administration and ends when the infusion is stopped. As with diazoxide, it should be used with caution in patients with impaired cerebral flow. SNP is the preferred drug in obtaining controlled hypotension in patients undergoing neurovascular surgery. Intravenous nitroglycerin is useful in patients prone to myocardial ischemia, but should be avoided in patients with increased intracranial pressure. Esmolol is effective in controlling both supraventricular tachyarrhythmias and severe hypertension. Its short onset of duration of action make it useful in the emergent setting, but because of its negative inotropic effect its use should be avoided in patients with low cardiac output. Verapamil should not be used in patients with preexisting conduction abnormalities. Nicardipine is a potent arteriolar vasodilator without a significant direct depressant effect on myocardium. As with other afterload reducing agents, it should not be used in patients with severe aortic stenosis. Because angiotensin-converting enzyme (ACE) inhibitors generally cause cerebral vasodilatation, enalaprilat may be particularly beneficial for patients who are at high risk of developing cerebral hypotensive episodes secondary to impaired cerebral circulation. Fenoldopam, a selective post-synaptic dopaminergic receptor (DA1) has been shown to be effective in treating severe hypertension with a lower incidence of side effects than SNP. Hypertensive urgencies can usually be managed with oral agents. Oral nifedipine, captopril, clonidine, labetalol, prazosin, and nimodipine have all been shown to be effective in these situations.
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PMID:Management of hypertensive urgencies and emergencies. 852 30

Hypertensive crisis is defined as a severe elevation in BP and is classified as either urgency or emergency. In hypertensive urgency there is no end-organ injury and no evidence that acute BP lowering is beneficial. Indeed, rapid uncontrolled pressure reduction may be harmful. Therefore, in hypertensive urgencies BP should be lowered gradually over 24 to 48 hours using oral antihypertensives. When the cause of transient BP elevations is easily identified, appropriate treatment should be given. When the cause is unknown, an oral antihypertensive should be given. The efficacy of available treatments appear similar; however, the underlying pathophysiological and clinical findings, mechanism of action and potential for adverse effects should guide choice. Captopril should be avoided in patients with bilateral renal artery stenosis or unilateral renal artery stenosis in patients with a solitary kidney. Nifedipine and other dihydropyridines increase heart rate whereas clonidine, beta-blockers and labetalol tend to decrease it. This is particularly important in patients with ischaemic heart disease. Labetalol and beta-blockers are contraindicated in patients with bronchospasm and bradycardia or heart blocks. Clonidine should be avoided if mental acuity is desired. In hypertensive emergency there is an immediate threat to the integrity of the cardiovascular system. BP should be immediately reduced to avoid further end organ damage. Sodium nitroprusside is the most popular agent. Nitroglycerin (glyceryl trinitrate) is preferred when there is acute coronary insufficiency. A beta-blocker may be added in some patients. Loop diuretics, nitroglycerin and sodium nitroprusside are effective in patients with concomitant pulmonary oedema. Enalaprilat is also theoretically helpful, especially when the renin system might be activated. Initial treatment of aortic dissection involves rapid, controlled titration of arterial pressure to normal levels using intravenous sodium nitroprusside and a beta-blocker. If beta-blockers are contraindicated, urapidil or trimetaphan camsilate are alternatives. Hydralazine is the drug of choice for patients with eclampsia. Labetalol, urapidil or calcium antagonists are possible alternatives if hydralazine fails or is contraindicated. For patients with catecholamine-induced crises, an alpha-blocker such as phentolamine should be given; labetalol or sodium nitroprusside with beta-blockers are alternatives. There are few, if any, comparative or randomised trials providing definitive conclusions about the efficacy and safety of comparative agents. Some investigators recommend decreasing the diastolic BP to no less than 100 to 110 mm Hg. A reasonable approach for most patients with hypertensive emergencies is to lower the mean arterial pressure by 25% over the initial 2 to 4 hours with the most specific antihypertensive regimen.
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PMID:Comparative tolerability profile of hypertensive crisis treatments. 970 48