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)

A specific subset of acute myocardial infarction was defined and named 'the hypertensive-hyperkinetic-coronary-active' subgroup. This subgroup included patients with acute myocardial infarction without pump failure or hypovolemia who continued to have hypertension and tachycardia, after relief of pain and who also had at least two recurrent ischemic episodes in the first days after a transmural event. Fifteen patients belonging to this group (group A) were studied in comparison with 15 other patients with acute myocardial infarction complicated by pump failure (group B). The alterations in hemodynamics, in circulating catecholamine levels and the clinical course during an intravenous infusion of isosorbide dinitrate were evaluated and the data obtained in the two groups were compared. The patients in group A had tachycardia, hypertension and upper normal filling pressures (pulmonary capillary wedge pressures: 15.8 +/- 1.8 mm Hg). They had high levels of circulating catecholamines (1,343 +/- 407 ng/l), a cardiac output of 5.9 +/- 0.6 liters/min and stroke work index of 78 +/- 11 (mean +/- SD). The effect of intravenous nitrates on the left ventricular function curves of the two groups was the following: a marked shift downward and slight shift to the left in group A, as opposed to a moderate but significant shift upward and marked shift to the left in group B. The episodes of recurrent ischemia subsided in 13 out of 15 patients from group A. It appears therefore that the hyperkinetic patients with acute infarction are characterized by a hypersympathetic response, a typical hemodynamic profile and a particular response to nitrate therapy directionally opposite to the changes obtained in patients with acute infarction complicated with failure.
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PMID:Hemodynamics, circulating catecholamines and response to intravenous nitrate therapy in a specific subset of acute myocardial infarction: the hypertensive-hyperkinetic-coronary-active group. 316 15

The relation between the duration of ischemic ST-segment depression (1 mm or more 60 ms after the J point) and the clinical awareness of chest pain was studied in 31 patients (aged 39-73 years) undergoing symptom-limited, graded treadmill exercise testing. The response of these patients to nitrate therapy (spray or sublingual tablet) given immediately on cessation of exercise was also studied. During exercise, angina pectoris appeared at an estimated workload of 4.6 +/- 2.2 metabolic equivalents (METS) (mean +/- SD), and pathological ST-segment depression at 4.9 +/- 1.9 METS (p = NS.) On cessation of exercise, angina disappeared after 3.0 +/- 1.9 min, but ST-segment depression persisted for more than twice as long (6.6 +/- 4.1 min) (p less than 0.0001). The ratio of time to ST-segment recovery/time to relief of pain (a quantitative measure of silent ischemia during recovery) increased with age (r = 0.49, p = 0.002), and in 16 patients over 60 years of age was higher than in 15 younger patients (3.6 +/- 2.5 vs. 2.1 +/- 1.4) (p less than 0.04). The silent ischemia ratio after exercise tended to decrease, although not significantly so (p = 0.2), in patients who received oral nitrates; there was no difference in the response to spray or tablet in this regard. We conclude that ST-segment depression frequently persists after relief of exercise-induced angina pectoris and more so in elderly patients.
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PMID:Persistent painless ST-segment depression after exercise testing and the effect of age. 329 58

The renal disposition of insulin in acute renal failure has not been evaluated. We used the isolated perfused rat kidney to test the hypothesis that acute renal failure (ARF) decreases renal insulin clearance. We used warm ischemia for 45 min, uranyl nitrate 5 mg/kg, ureter ligation, and nonfiltering kidneys as methods of inducing ARF. Comparisons were made with normal control kidneys. The concentrations of insulin in perfusate and urine was determined by radioimmunoassay. Acute renal failure caused significant reductions in glomerular filtration rate, sodium and potassium reabsorption, and an increased urine pH. Warm ischemia and uranyl nitrate toxicity caused a 50% decrease in the renal clearance of insulin. Nonfiltering kidneys cleared insulin at a rate 90% decreased from controls. Ureteral ligation caused a 32% decrease in insulin clearance. Filtration was necessary for insulin to be cleared from perfusate. We conclude that ARF decreased renal insulin clearance through a decrease in insulin uptake from both the tubular lumen and peritubular surface.
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PMID:Effect of acute renal failure on insulin disposition in the isolated perfused rat kidney. 331 99

Vasodepressor prostanoids have been suggested to regulate renal hemodynamics after nephrotoxic injury and thus protect the kidney against the effects of prolonged ischemia. This study assessed whether changes in two microvascular vasodilator prostanoids would correlate with changes seen in renal hemodynamics in rabbits with nephrotoxic renal injury produced by either uranyl nitrate or mercuric chloride. Rabbits were killed at 3, 24, and 72 h after the nephrotoxin injections and 6-ketoprostaglandin (PG) F1 alpha and PGE2 synthesis was measured in vitro in isolated renal microvessels. At the end of 24 h, synthesis of both prostanoids was significantly increased in all nephrotoxin-treated animals, an observation not noted at the end of 3 h. At 72 h, 6-keto-PGF1 alpha production remained elevated. Pretreatment with mepacrine blocked the increased prostanoid production seen in uranyl nitrate-treated animals. Thus, renal microvascular vasodilator prostanoid biosynthesis is increased 24-72 h after nephrotoxin administration. These data suggest that the biosynthesis of prostacyclin and PGE2 may contribute to the maintenance of renal blood flow in the first few days after acute renal injury and further suggest that a mechanism for this increase may be stimulation of phospholipase A2.
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PMID:Alterations in rabbit renal microvascular prostanoid synthesis in acute renal failure. 336 78

Although nitrates are the basic treatment for patients with ischemic heart disease and numerous clinical studies have compared the anti-ischemic effects of different combinations with beta-blockers and/or calcium antagonists, no study is known on a controlled intraindividual comparison of the combination nitrate plus beta-blocker with the combination nitrate plus a heart rate-decreasing calcium-antagonist. Therefore we performed a randomized, double-blind and crossover study to compare the effects of 80 mg isosorbide dinitrate in slow-release form (ISDN, once-daily) plus 120 mg verapamil (t.i.d.) with those of 80 mg ISDN plus 80 mg propranolol (b.i.d.). After these two phases of 3 weeks' duration respectively, patients received the combination of all three drugs with the same dosages in a single-blind manner. In addition to the standard inclusion criteria, a pathological exercise-ECG even after ISDN was required as well as a left ventricular ejection fraction (EF) of greater than or equal to 35%. This protocol could be completed in 26 of the 30 enrolled patients. The combination ISDN plus verapamil proved to exert the same anti-ischemic effects as the combination ISDN plus propranolol. The triple therapy showed a further improvement of exercise induced ischemia without deterioration of the EF at rest or during exercise. Even though only this triple therapy led to an optimal anti-ischemic result in about one third of the patients, it should be initiated cautiously, since symptomatic bradycardia may occur.
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PMID:Equal anti-ischemic properties of isosorbide dinitrate plus verapamil and isosorbide dinitrate plus propranolol. A randomized, double-blind and crossover study. 354 14

There is increasing evidence that constant nitrate plasma levels, as induced by at least three-times-daily ingestions of isosorbide dinitrate in sustained-release form, lead to an attenuation or even complete loss of the anti-ischemic effects (nitrate tolerance). Therefore, the dependence of tolerance development on dosage intervals according to once-daily and twice-daily ingestions was assessed. Tablets of isosorbide dinitrate (80 mg) in sustained-release form were administered once-daily at 8 A.M. (dosage interval 24 hours) or twice-daily at 8 A.M. and 8 P.M. (dosage interval 12 hours), as well as at 8 A.M. and 2 P.M., respectively (maximal dosage interval 18 hours). A total of 34 patients with angiographically proven coronary artery disease, a history of stable, exercise-dependent angina pectoris, and a reproducible, exercise-induced ST-segment depression of at least 0.15 mV (1.5 mm), who initially showed a response to 80 mg of isosorbide dinitrate, were enrolled. The anti-ischemic effects of isosorbide dinitrate on exercise-induced ischemia were objectively determined by the measurement of exercise-induced ST-segment depression before as well as two, six, and 12 hours after the ingestion at the first and the 15th day of the studies. Since the dosage interval of 12 hours resulted in constant plasma levels, the initially beneficial anti-ischemic effects of isosorbide dinitrate were considerably attenuated after two weeks of treatment. In contrast, the once-daily regimen with its intermittent peaks and valleys of nitrate plasma levels showed identical anti-ischemic effects at the 15th day as compared with the first day. Ingestions at 8 A.M. and 2 P.M. also circumvented the development of nitrate tolerance, however, combined with an even more pronounced anti-ischemic effect after 12 hours as compared with the once-daily regimen. Thus, the circumvention of nitrate tolerance requires a daily "nitrate-poor" interval. The best compromise between a maximal possible anti-ischemic effect and the circumvention of tolerance development was found for the "eccentric" dosage regimen in which the tablets were ingested in the morning and early afternoon.
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PMID:Induction and circumvention of nitrate tolerance applying different dosage intervals. 367 93

During Ergonovine-test a patient with Prinzmetal angina presented (in I, aVL, V3-V6) ST downsloping which, after a temporary phase of alternative normalization (AST) beat to beat in V5, progressed to ST upsloping with typical angina. The M-mode echo-study first discovered, before than ecg, septal impairment (hypokinesia which increased to akinesia in the AST phase) and also asynergy of posterior wall of left ventricle. After intravenous nitrate echo-alterations reversed more rapidly than ecg one (transitional phase of ST decrease). The authors relate the AST to temporary alternative pseudonormalization caused by a phase of electrical instability during progressive vasospastic ischemia involving first the endocardial layers and after the epicardium of a single myocardiocoronary district. Probably also other partially opposite ischaemic districts, as suggested from echo data of posterior wall asynergy took a part in these events. This rare ST-alternans type as new pseudonormalization phenomenon and the usefulness of echo-study during ischaemic attacks are stressed.
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PMID:[Clinical, electrocardiographic and echocardiographic findings in a case of vasospastic angina with alternating pseudonormalization of the ST segment]. 383 2

Nitroglycerin (NTG) and isosorbide dinitrate (ISDN) are potent dilators of vascular smooth muscle. The organic nitrates produce venodilation at very low doses, with little additional vasodilation of the venous circulation with increasing dosage. Nitrates increase arterial diameter and improve arterial conductance at low to moderate doses, and at high doses these agents produce dilation of the arteriolar or resistance vessels of the body. The overall hemodynamic response to nitrate administration will be modulated by the degree of sympathetic reflex discharge, the presence or absence of congestive heart failure, the dosage of administered nitrate, and the presence or absence of nitrate tolerance. Regional circulatory effects of the organic nitrates include a decrease in vascular resistance and an increase in arterial blood flow to the arms and legs. Venodilation also occurs in the extremities. In the splanchnic and mesenteric circulations, nitrates induce an initial vasodilative response followed by reflex vasoconstriction. Hepatic blood flow changes little in the normal state. Pulmonary blood flow decreases and pulmonary artery and venous pressures fall after nitrate administration. Renal blood flow remains essentially unchanged or decreases slightly after NTG administration, although reflex sympathetic activity may cause secondary vasoconstriction. The antianginal effects of nitrates have long been thought to be related to their systemic or peripheral actions, which reduce myocardial oxygen requirements through decreases in left ventricular preload and afterload. There is, however, considerable evidence that nitrates have important direct effects on the coronary circulation in both the normal and the ischemic heart. Such actions include coronary artery dilation, increased collateral blood flow, and enhanced oxygenation and nutrient perfusion to zones of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of nitroglycerin and long-acting nitrates. 392 41

Minimally invasive evaluation of the behavior of the right and the left ventricle can be obtained in a dynamic way by using technetium-99 (99Tc) scintographic ventriculography. The "first pass" technique is particularly appropriate to the investigation of short-acting agents, such as nitroglycerin and other nitrates, but information on a 1-minute to 2-minutes steady state response can be obtained by using the "gated blood pool" method. Studies in patients with and without coronary heart disease have identified apparent improvement in regional and global left ventricular ejection fractions associated with afterload reduction caused by such interventions. However, part of the normalization of regions of previously abnormal myocardial contraction may be due to more uniform transmural distribution of coronary blood flow. Such techniques, including nitrate administration, have been used to define regional ischemia suitable for revascularization procedures. Sequential thallium studies also suggest that nitroglycerin reduces or prevents stress induced ischemia, although the mechanism (afterload versus coronary vasodilation) has not been completely elucidated. In the future subtraction angiographic techniques may lead to a more accurate estimate of regional distribution of blood flow and its pharmacologic manipulation. Digital techniques will also facilitate accurate measurement of coronary vascular narrowing in a manner that will serve to elucidate the direct actions of nitrates and similar substances on the coronary circulation.
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PMID:Newer technologies for study of the action of nitrates in coronary circulation and myocardial function. 392 43

The strategy of treatment in vasospastic angina is mainly based on the results of coronary angiography. In a series of 165 patients with coronary spasm documented by angiography, 51 patients (31 per cent) had angiographically normal arteries and 69 per cent had organic atherosclerotic lesions. Patients with fixed atherosclerotic lesions were divided in two subgroups depending on whether the lesions were operable. The first subgroup (47 cases) comprised patients with operable lesions and coronary spasm. They underwent aorto-coronary bypass associated with a procedure to prevent spasm (plexectomy) (40 cases). Depending on the site of the lesions, some patients with operable lesions may benefit from coronary angioplasty followed by treatment with calcium antagonist drugs. Patients in the second subgroup (67 cases) with inoperable fixed atherosclerotic lesions were treated with calcium antagonists. Betablockers, which may be considered in organic coronary artery disease, are theoretically contra-indicated because of the vasospastic factor. The remaining patients with "angiographically normal" vessels (51 cases) were treated with nitrate derivatives and calcium antagonists. Treatment should be directed to the suppression of the clinical symptoms and, above all, of ECG signs of ischemia as proved by repeated Holter monitoring. The clinical course may also be assessed by repeated provocation tests. Results may depend on the doses and their timing during the 24 hour period. Duration of treatment in patients with angiographically normal vessels has not yet been established. Isolated cardiac denervation may be indicated in these patients who fail to respond to medical treatment (8 cases).
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PMID:[Strategy of the treatment of vasospastic angina pectoris]. 640 40


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