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)

This study was designed to analyze the electrolytes changes in myocardial cells, and to clarify the effect of diltiazem, a calcium channel blocker on myocardial ischemia during open heart surgery. Thirty patients who underwent open heart surgery using cold glucose-insulin-potassium (GIK) cardioplegic solution were divided into following three groups. C group: diltiazem was not administered. CD group: cardioplegic solution containing diltiazem 7.5 mg/L was used. DP group: diltiazem 1.5 micrograms/kg/min was given continuously by intravenous administration from the day before operation to the day after operation. Atrial wall biopsies were performed before aortic cross clamp (non-ischemic status), after 60 minutes' ischemia, and 5 minutes after releasing aortic cross clamp (reperfusion). The specimens were freshly frozen and measured for various electrolytes by means of X-ray microprobe analysis. In C group, potassium level decreased during both ischemia and reperfusion, while calcium level increased during ischemia and significantly increased during reperfusion period. In DC and DP groups, calcium accumulation during reperfusion was suppressed, and potassium level which had been lowered during ischemia recovered to the level of non-ischemic status during reperfusion. Sodium and chlorine showed an increase during ischemia in each group. However, sodium accumulation in DC and DP groups tended to recover during reperfusion. DP and DC groups were considered to be superior to C group in terms of cardiac index and left ventricular work. This may be due to afterload reduction as evidenced by low systemic vascular resistance. Intracellular electrolytes environment during reperfusion and hemodynamics during early postoperative periods were excellent in DP group. CPK-MB was significantly lower in both CD and DP groups than in C group. These data suggested that diltiazem could suppress intracellular calcium accumulation and keep homeostasis of sodium-potassium pump mechanism in membrane during reperfusion. It is concluded that diltiazem is useful to protect myocardium from ischemia during open heart surgery.
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PMID:[The protective effect of diltiazem, a calcium channel blocker on myocardial ischemia during open heart surgery--an analysis of electrolyte changes in myocardial cells]. 234 17

The endogenous compound adenosine may play a role in limiting myocardial ischemia-reperfusion injury through its ability to cause vasodilation, modulate cardiac adrenergic responses, inhibit neutrophil function, or modulate energy supply and demand of the myocardium. The local anesthetic lidocaine has been shown to be protective against myocardial ischemia-reperfusion injury, although its mechanism of action remains unresolved. We hypothesized that administration of exogenous adenosine during reperfusion would limit the size of the infarct that results from a period of ischemia and reperfusion only when the animals are treated with lidocaine. Male, mongrel dogs (13.0-20.0 kg) were anesthetized (30 mg/kg i.v. sodium pentobarbital), and a left thoracotomy was performed. The left circumflex coronary artery (LCx) was isolated and instrumented with an electromagnetic flow probe, a 25-gauge nonobstructing intracoronary catheter, and a critical stenosis. The dogs were allocated randomly to one of four groups: 1) control, n = 13, (saline), 2) adenosine, n = 13, (0.15 mg/kg/ml/min i.c. for the first hour of reperfusion), 3) lidocaine, n = 9, (2.0 mg/kg i.v. given immediately before coronary artery occlusion and just before reperfusion), or 4) adenosine plus lidocaine, n = 11. The LCx was occluded for 90 minutes and reperfused for 6 hours. Regional myocardial blood flow (RMBF) was determined (n = 6 per group) at 80 minutes of occlusion and at 45 minutes of reperfusion with radiolabeled microspheres. RMBF determinations revealed an increase in blood flow to the inner two thirds of the myocardium at 45 minutes of reperfusion only in the presence of the combined treatment. Adenosine treatment alone or lidocaine treatment alone did not affect RMBF. Quantification of infarct size (triphenyltetrazolium method) expressed as a percent of the area at risk revealed a significant limitation of infarct size only in the group treated with both adenosine and lidocaine: control, 47.8 +/- 6.6%; adenosine, 45.0 +/- 3.2%; lidocaine, 46.9 +/- 6.0%; and adenosine and lidocaine, 20.8 +/- 5.6%. Statistical analyses were performed with two-way analysis of variance to account for the two individual drug treatments. The findings show that intracoronary administration of exogenous adenosine, at the dose used, is only effective at limiting myocardial infarct size when administered to lidocaine-treated animals.
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PMID:Combined adenosine and lidocaine administration limits myocardial reperfusion injury. 237 6

The elevation of cardiomyocyte membrane permeability has been demonstrated during pituitrin-isadrin-induced myocardial ischemia. Preventive 7-day oral administration of an antioxidant dibunol (30 and 120 mg/kg) preserved sarcolemmal integrity, decreased myocardial membrane permeability to sulfacetamide sodium, and reduced peroxide and mechanical erythrocyte hemolysis. Inhibition of lipid peroxidation with an antioxidant dibunol improved myocardial injury and decreased the death rate of animals with catecholamine-induced myocardial ischemia. These data suggest the involvement of lipid peroxidation in the development of ischemic myocardial injury.
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PMID:[Significance of sarcolemma damage in the pathogenesis of myocardial ischemia induced by pituitrin-isadrin and its correction using the antioxidant dibunol]. 243 Jun 40

We administered diltiazem HCl i.v. (0.05 mg/kg in bolus followed by 0.01 mg/kg/min for 45 min), and determined the changes in blood pressure (BP), glomerular filtration rate (GFR), renal blood flow (RBF), total renal resistance, urinary volume (UV), urinary sodium (UNa) and potassium excretion, urea and osmolar clearance, and tubular reabsorption ratio of sodium (TRNa%). The serum concentration of diltiazem achieved was similar to the maximum level after a single oral dose of 120 mg. GFR and RBF were measured by i.v. infusion of sodium thiosulfate and sodium rho-amino-hippurate, respectively, as indicators. The subjects included 12 cases of essential hypertension (EH), 10 of chronic glomerular nephritis (CGN) with hypertension, 12 of CGN without hypertension, 12 of ischemic heart disease (IHD), and 10 of normotensive controls. BP decreased in hypertensives but not in normotensives. In patients with EH, GFR and RBF increased markedly (by 25.3 +/- 33.8% and 30.7 +/- 39.5%, respectively). In patients with IHD, GFR increased slightly by 9.8 +/- 17.6%, whereas in patients with CGN with hypertension, GFR decreased by -4.3 +/- 14.3%. No significant change of these indices was observed in normal subjects and in patients with CGN without hypertension. UV and UNa increased and TRNa% decreased in all groups. Urea and osmolar clearance increased in almost every group.
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PMID:Clinical effects of intravenous diltiazem hydrochloride on renal hemodynamics. 243 98

Vasodilators may provoke myocardial ischemia in patients with coronary heart disease. Therefore, we analyzed in conscious dogs the effect of angiotensin-converting enzyme (ACE) inhibition by enalaprilat on parameters potentially important to provocation of myocardial ischemia, such as sympathetic activity, myocardial oxygen consumption, and vascular tone in coronary conduit and resistance vessels. Under normal sodium intake (2-4 mEq/kg/day), enalaprilat (0.03 and 0.3 mg/kg i.v. during 5-min infusion with 30-min intervals, n = 8) did not modify the norepinephrine release rate into plasma (a parameter of overall sympathetic activity). The higher dosage reduced myocardial oxygen consumption (to 87 +/- 2% of control), mean arterial pressure (MAP) (to 90 +/- 1%) and coronary conduit artery tone (normalized delta diameter: +3.2 +/- 0.7%) without dilating coronary resistance vessels. Following renin-angiotensin activation by sodium deprivation (3 X 1 mg/kg furosemide plus 7 days sodium intake less than 0.2 mEq/day), enalaprilat similarly lowered myocardial oxygen consumption and reduced vascular tone both in coronary conduit (normalized delta diameter: +4.0 +/- 0.9%) and resistance vessels (delta coronary flow: +45 +/- 12%). Although MAP declined to 76 +/- 6%, heart rate and norepinephrine release rate were not modified significantly. We propose that the dilation of epicardial arteries results from a direct intramural action. Enalaprilat seems unlikely to provoke myocardial ischemia even in states with a strongly activated renin-angiotensin system.
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PMID:Dilation of epicardial arteries in conscious dogs induced by angiotensin-converting enzyme inhibition with enalaprilat. 243 1

1. Among the dysionemias hyper- and hypokalemia are particularly important for clinical arrhythmogenesis. Disorders in sodium- and calcium concentrations, however, are relevant only in single cases. The impact of magnesium concentration disorders on cardiac rhythm is not yet totally elucidated. 2. In hypokalemia tachycardic arrhythmias are most important, while bradycardic and tachycardic arrhythmia can be caused by hyperkalemia. An important factor in arrhythmogenesis is the rate of development of hypo- or hyperkalemia. Hypokalemically-induced arrhythmia can be suppressed by potassium substitution. 3. Although the importance of a magnesium dysionemia for arrhythmogenesis has not been confirmed, magnesium can be used for the treatment of arrhythmias with good results. Besides an antiarrhythmic efficacy, an antifibrillatory activity is suggested in acute myocardial ischemia.
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PMID:[Ion regulation disorders and cardiac arrhythmia. The relevance of sodium, potassium, calcium, and magnesium]. 247 Mar 84

In the present study, 52 patients with cirrhosis, portal hypertension, and variceal hemorrhage underwent either an elective or an emergency side-to-side portacaval shunt operation. Vasopressin was infused intravenously at 60 units/hour from just prior to abdominal incision until completion of the anastomosis. Eight of 35 patients who received vasopressin alone (23 percent) tolerated increased doses of 75 to 90 units/hour to obtain hemostasis. Four of 52 patients required simultaneous infusion of sodium nitroprusside to correct systemic hypertension. An additional 15 percent reduction in portal venous pressure occurred in these patients. Eleven of 13 patients with vasopressin-induced myocardial ischemia responded to simultaneous infusion of nitroglycerin. Further prospective studies are indicated to adequately delineate the dose and duration of therapy with either nitroprusside or nitroglycerin for simultaneous administration with intravenous vasopressin.
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PMID:Simultaneous infusion of nitroglycerin and nitroprusside to offset adverse effects of vasopressin during portosystemic shunting. 249 34

Intravenous nitroglycerin lowers left ventricular filling pressure and systemic vascular resistance in patients with acute myocardial infarction. At lower infusion rates (less than 30 micrograms/min) nitroglycerin acts principally as a venodilator, while at higher infusion rates a balanced venous and arterial dilating effect is seen. Patients with left ventricular failure demonstrate increased or maintained stroke volumes, while patients without failure will show a decrease in stroke volume. All hemodynamic subgroups will show a reduction in left ventricular filling pressures and in electrocardiographic evidence of regional myocardial ischemia. Longer-term infusions (24-48 h) have been associated with a reduction in short-term mortality and evidence of myocardial preservation, as evidenced by improved left ventricular function or indices of infarct size. Studies comparing intravenous nitroglycerin and sodium nitroprusside have revealed increases in intercoronary collateral flow with nitroglycerin, in contrast to decreases with nitroprusside, suggesting a coronary steal with nitroprusside. Current clinical practice would recommend intravenous nitroglycerin as initial adjunctive therapy for patients receiving intravenous thrombolytic therapy and/or acute percutaneous transluminal angioplasty within 4-6 h of the onset of symptoms of acute myocardial infarction, with the goal of optimizing collateral flow until reperfusion can be accomplished. Patients treated later than 6 but less than 12-14 h after symptom onset should still receive intravenous nitroglycerin for 24-48 h with the hope of reducing infarct size. Likewise, congestive heart failure and arterial hypertension complicating acute infarctions as well as postinfarction unstable angina are additional current indications for the use of intravenous nitroglycerin in patients with acute myocardial infarction.
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PMID:Role of nitroglycerin in acute myocardial infarction. 250 Oct 31

The effects of glycerol trinitrate (GTN), sodium nitroprusside and isoket on central hemodynamics, myocardial contractility and myocardial function have been compared. 65 patients with ischemic heart disease have been examined. All the patients were divided into 3 groups depending on the drug studied. GTN was administered sublingually at a dose of 0.5 mg, while sodium nitroprusside and isoket were infused at doses of 1.5 micrograms (kg min) and 400 micrograms/min, respectively. It has been shown that GTN and isoket effects on central hemodynamics were mainly mediated by their venodilating action and preload reduction, thus promoting to the improvement of the myocardial function. Hemodynamic effects of sodium nitroprusside on the cardiovascular system are mediated by its dilating action on the arterial bed and afterload reduction.
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PMID:[Comparative assessment of the effect of nitroglycerin, sodium nitroprusside and isoket on hemodynamics in patients with ischemic heart disease]. 250 11

The efficacy of nicardipine and nitroprusside in preventing poststernotomy hypertension was compared in two groups of 45 patients undergoing coronary artery surgery. Patients were anesthetized with fentanyl, 100 micrograms/kg, and oxygen. Group N received nicardipine at an initial rate of 3 micrograms/kg/min. Group S received sodium nitroprusside at an initial rate of 1 microgram/kg/min. The vasodilators were started before surgery, and infusion rates were adjusted to maintain systolic blood pressure between 80% and 120% of postintubation (baseline) values. Additional measurements were obtained before incision and after sternotomy. In both groups, arterial blood pressure could be controlled effectively in all patients. In group S, pulmonary artery pressure (PAP) decreased before incision. At this time, systemic vascular resistance (SVR) decreased in both groups. After sternotomy, PAP returned to baseline values in group S. In both groups, heart rate, rate-pressure product, and cardiac index increased, while SVR remained decreased. In the period from induction of anesthesia to the start of cardiopulmonary bypass, the incidence of myocardial ischemia was greater (P less than 0.01) in group S (24%) than in group N (9%). Between the groups, the concentration of creatine phosphokinase MB was not significantly different in the first 24 hours postoperatively. In conclusion, it was shown that nicardipine may be a suitable alternative to nitroprusside for the prevention of poststernotomy hypertension and myocardial ischemia in patients undergoing coronary artery surgery.
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PMID:The efficacy of nicardipine and nitroprusside in preventing poststernotomy hypertension. 252 Oct 26


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