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)

Although silent ischemia may be linked to increases in cardiovascular morbidity and mortality, the long-term effects of a strategy aimed at the detection and treatment of this asymptomatic condition have not been fully explored. We therefore have developed the Atenolol Silent Ischemia Trial (ASIST), the first multicenter, randomized, prospective study of the prognostic implications of silent ischemia in asymptomatic and minimally symptomatic patients with coronary artery disease. Inclusion criteria for study patients were documented coronary artery disease, evidenced angiographically or by previous myocardial infarction, and transient ischemia, evidenced by abnormalities of regional wall motion, stress thallium-201, or exercise electrocardiogram. The main objective of ASIST is to assess the influence of frequency and duration of symptomatic and asymptomatic ischemic episodes on the occurrence of fatal and nonfatal cardiac events. Atenolol, a beta 1-selective adrenergic blocker, was chosen as the therapeutic intervention because of its potential benefits in treating both symptomatic and asymptomatic ischemia. Ambulatory electrocardiographic monitoring will be used to measure the frequency and duration of ischemic episodes during daily life. The predictive ability of short-term (4-week) effects on long-term (52-week) response to atenolol treatment is also being assessed, along with the economic impact of this diagnostic and therapeutic strategy. Given the current emphasis on reducing morbidity and mortality associated with coronary artery disease, ASIST results should shed light onto the long-term management and prognostic implications of this otherwise asymptomatic condition.
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PMID:The prognostic and economic implications of a strategy to detect and treat asymptomatic ischemia: the Atenolol Silent Ischemia Trial (ASIST) protocol. 181 Jun 81

The effects of regression of left ventricular hypertrophy following atenolol and bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats (SHR) were studied. Atenolol (50 mg/kg/day) and bunazosin (5 mg/kg/day) were administered to SHR from 19 to 26 weeks of age, whereas tap water was given to control SHR and normotensive Wistar-Kyoto rats (WKY). Both atenolol and bunazosin significantly decreased arterial blood pressure and significantly decelerated the increase in left ventricular weight in SHR. At the end of the long-term treatment, hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The pressure-rate product and the extent of recovery of the coronary flow after reperfusion following 30 min of ischemia in the bunazosin-treated SHR were significantly higher than those in the control SHR and the atenolol-treated SHR. The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were significantly lower than those in the reperfused WKY. Both atenolol and bunazosin improved the restoration of ATP and CrP in SHR after reperfusion following 30 min of ischemia. In conclusion, antihypertensive therapy with either atenolol or bunazosin was effective in preventing cardiac hypertrophy and ischemic damage caused by different mechanisms. Factors resulting from stimulation of the cardiac alpha 1 adrenoceptor may play an important role in the development of hypertensive cardiac hypertrophy, just as factors resulting from stimulation of the beta 1-adrenoceptor do.
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PMID:Effects of regression of left ventricular hypertrophy following atenolol or bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats. 183 20

Diffuse communications between the left coronary artery and the left ventricular cavity were found in a 54-years-old man presenting with angina pectoris and reversible ischemia documented on stress Thallium scintigraphy. During atrial pacing the patient experienced chest pain which was accompanied by lactate production. Atenolol, but not nifedipine, did ameliorate the symptoms. The anatomical types and the embriogenesis of coronary microfistulas along with possible mechanisms of ischemia are discussed.
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PMID:[Multiple coronary fistulas to the left ventricle. An unusual cause of myocardial ischemia]. 275 43

Coronary artery occlusion produces myocardial acidosis, which can be attenuated by propranolol or sotalol. The present study was undertaken to determine which beta adrenoceptors, beta-1 or beta-2, contribute to the ischemic myocardial acidosis. Dogs anesthetized with pentobarbital were used. In the first series of experiments, blood flow in the left anterior descending coronary artery was reduced by an occluder to about one-third of the original flow. Myocardial pH was measured by means of a micro pH electrode inserted into the left anterior descending coronary artery area at the depth of about 8 mm. The myocardial pH decreased from 7.44 to 7.55 to 6.73 to 6.89, 30 min after partial occlusion being the time immediately before an i.v. injection of drugs. Atenolol (1 mg/kg) attenuated significantly the decrease in myocardial pH that had been induced by partial occlusion, whereas IPS 339 (360 micrograms/kg) and ICI 118,551 (300 micrograms/kg) did not. The pH effect of atenolol was confirmed even in the paced heart. In the second series of experiments, the antagonistic action of these drugs on the isoproterenol-induced increase in heart rate and myocardial contractile force and the decrease in diastolic blood pressure was investigated. By this experiment, it was confirmed that atenolol has the beta-1 adrenoceptor antagonistic action, and the IPS 339 and ICI 118,551 have the beta-2 antagonistic action. These results suggest that the activation of beta-1 adrenoceptors contribute to the myocardial acidosis during ischemia.
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PMID:Attenuation by atenolol of myocardial acidosis during ischemia in dogs: contribution of beta-1 adrenoceptors to myocardial acidosis. 285 88

Glycerol 3-phosphate acyltransferase (GPAT) and Triglyceride lipase (TGL) were measured in homogenates from non-ischaemic and ischaemic tissue from the isolated perfused rat heart. Ischaemia was produced by occlusion of the left descending coronary artery for 10 min. Compared to activities measured in tissue from normally perfused hearts, GPAT activity measured in tissue from the ischaemic area was considerably reduced. TGL activity in the ischaemic area was markedly increased compared to activity measured in normally perfused hearts. No change was seen in GPAT or TGL activity measured in tissue from the non-ischaemic area. The change in activities produced by ischaemia were prevented by pre-perfusion with the cardio-selective beta-antagonist Atenolol. Reperfusion of the ischaemic area resulted in TGL activity returning to the value measured in tissue from normally perfused hearts. However, GPAT activity, after 1 min of reperfusion, fell to a value lower than after 10 min ischaemia. The reperfusion-induced fall in GPAT activity was prevented by pre-perfusion with the alpha 1 antagonist Doxasozin. Pre-perfusion of the alpha 2 antagonist Yohimbine resulted in a prolongation of the increased TGL activity in the ischaemic area during reperfusion. All changes in enzyme activities were prevented by injection of 6 OH-dopamine 24 h before hearts were removed. These changes in enzyme activities show that during ischaemia there is an increased beta-adrenergic drive. On reperfusion the beta-adrenergic drive is removed but an alpha 1 adrenergic drive becomes apparent.
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PMID:The effect of coronary artery occlusion and reperfusion on the activities of triglyceride lipase and glycerol 3-phosphate acyl transferase in the isolated perfused rat heart. 286 56

Once-daily atenolol and celiprolol were compared in a placebo-controlled crossover study of 16 patients with stable angina pectoris. Atenolol and celiprolol equally and significantly reduced frequency of angina and electrocardiographic evidence of cardiac ischemia. Celiprolol, however, produced less suppression of the double product at 1 mm of ST-segment depression than atenolol, suggesting that actions other than reduction of heart rate may contribute to its antianginal efficacy.
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PMID:Atenolol and celiprolol for stable angina pectoris. 289 33

The authors performed a long-term, double-blind, crossover, randomized study on the effects of two drugs (atenolol, 100 mg/day, or nifedipine, 10 mg t.i.d.) when administered alone or in combination on the exercise tolerance in 10 patients with stable angina on effort (mean age 52 +/- 4 years, 8 males and 2 females) and documented significant (greater than or equal to 70%) obstructive coronary lesions at angiography. None of the drug treatments improved exercise duration or maximal sustained work load. Atenolol decreased significantly ST segment depression to -1 +/- 0.8 from -1.91 +/- 0.7, baseline and -2.05 +/- 0.5, placebo. Nifedipine was not better than placebo. The atenolol plus nifedipine treatment was better than placebo (p less than 0.001) or nifedipine alone (p less than 0.05) but was not more significantly efficacious than atenolol alone. Long-term management of exertional angina can be usefully performed using atenolol. The use of nifedipine at the present dose of 10 mg, although well tolerated, did not improve the ST signs of ischemia.
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PMID:Atenolol and/or nifedipine in effort angina: which is the treatment of choice for exercise coronary protection? 319 3

Experiments were carried out on rats after coronary arterial ligation. In the myocardial infarction region there is the border zone or reversibly damaged zone which may be partially saved from necrosis by using beta-blocking agents. Atenolol, dibunol, Astragalus dasyanthus pall. moderately decrease the myocardial damage area at permanent and transient ischemia.
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PMID:[Effect of atenolol, dibunol, peroxidase and Astragalus dasynthus on the morphometric parameters of myocardial infarction]. 343 24

We examined the importance of decreased heart rate in the beneficial effect of beta-adrenergic blockade on exercise-induced regional myocardial ischemia and contractile dysfunction in conscious dogs with single vessel coronary stenosis (ameroid constrictor). Studies were performed during control treadmill exercise, which produced regional myocardial ischemia (blood flow measured with microspheres) and wall dysfunction (measured using sonomicrometers). A second run was performed after the administration of atenolol (0.3-1.0 mg/kg i.v.), and the reduced heart rate caused by atenolol during early steady-state running was then prevented by atrial pacing during the latter portion of the run. Atenolol reduced the exercise heart rate from 217 +/- 25 beats per minute (SD, n = 9) to 166 +/- 15, and ischemic zone wall thickening during systole improved from 27 +/- 22% of the resting value in the control run to 50 +/- 25% of the resting value in the atenolol run (p less than 0.01). Atrial pacing then increased heart rate to 217 +/- 23 beats per minute, and regional wall thickening deteriorated to 15 +/- 25% of the resting value. Regional subendocardial blood flow in the ischemic zone during atrial pacing with atenolol was slightly less than that observed in the control run, in both ischemic and control zones, indicating no remaining beneficial effect of atenolol when heart rate reduction was eliminated. We conclude that the only significant mechanism for the improvement in exercise-induced ischemia and wall motion produced by atenolol is a reduction in the exercise heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of beneficial effect of beta-adrenergic blockade on exercise-induced myocardial ischemia in conscious dogs. 359 48

We investigated the effects of Defibrotide (D), a natural polydeoxyribonucleotide, on acute myocardial ischemia (AMI) in anesthetized cats. A permanent ligature was placed around the left anterior descending coronary artery (LAD) 12-14 mm from its origin. Ventricular fibrillation and death were exceptional and when they occurred the cats were not included in the evaluation. Pretreatment of cats with D, 32 mg Kg-1 h-1, i.v. infusion, maintained throughout the 5 h occlusion period, reduced AMI-ST segment increases and increased the diminished pressure-rate index (PRI). AMI-induced changes in lactate, ATP and CPK in ischemic tissue were prevented by D. PGI2 gave the same results as D. Atenolol prevented the loss of myocardial CPK, but had no favourable effects on lactate and ATP in ischemic tissue. The beneficial effects of D in AMI reported here could be partly attributed to its ability to enhance PGI2 release from vascular walls; D might also relieve ischemia by improvement of local tissue oxygenation, energy supplies and platelet function by its ability to deaggregate platelet clumps.
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PMID:Cardioprotective effects of defibrotide in acute myocardial ischemia in the cat. 389 Feb 60


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