On the nature of protection by propranolol against myocardial necrosis after temporary coronary occlusion in dogs

Reimer, Keith A.; Rasmussen, Margaret M.; Jennings, Robert B.

doi:10.1016/0002-9149(76)90391-x

Cited by 92 publications

(37 citation statements)

References 17 publications

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“…Experimental data have strongly suggested that intravenous ␤-blocker administration can decrease infarct size if an adequate amount of ␤-blocker can be delivered to the ischemic zone before irreversible damage. 7,9,10 The largest amount of myocardial salvage occurs if the ␤-blocker is given before coronary occlusion, although animal data have demonstrated some degree of myocardial salvage when intravenous ␤-blocker is given as long as 3 to 4 hours after coronary occlusion. 10,15 Furthermore, studies using transient occlusion followed by reperfusion tend to show more myocardial salvage than preparations with permanent occlusion.…”

Section: Discussionmentioning

confidence: 99%

“…6 Experimental studies have shown that intravenous administration of the ␤-blocker propranolol before coronary artery occlusion can significantly reduce the electrocardiographic, enzymatic, and histological indices of myocardial infarction (MI). [7][8][9][10] Clinical PCI studies have shown that intracoronary (IC) propranolol delays the development of ischemia during balloon occlusion as determined by the time to and extent of ST-segment elevation on IC and surface ECGs. 11,12 Currently, there are no data evaluating the impact of adjunctive IC ␤-blocker therapy before PCI on postprocedural MI, as reflected by biochemical marker release, and on clinical…”

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confidence: 99%

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Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary β-Blocker

et al. 2003

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Background-Experimental studies have demonstrated that intravenous ␤-blocker administration before coronary artery occlusion significantly reduces myocardial injury. Clinical studies have shown that intracoronary (IC) propranolol administration before percutaneous coronary intervention (PCI) delays myocardial ischemia. The present study tested the hypothesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardial infarction (MI) and short-term adverse outcomes after PCI. Methods and Results-Patients undergoing PCI (nϭ150) were randomly assigned in a double-blind fashion to receive IC propranolol (nϭ75) or placebo (nϭ75). Study drug was delivered before first balloon inflation via an intracoronary catheter with the tip distal to the coronary lesion. Biochemical markers were evaluated through the first 24 hours and clinical outcomes to 30 days. Evidence of MI with creatine kinase-MB elevation after PCI was seen in 36% of placebo and 17% of propranolol patients (Pϭ0.01). Troponin T elevation was seen in 33% of placebo and 13% of propranolol patients (Pϭ0.005). At 30 days, the composite end point of death, postprocedural MI, non-Q-wave MI after PCI hospitalization, or urgent target-lesion revascularization occurred in 40% of placebo versus 18% of propranolol patients (hazard ratio 2.14, 95% CI 1.24 to 3.71, Pϭ0.004). Conclusions-IC

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary β-Blocker

et al. 2003

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“…Propranolol has been shown to exert a beneficial effect on myocardial ischemia both in experimental animals and in man (2,7,9,19,(33)(34)(35)(36)(37). Although most ofthese studies are based on indirect methods for measuring ischemic injury, in others the salutary effects of propranolol have been based on morphologic observations (34,35,37).…”

Section: Changes In Pmco2 and 127xenon Washout In Ischemic Tissuementioning

confidence: 99%

Assessment of the Efficacy of Interventions to Limit Ischemic Injury by Direct Measurement of Intramural Carbon Dioxide Tension after Coronary Artery Occlusion in the Dog

Hillis¹,

Khuri²,

Braunwald³

et al. 1979

J. Clin. Invest.

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A B S T R A C T Although nuimerous interveintions have been shown to exert a salutary effect on the ischemic inyocardium, the severity of ischemia generally has been measured by indirect techniques. In the present investigation the effect of ischemia on intramural carbon dioxide tension (PmCO2) was measured directly in the open-chest, anesthetized dog with a mass spectrometer during repetitive 10-min coronary artery occlusions separated by 45-min periods of reflow; simultaneously, regional myocardial blood flow in the ischemic area was measured by "27Xenon washout. In all dogs the increase in PmCO2 from before to 10 min after the first occlusion (APmCO2) exceeded that during subse(luent occlusions. In those dogs not receiving an intervention (controls), APmCO2 during the third occlusion was similar to that during the second occlusion. When propranolol, hyaluronidase, and nitroglycerin were administered to different groups of dogs before the third occlusion, each caused significantly smaller elevations in APmCO2 than those occurring during the control second occlusion, and the comnbination of all three interventions induced the smallest increase in APmCO2. Regional myocardial blood flow rose with hyaluronidase and was unchanged with propranolol,

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“…Though propranolol has not been found to prevent the ventricular fibrillation that often occurs in dogs at the onset of reperfusion (Sommers & Jennings, 1972), this agent reduced the amount of necrosis that develops in the dog heart after 40 min of temporary coronary occlusion (Reimer, Rausmussen & Jennings, 1973). This protective effect of propranolol was related to ,B-adrenoceptor blockade (Reimer, Rasmussen & Jennings, 1976).…”

Section: Introductionmentioning

confidence: 87%

Cardiovascular Effects of Acebutolol Following Coronary Artery Occlusion and Reperfusion in Anaesthetized Dog

Chernecki

Das

Dhalla

et al. 1978

British J Pharmacology

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The effects of 5 mg/kg acebutolol given intravenously were investigated in anaesthetized dogs after (a) ligation of the left anterior descending coronary artery and (b) coronary reperfusion following 60 min of ligation of the left anterior descending coronary artery. Coronary artery ligation produced, after 4 to 6 h, persistent multiple ventricular ectopic beats and abnormalities of R and T waves and of the S‐T segment. Administration of acebutolol, after the development of persistent ventricular arrhythmias, restored normal sinus rhythm within 5 min of injection. Electrocardiographic abnormalities were also reduced. Coronary artery reperfusion (following 60 min of ligation) resulted in multiple ventricular ectopic beats, ventricular tachycardia and/or ventricular fibrillation. Pretreatment with acebutolol, 15 min before starting reperfusion, markedly reduced the arrhythmias. Acebutolol did not affect peak inspiratory airway pressure. Acebutolol produced significant bradycardia and slight, transient, hypotension. It was without effect on left ventricular systolic pressure, left ventricular end‐diastolic pressure, cardiac output or pulmonary arterial pressure. These results suggest beneficial effects of acebutolol in myocardial ischaemia and coronary reperfusion, without any significant risk of cardiodepression or bronchospasm.

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On the nature of protection by propranolol against myocardial necrosis after temporary coronary occlusion in dogs

Cited by 92 publications

References 17 publications

Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary β-Blocker

Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary β-Blocker

Assessment of the Efficacy of Interventions to Limit Ischemic Injury by Direct Measurement of Intramural Carbon Dioxide Tension after Coronary Artery Occlusion in the Dog

Cardiovascular Effects of Acebutolol Following Coronary Artery Occlusion and Reperfusion in Anaesthetized Dog

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