Circulation
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Little is known regarding specific biologic and pharmacologic differences between human internal mammary arteries and saphenous veins. To better define the role of alpha-adrenoceptor-mediated vasoconstriction in human internal mammary arteries and saphenous veins, we obtained fresh specimens of both vessels from 32 patients undergoing coronary artery bypass surgery. Dose-response curves were generated for the relatively selective alpha 1-receptor agonist phenylephrine, the alpha 2-receptor agonist BHT-920, and the alpha 1- and alpha 2-receptor agonist norepinephrine. ⋯ Dose-response curves for phenylephrine and BHT-920 were shifted to the right for both vessels in the presence of the alpha 1-receptor antagonist prazosin and the alpha 2-receptor antagonist yohimbine, respectively. Norepinephrine elicited contraction at a lower concentration in saphenous veins than in internal mammary arteries with a mean EC50 of 7.8 X 10(-8) M for saphenous veins and a mean EC50 of 3.4 X 10(-7) M for internal mammary arteries (p less than 0.05). The results suggest that alpha-adrenoceptor-mediated vasoconstriction is caused primarily by alpha 1-receptors in human internal mammary arteries and by alpha 1- and alpha 2-receptors in human saphenous veins.
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Comparative Study
Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine.
Pure alpha-adrenergic agonists, such as phenylephrine, and mixed alpha- and beta-adrenergic agonists, such as epinephrine, raise perfusion pressure for heart and brain during cardiopulmonary resuscitation (CPR). However, with the high doses used during CPR, these drugs may directly affect vascular smooth muscle and metabolism in brain and heart. We determined whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 micrograms/kg/min) or epinephrine (4 micrograms/kg/min) leads to equal organ blood flow, cerebral O2 uptake, and cerebral electrophysiologic function. ⋯ During CPR and at 2 hours after resuscitation, there were no differences between drug groups in the level of regional cerebral or coronary blood flow, cerebral O2 uptake, or evoked potentials. Therefore, with minimal delay in the onset of CPR and with equipotent pressor doses of phenylephrine and epinephrine, we found no evidence that one agent provides superior coronary or cerebral blood flow or that epinephrine by virtue of its beta-adrenergic properties adversely stimulates cerebral metabolism at a critical time that would impair brain electrophysiologic function. Moreover, epinephrine did not preferentially impair subendocardial blood flow as might be expected if it enhanced the strength of fibrillatory contractions.
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Multicenter Study Comparative Study Clinical Trial
ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction.
Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. ⋯ In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.
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Modest survival benefits have been reported in patients with acute myocardial infarction complicated by cardiogenic shock who were treated with early surgical revascularization or thrombolytic therapy. To determine whether coronary angioplasty improves survival, 87 patients with cardiogenic shock complicating acute myocardial infarction at the University of Michigan, Ann Arbor, Michigan, from 1975 to 1985 were retrospectively analyzed. Patients in group 1 (n = 59) were treated with conventional therapy; patients in group 2 (n = 24) were treated with conventional therapy and angioplasty. ⋯ The 30-day survival was significantly improved for group 2 patients (50% vs. 17%, p = 0.006). Survival in group 2 patients with successful angioplasty was 77% (10 of 13 patients) versus 18% (two of 11 patients) in patients with unsuccessful angioplasty, (p = 0.006). The findings suggest that angioplasty improves survival in cardiogenic shock compared with conventional therapy with survival contingent upon successful reperfusion of the infarct-related artery.