Combined Effects of Buffer and Adrenergic Agents on Postresuscitation Myocardial Function

• Published in: The Journal of pharmacology and experimental therapeutics Vol. 291; no. 2; p. 773
• Main Authors: Sun, S, Weil, M H, Tang, W, Povoas, H P, Mason, E
• Format: Journal Article
• Language: English
• Published: United States American Society for Pharmacology and Experimental Therapeutics 01.11.1999
• Subjects: Adrenergic beta-Agonists - pharmacology; Animals; Blood Pressure - drug effects; Buffers; Coronary Vessels - drug effects; Drug Interactions; Electric Countershock; Epinephrine - pharmacology; Heart - drug effects; Hemodynamics - drug effects; Male; Propanolamines - pharmacology; Random Allocation; Rats; Rats, Sprague-Dawley; Resuscitation - adverse effects; Resuscitation - mortality; Sodium Bicarbonate - therapeutic use; Time Factors; Tromethamine - therapeutic use; Vascular Resistance - drug effects
• ISSN: 0022-3565; 1521-0103

Although buffer agents alone have failed to improve the success of resuscitation, we now examine the widely held concept that it is the combined effect of alkaline buffer and adrenergic agents that improves outcomes of cardiopulmonary resuscitation. In the present report, the effects of both CO 2 -consuming and CO 2 -generating buffer agents in combination with adrenergic vasopressor drugs were investigated. Ventricular fibrillation was electrically induced in Sprague-Dawley rats weighing between 450 and 550 g. Precordial compression and mechanical ventilation were initiated after 8 min of untreated ventricular fibrillation. Animals were then randomized to receive bolus injections of either inorganic sodium bicarbonate buffer, organic tromethamine buffer, or saline placebo. The β 1 adrenergic effects of epinephrine were blocked with esmolol. The vasopressor amine was injected 2 min after injection of the buffer agent. Electrical defibrillation was attempted at the end of 8 min of precordial compression. In 15 additional animals, the sequence of administration of the adrenergic vasopressor and buffer agents was reversed such that the adrenergic vasopressor was injected before the buffer agents. All animals were restored to spontaneous circulation. Both bicarbonate and tromethamine significantly decreased coronary perfusion pressure from 26 to 15 mm Hg and reduced the magnitude of the vasopressor effect of the adrenergic vasopressor. When the vasopressor preceded the buffer, declines in coronary perfusion pressure after administration of buffer agents were prevented. In each instance, however, greater impairment of postresuscitation myocardial function and decreased postresuscitation survival were observed after treatment with buffer agents.