Acute effects of adrenergic agents on post-defibrillation arrest time in a cultured heart model

Abstract

Possible drug interactions with electrical defibrillation were examined. We tested the hypothesis that adrenergic agents (epinephrine, norepinephrine, isoproterenol) and a calcium channel blocker (verapamil), when applied acutely, alter the duration of arrest following a defibrillator shock. A secondary hypothesis (based on observations) was that the drugs alter the occurrence of changes to normal rhythms following the shock. Dissociated heart cells from 10-day chicken embryos were cultured to form spherical aggregates and plated in petri dishes. In the experiments, the spheres were paced at 0.75 V/cm above contraction threshold, and a biphasic defibrillator shock was applied for 1 ms at 46 V/cm. The arrest time and occurrence of rhythm changes were recorded. The adrenergic agents shortened the duration of arrest following a defibrillator shock, while the calcium channel blocker lengthened the arrest time. Comparisons with the control proportion of double beats showed no significant change with the adrenergic agents and a decrease with verapamil.

Acute effects of nonexcitatory electrical stimulation during systole in isolated cardiac myocytes and perfused heart

“…In order to asses CCM therapy in various patient populations and its potential interactions with other therapies (e.g., pharmaceuticals (Krauthamer and Smith )), it is important to know how the electrical fields corresponding to CCM affect myocyte dynamics, particularly regarding inotopicity as regulated by [Ca 2+ ] i . For example, if CCM increases myocyte force development, the cellular effect could enhance sympathetic effects; however, if CCM decreases myocyte force development, the overall effect of CCM may be suboptimal and could be altered to minimize the deleterious cellular behavior.…”

Mecanismos envolvidos na depressão contratil e lesão de miocitos cardiacos submetidos a campos eletricos de alta intensidade

“…O aumento do coeficiente de Hill indica que o efeito protetor do ISO foi restrito a campos de menor intensidade (50-80 V/cm), mas não se manifestou para valores mais altos de E, para os quais a letalidade foi semelhante àquela em células controles (80-130 V/cm). Krauthamer & Smith, (2004) relataram que a estimulação de adrenoceptores β encurta o período de inatividade elétrica (atribuído à eletroporação) após choque do tipo desfibrilatório em cultura de células cardíacas. Estes resultados são consistentes com os nossos, já que sugerem menor grau de eletroporação (e/ou reparo mais eficiente) em resposta a choques de uma dada amplitude.…”