Genetic deletion of NOS3 increases lethal cardiac dysfunction following mouse cardiac arrest.

ABSTRACT:

Study aims

Cardiac arrest mortality is significantly affected by failure to obtain return of spontaneous circulation (ROSC) despite cardiopulmonary resuscitation (CPR). Severe myocardial dysfunction and cardiovascular collapse further affects mortality within hours of initial ROSC. Recent work suggests that enhancement of nitric oxide (NO) signaling within minutes of CPR can improve myocardial function and survival. We studied the role of NO signaling on cardiovascular outcomes following cardiac arrest and resuscitation using endothelial NO synthase knockout (NOS3(-/-)) mice.

Methods

Adult female wild-type (WT) and NOS3(-/-) mice were anesthetized, intubated, and instrumented with left-ventricular pressure-volume catheters. Cardiac arrest was induced with intravenous potassi

SUBMITTER: Beiser DG 

PROVIDER: S-EPMC3018673 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature