REDUCTION OF ISCHEMIC MYOCARDIAL DAMAGE IN DOG BY LIDOCAINE INFUSION

  • 1 January 1977
    • journal article
    • research article
    • Vol. 87  (2) , 399-+
Abstract
The effects of lidocaine infusion on the ultrastructural damage induced in cardiac muscle by normothermic cardiopulmonary bypass were assessed in 15 dogs. Six dogs received no medication other than sodium pentobarbital (25 mg/kg, i.v.) while 9 dogs were treated with lidocaine after anesthesia. Lidocaine was given as a 2-mg/kg loading dose 10 min prior to ischemic arrest and a 2 mg/min continuous infusion during the entire experimental period. Biopsy samples of the left ventricular apex were taken 15 and 45 min after the start of ischemic arrest and 5 min after resumption of coronary blood flow. Biopsy samples were also obtained from 4 animals after thoracotomy to serve as controls for experimental procedures. Myocardial ultrastructure in the 4 control animals was comparable to previous reports. Five of 6 of the nontreated dogs and 8 of 9 lidocaine-treated dogs survived the entire period of ischemia and 5 min of coronary reperfusion. The extent of ultrastructural damage varied considerably between the 2 groups. In the experimental dogs receiving no lidocaine, mitochondria were swollen, cristae were absent, the mitochondrial matrix was cleared and sarcomeres were disrupted. Myelin figures and contraction bands were also observed. None of the surviving lidocaine-treated animals had ultrastructural changes comparable to the worst ones in nontreated dogs. Damage was limited to some swelling of mitochondria with focal clearing of matrix. Most cristae remained intact. There were no myelin figures and few contraction bands. Lidocaine possibly protects the integrity of ischemic myocardium and this protection possibly resulted from stabilization of plasma and/or mitochondrial membranes.