Pre-clamp cardioprotection by protein kinase C (PKC) inhibitor improves left ventricular function following canine normothermic arrest.
J Cardiovasc Surg (Torino)
; 37(2): 141-3, 1996 Apr.
Article
em En
| MEDLINE
| ID: mdl-8675519
ABSTRACT
Since protein kinase C (PKC) has been proven to be a mediator of neutrophil activation and of intracellular calcium homeostasis, its inhibition could protect the myocardium from the deleterious effects of ischemic/reperfusion inury (IRI). The principal objective of this study was to evaluate the efficacy of the PK inhibitor SPC-100270 (2S,3S)-2-amino, 3-octadecanediol in a canine model of IRI. A double-blind study was conducted in which 19 coonhound dogs received either SPC-100270 or a vehicle before going on cardiopulmonary bypass (CPB). After 60 minutes of global normothermic (37 degree C) cardiac arrest (cross-clamp time 65-81 minutes for SPC-100270 and 65-72 minutes for control) and discontinuation of CBP, an epicardial short axis view echocardiogram was performed and reviewed by a double-blinded observer to determine the ejection fraction (EF). EF value exceeded 20% in 5 out of 9 SPC-100270 animals (27%-44%) and in 0 of 10 controls (0%-16%). These data show that SPC-10027 significantly (p=0.01 by Fisher's Exact Test) increased the probability that the animals would exhibit an EF greater than 20%.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Esfingosina
/
Proteína Quinase C
/
Traumatismo por Reperfusão Miocárdica
/
Função Ventricular Esquerda
/
Inibidores Enzimáticos
Tipo de estudo:
Diagnostic_studies
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
J Cardiovasc Surg (Torino)
Ano de publicação:
1996
Tipo de documento:
Article
País de afiliação:
Estados Unidos