Although somewhat less potent than 16:0-alkyl-PAF (1-O-hexadecyl2-acetyl-sn-glycero-3-phosphocholine), the acute cardiovascular alterations following the intravenous bolus administration of 18:0-alkyl-PAF include the development of transient right ventricular hypertension and sustained systemic hypotension. In the present study, the differential effects of indomethacin (5mg/kg) on the cardiovascular alterations induced by 16:0-and 18:0-alkyl-PAF in anesthetized, instrumented rabbits were examined. 16:0-alkyl-PAF (0.5 nmole/kgl 18:0-alkyl-PAF (1.0 nmole/kg) Control Indomethacin Control Indomethacin (n=7) (n=7) (n=11) (n=8) RVP 100±4 107±3 96±6 101±6 MAP 88±5 84±5 85±6 63±3* CO 87±4* 82±4 72±4 88±6* SVR 102±1 108±11 118±8 65 ±3* (Responses 10 min post-PAF were calculated as a percentage of pre-challenge and presented as the mean±SE; n=number of animals; RVP, right ventricular pressure; MAP, mean arterial pressure; CO, cardiac output; SVR, systemic vascular resistance; *=significantly different than 18:0-alkyl-PAF) Although the magnitude of RVP and MAP changes induced by various molecular species of PAF are comparable, the physiological basis for these alterations are dependent upon'individual molecular species of PAF and are differentiallv modulated bv oroducts of arachidonic acid metabolism.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology