| pubmed-article:7124058 | pubmed:abstractText | Reflex sympathetic nerve activation obscures the direct myocardial effect of Nifedipine after intravenous administration. Consequently, in 10 patients with coronary artery disease 0.1 mg of Nifedipine were injected into the left coronary artery to evaluate its specific effect on coronary sinus blood flow (CSF), coronary vascular resistance (CVR), and myocardial oxygen consumption (MVO2). One minute after Nifedipine, CSF increased from 115 +/- 15 to 193 +/- 47 ml/min (p less than 0.001), and CVR decreased from 0.92 +/- 0.16 to 0,54 +/- 0.12 mm Hg X min X ml-1 (p less than 0.001). Mean aortic pressure dropped from 107 +/- 5 to 99 +/- 3 mm Hg (p less than 0.01). MVO2 was reduced from 14.6 +/- 2.6 to 11.7 +/- 2.8 ml O2 X min-1 (p less than 0.05). After five minutes CSF (113 +/- 18) and MVO2 (14.9 +/- 3.1) had returned to their preinjection level. Additionally, CSF and MVO2 were measured during rapid atrial pacing (mean rate 118 +/- 6 min-1). Average CSF and MVO2 values were 172 +/- 63 and 19.8 +/- 5.0 before and 177 +/- 69 and 20.6 +/- 7.3 approximately 6 minutes after Nifedipine injection. Conclusions: Intracoronary Nifedipine results in coronary vasodilation and subsequently in an increase in coronary flow. The concomitant reduction in MVO2 provides evidence for an oxygen sparing, negative inotropic effect of Nifedipine, which, however, is of very limited duration. A sustained oxygen-saving effect during periods with increased oxygen demand could not be shown. | lld:pubmed |
