Myocardial hypoxia is thought to be an important stimulus for increasing interstitial adenosine concentration. The adenosine hypothesis of coronary control was investigated during steady-state hypoxia by making measurements of coronary venous and epicardial well adenosine concentrations in adrenergically intact dogs and in animals with cr-and (-receptor Materials and Methods General PreparationTwenty-four mongrel dogs (25-36 kg) of either sex were studied. Dogs were sedated with morphine sulfate (2.5 mg/kg s.c.) and anesthetized with a-chloralose (100 mg/kg i.v.). An adequate level of anesthesia was maintained by 500-mg supplements of a-chloralose as needed. Metabolic acidosis secondary to a-chloralose anesthesia was corrected by intravenous infusion of 1.5% sodium bicarbonate solution.The dogs were intubated and mechanically ventilated with a positive-pressure respirator (model 607, Harvard Apparatus, South Natick, Mass.) with end-expiratory pressure between 0 and 5 cm H20. End-expiratory CO2 was measured (model LB-2, Beckman Instruments, Fullerton, Calif.) and held between 4.5% and 5

Background-Sodium nitroprusside is one of several agents considered effective for treating the no-reflow phenomenon during acute coronary interventions. However, the coronary hyperemic dose responses and systemic hemodynamic effects of intracoronary nitroprusside have yet to be determined in humans. The purpose of this study was to compare the hyperemic and hemodynamic responses of intracoronary nitroprusside to intracoronary adenosine in patients during cardiac catheterization with angiographically normal anterior descending arteries. Methods and Results-In 21 patients, coronary blood flow velocity (0.014-inch Doppler flow wire), heart rate, and blood pressure were measured in unobstructed left anterior descending coronary arteries at rest, after intracoronary adenosine (30-to 50-g boluses), and after 3 serial doses (0.3-, 0.6-, and 0.9-g/kg boluses) of intracoronary nitroprusside. Coronary reserve was calculated as hyperemia/basal coronary flow velocity. In an additional 9 patients with intermediate stenoses (53Ϯ7%), 14 fractional flow reserve (FFR) measurements (using 0.014-inch pressure wire) were performed with both intracoronary adenosine and nitroprusside (0.6 g/kg). Intracoronary nitroprusside produced equivalent coronary hyperemia with a longer duration (Ϸ25%) compared with intracoronary adenosine. Intracoronary nitroprusside (0.9 g/kg) decreased systolic blood pressure by Ͻ20%, with minimal change in heart rate, whereas intracoronary adenosine had no effect on these parameters. FFR measurements with intracoronary nitroprusside were identical to those obtained with intracoronary adenosine (rϭ0.97). Conclusions-Compared with adenosine, intracoronary nitroprusside produces an equivalent but more prolonged coronary hyperemic response in normal coronary arteries. Intracoronary nitroprusside, in doses commonly used for the treatment of the no-reflow phenomenon, can produce sustained coronary hyperemia without detrimental systemic hemodynamics. On the basis of FFR measurements compared with adenosine, sodium nitroprusside also appears to be a suitable hyperemic stimulus for coronary physiological measurements.

Myocardial perfusion reserve derived by real-time infusion MBV measurements correlates with Doppler flow wire-derived CFR. Therefore, MPR may be a potential surrogate for Doppler flow wire-derived CFR in patients with angiographically normal coronary arteries.

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The adjunctive use of atropine in HTX patients during DSE aids in reaching 85% of maximum predicted HR in some patients. Furthermore, resting HR may predict the additional need of atropine during DSE.