Figure 3.

A, Representative control and S+U provoked angiograms are shown at smallest recorded diameters in a P-treated monkey compared with a placebo-treated ovx control. Each angiogram is from 3 minutes after the second S+U injection. The vasospasm that occurred in the placebo ovx is typical of the ovx group. There was prolonged (for >5 minutes) vasoconstriction in 5 of 5 placebo monkeys. In contrast, 7 of 7 DP9-treated monkeys were protected (no vasospasm or sustained vasoconstriction to <33% of control diameter occurred at any point in the protocol). B, Angio-graphically measured minimum diameters (φ) as a percent of control diameter (recorded before vasospasm challenge) in response to intracoronary injections over 30 seconds of the provocative stimulus (S+U successive injections) are shown as means ± SE. The provoking constrictor stimulus of S+U [100 μmol/L serotonin + 1 μmol/L U46619 (syringe concentration)] is estimated to be diluted 15 times by coronary blood flow, ie, to 6.7 μmol/L serotonin + 67 nM U46619, that would appear in the epicardial coronary arteries. Vasospasm-like constrictions were considered to be a reduction to <33% of control diameter for >5 minutes. The average minimum φ in placebo ovx (25.47% ± 9.58%) met the criterion of reduction to <33% of control diameter and are indicative of hyperreactivity and vasospasm-like constrictions that occurred in 5 of 5 ovx monkeys. In contrast, the average minimum φ in P-treated monkeys (60.08% ± 5.62%) are indicative of protection against hyperreactivity in all 7 P-treated monkeys. *Significant differences from placebo (P<0.05).