Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of dezocine, an agonist-antagonist opioid analgesic, on enflurane MAC (EMAC) was measured in dogs and, in a separate study, the hemodynamic effects of IV bolus doses of dezocine in the presence of a stable end-tidal enflurane concentration were measured. Study 1 (n = 8)--EMAC Reduction: Dezocine reduced EMAC in a dose-dependent fashion by a maximum of 58 +/- 3% (mean +/- SEM) after injection of 20 mg/kg. Cardiac toxicity prevented administration of higher doses. Study 2--Hemodynamics: Group 1 (n = 7) received dezocine 0.2, 1.5, 5, and 20 mg/kg IV each as a bolus over 30 sec. Group 2 (n = 5) was studied in exactly the same manner except that instead of dezocine, each dog received drug carrier solution alone (carrier). Significant hemodynamic differences between carrier and drug groups were observed only at the 20 mg/kg dose level, which produced death in one dog and a decrease in mean aortic pressure to 39 +/- 5% of baseline, in cardiac output to 60 +/- 9% of baseline, and in stroke volume to 69 +/- 9% of baseline in the remaining dogs. It is concluded that dezocine produces a dose-dependent reduction in EMAC limited by cardiovascular toxicity. This toxicity appears to be related to direct myocardial depression by high doses of dezocine in the presence of enflurane.
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PMID:Dezocine-MAC reduction and evidence for myocardial depression in the presence of enflurane. 366 62

The hemodynamic and respiratory effects of dezocine and ciramadol, two agonist-antagonist analgesics, were compared with those of morphine in 30 patients undergoing diagnostic cardiac catheterization. Each subject received a single intravenous dose of dezocine (0.125 mg/kg), ciramadol (0.6 mg/kg), or morphine (0.125 mg/kg) in a double-blind fashion. Hemodynamic and respiratory parameters were measured at baseline and 5, 10, and 20 minutes after dosing. Dezocine increased the cardiac index (CI; 2.67 to 2.92 L/min/m2), stroke volume index (SVI; 43.6 to 47.6 ml/beat/m2), left ventricular stroke work index (LVSWI; 57.4 to 64.7 gm-m/m2), and pulmonary vascular resistance (PVR; 105.6 to 154.0 dynes X sec/cm5). Ciramadol increased the CI (2.78 to 3.22 L/min/m2), SVI (40.9 to 48.2 ml/beat/m2), LVSWI (51.1 to 57.9 gm-m/m2), and mean pulmonary arterial pressure (PA; 14.7 to 18.9 mm Hg). Morphine had no effect on CI, SVI, LVSWI, PA, or PVR, but it significantly lowered systolic and diastolic blood pressures. There were no appreciable changes in heart rate, left ventricular end-diastolic pressure, mean arterial pressure, or mean pulmonary capillary wedge pressure after any of the drugs. All three drugs significantly decreased systemic vascular resistance. There were no clinically significant changes in respiratory parameters. We conclude that dezocine, ciramadol, and morphine have no clinically important adverse effects on cardiac performance.
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PMID:Hemodynamic and respiratory effects of dezocine, ciramadol, and morphine. 383 74