The effect of extracorporeal photopheresis (EP) on various cytogenetic parameters has been investigated. During EP the photoactivatable agent 8-methoxypsoralen (8-MOP) was administered orally. After 2 h a leukocyte-enriched blood fraction was collected by haemocentrifugation, irradiated with UVA extracorporeally, and reinfused to the patient. Two patients suffering from cutaneous T-cell lymphoma showed a marked clinical improvement in response to therapy. In order to investigate the cytogenetic effects and mutagenic risk of EP, the mitotic index (MI), the type and number of chromosomal aberrations and the rate of sister chromatid exchanges (SCE) were studied. Following EP treatment the patients' lymphocytes were cultured and stimulated with phytohaemagglutinin (PHA) for 48 or 72 h. The cultured lymphocytes showed a decreased MI after 48 h as an indicator of cytotoxic effects, but not after 72 h. In lymphocyte cultures not stimulated with PHA, the MI was decreased even after 72 h. The number of chromosomal aberrations and SCE were increased upon treatment, but only transiently, returning to basal levels between consecutive treatments. Our data provides no evidence for increased mutagenic risk as a consequence of effective EP treatment.
The cardiovascular effects of the H2-receptor-antagonists cimetidine and ranitidine have been compared in a randomized double-blind crossover study. The experiments were performed in seven anesthetized mongrel dogs. Cimetidine (200 mg) and ranitidine (50 mg) were infused i.v. for 2 min. The time interval between cimetidine and ranitidine application was always 3 h. The direct comparison of the drug effects on blood pressure shows a significant difference between cimetidine and ranitidine (P less than 0.001). Apart from the sequence of application, cimetidine causes a significant decrease (P less than 0.01) in total peripheral resistance (-271 +/- 50 dyn . s . cm-5) resulting in a decrease in mean blood pressure (-9 +/- 1.1 mmHg). In contrast to cimetidine, none of the recorded parameters are altered significantly by ranitidine. Heart rate, left ventricular end-diastolic pressure, myocardial contractility (dP/dtmaxLV), mean right atrial pressure, mean pulmonary artery pressure, and cardiac output are not affected significantly by either drug. Due to our results it might be concluded that the cimetidine-induced hypotension is mediated by peripheral vasodilation.
Possible in vivo interactions of serotonin and noradrenaline were investigated in 7 anesthetized mongrel dogs. The hemodynamic effects of three different doses of serotonin (10, 50 and 100 μg/kg/min) were analyzed with and without noradrenaline treatment (0.05–0.1 μg/kg/min). There were no significant differences in peripheral and cardiac responses between the pure serotonin effect and the hemodynamic effects of a parallel serotonin-noradrenaline infusion. The discussed amplifying effect of serotonin on the adrenergic system could not be observed in the total canine cardiovascular system.
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