Human postmortem digital arteries obtained between 6 and 60 hours after death were used for in vitro studies of vascular smooth muscle physiology and pharmacology. Isometric tension was recorded from spiral strips in tissue baths at 37°C. The responses were durable and reproducible and were similar to those of 10 operative specimens of visceral arteries. The contractile force of the preparations was unrelated to the time elapsed since death. Norepinephrine, 5-hydroxytryptamine, and barium chloride gave the strongest responses; histamlne and potassium chloride were weaker agonists. Hie order of sensitivities to the agonists tested was angiotensin > 5hydroxytryptamine > norepinephrine > histamlne > barium chloride > potassium chloride. Both competitive (phentolamlne) and noncompetitive (phenoxybenzamlne) antagonism of DorepiDephrine was demonstrated. Pbentolamine was also a weak inhibitor of 5-hydroxytryptamine. Cyprobeptadine was a potent antagonist of 5-hydroxytryptamine, but had less effect against norepinephrine. This suggests the presence of separate receptors for 5hydroxytryptamine and norepinephrine in these vessels. The response to barium chloride was inhibited by the calcium-antagonist, verapamil. The o-adrenoceptor antagonist, phentolamlne, was not effective against barium chloride. We conclude that human postmortem digital arteries can be studied effectively in vitro. The preparation should be useful for the evaluation of drugs that are thought to act at a peripberal vascular site.
The proliferation of haemolytic plaque-forming cells in the spleen of preleukaemic AKR mice following primary immunization with sheep red cells was slightly delayed and the peak response was not as high as in normal mice. In leukaemic A K R mice, although there were normal numbers of background plaque-forming cells in the spleens of unimmunized animals, these cells failed to proliferate following antigenic stimulation and no detectable haemolysin antibody response occurred before the seventh day f o Ilo wing immunization.Haemagglutinin responses were normal in preleukaemic A K R mice but were depressed severely in mice with thymic lymphomata or generalized lymphoid leukaemia.The present results do not support the concept that severe immunological deficiencies are a necessary prerequisite of the preleukaemic state.
Chloramphenicol in the newborn infant. A physiological explanation of its toxicity when given in excessive dose. New Engl. J. Med., 262, 787-794. system do not change with increasing age.
The contractile responses of spiral strips of human digital arteries to samples of a suspension of human platelets aggregated by thrombin have been studied at different time intervals after aggregation. Platelets added to the arterial strips 1 min after aggregation of the platelets produced contractile responses which were significantly greater than those produced by corresponding platelets added 20 min after aggregation. When platelets were aggregated in the presence of indomethacin or the thromboxane synthetase antagonist 1-benzylimidazole, contractile responses produced by the platelets 1 min after aggregation were significantly reduced. They were then not significantly different from those produced by addition of the aliquots 20 min after aggregation, which were unaffected. Pretreatment of the arteries with the serotonin antagonist ketanserin nearly abolished the contractile responses produced by addition of the platelets 20 min after aggregation, and significantly reduced those produced by addition of the platelets 1 min after aggregation. Ketanserin did not affect the contractile responses of the arteries to potassium chloride, prostaglandin F2 alpha, or the endoperoxide analogue U-46619, but antagonized the contractile effects of exogenous serotonin. Combination of pretreatment of the arteries with ketanserin and aggregation of the platelets in indomethacin or 1-benzylimidazole virtually abolished contractile responses to platelets added both 1 min and 20 min after aggregation. Tensions developed to different dilutions of platelets added 1 min after aggregation to arteries pretreated with ketanserin were not significantly different from those obtained to the same dilutions added 20 min after aggregation to arteries not pretreated with ketanserin.(ABSTRACT TRUNCATED AT 250 WORDS)
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