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Serotonin, a naturally occurring vasoconstrictor of mesenteric blood vessels, inhibited by 80% the secretion of fluid into closed intestinal loops induced by cholera toxin. Isoproterenol, a vasodilator, stimulated secretion by 50%. These results indicate that the massive fluid production induced by cholera toxin can be modified by vasoactive agents.

In an attempt to elucidate the nature of the binding of PHA to lymphocytes, these cells were exposed to different enzymes before cultivation with PHA. The degree of stimulation was measured as 14C-thymidine incorporation into the acid insoluble fraction. It appears that certain enzymes, known to act on cell surfaces, suppress the PHA response while others leave it unchanged or even enhance the PHA effect. Trypsin and neuraminidase belong to the former group. Several hours after enzyme digestion lymphocytes are refractory to PHA treatment but gradually they recover their potential, implying that a regeneration of the surface has to occur before the PHA response can be initiated. Common monosaccharides had little or no effect on the PHA stimulation.

Human lymphocytes treated with neuraminidase (from Vibrio cholera) are more susceptible to lysis with antiserums directed against HL-A antigens in the cytotoxicity test than are the corresponding cells incubated in buffer. Enzymetreated cells are also lysed by antibodies other than those directed against HL-A, but control cells are not. The extra sensitivity to antibody disappears after 2 to 6 days in tissue culture.