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The leukemic phase of mantle cell lymphoma (mantle cell leukemia) is defined as an absolute lymphocyte count of greater than 4,000/microliter and characterized by the presence of relatively small, slightly irregular lymphocytes in the peripheral blood. Although a variant of mantle cell lymphoma with blastic morphsology exists and has been previously well described, a blastic morphologic variant of mantle cell leukemia has not been described. We report such a case in a 74-year-old male who presented with splenic rupture and an elevated white blood cell (WBC) count. The diagnosis was based on flow cytometric immunophenotyping and the cytomorphology of the peripheral blood.

Intravenous administration of nicotinic acid to the anesthetized dog prior to thermal trauma reduced plasma loss at 10 minutes after burn from 7 milliliters per kilogram to less than 2 millimeters per kilogram. During the next 50 minutes plasma loss was the same in treated and untreated animals. An additional dose of nicotinic acid 30 minutes after burn prevented this further loss.

By means of direct arterial perfusion of the adrenal glands in the dog it has been shown that synthetic lysine vasopressin stimulates the secretion of hydrocortisone. This effect is not mediated via the adenohypophysis or any other organ but is rather the result of direct stimulation of the adrenal cortex by vasopressin itself.

The effects of block of autonomic ganglia by chlorisondamine and by hexamethonium, the administration of neostigmine and of atropine upon blood pressure, nervous transmission through the superior cervical ganglion, stimulation of autonomic ganglia by dimethylphenylpiperazinium, and the carotid occlusion reflex, have been studied in the dog anaesthetized with sodium pentobarbitone. The results of these studies have shown: (1) A ganglion blocking agent blocks synaptic transmission in the superior cervical ganglion at the same time as it lowers blood pressure. Neostigmine administered after ganglion-block raises the blood pressure without much change in the response to stimulation of the preganglionic cervical sympathetic nerve. (2) If the effects of preganglionic nerve stimulation are recorded as a contraction of the nictitating membrane, a ganglion-blocking agent also abolishes this response at the same time as it blocks the reflex rise in blood pressure produced by occlusion of both common carotid arteries. Neostigmine administered under these conditions does not affect the responses of the nictitating membrane, but restores the carotid occlusion reflex. This restoration of reflex activity is sensitive to atropine, as is the blood pressure rise. (3) At the same time that neostigmine restores the carotid occlusion reflex, there is no restoration of sensitivity of autonomic ganglia to chemical stimulation by dimethylphenylpiperazinium. In these animals atropine not only blocked the restored carotid occlusion reflex, but produced a further inhibition of the pressor response to dimethylphenylpiperazinium. It is concluded that neostigmine may raise blood pressure by partially restoring autonomic ganglionic transmission, but that total ganglionic function is not restored.