This study examined the hypothesis that descending inhibitory pathways from brain stem to spinal cord mediate the analgesic effect of both electrical brain stimulation and morphine. In the first set of experiments, the effect of subtotal midthoracic spinal cord lesions on the analgesic effect of electrical stimulation in the periaqueductal gray matter of the rat was examined. In the second, the effect of similar cord lesions on the analgesic effect of intraperitoneal morphine was studied. In both cases, a lesion of the dorsal part of the lateral funiculus (DLF) reduced or abolished the analgesia of the hindlimbs. Analgesia of the forelimbs was unaffected. Lesions of the dorsal columns, which include the corticospinal tract, or lesions of the ventral part of the lateral funiculus had no effect on analgesia. It is concluded that an inhibitory pathway, which descends in the dorsal part of the lateral funiculus and which probably originates in the nucleus raphe magnus of the medulla, mediates the descending control found in both morphine and stimulus-produced analgesia.

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The total weight of the normal adult human heart as well as that of each ventricle is proportional to body size. Body weight is superior to height as a predictor of total heart and isolated ventricular weights. Ventricular wall thickness is an insensitive means of assessing ventricular hypertrophy. Heart weight is a poor predictor of isolated right ventricular mass but a slightly better predictor of isolated left ventricular mass. The only method of determining the presence or absence of hypertrophy with confidence is to use the Fulton technique for isolated ventricular weights. The use of an arbitrary upper and lower limit, as currently used, for isolated ventricular weights obtained by Fulton's method may, however lead to errors in determining the presence or absence of ventricular hypertrophy.