Inverted Meckel's diverticulum.

Although Meckel's diverticulum is a relatively common anomaly, inverted Meckel's diverticulum has been reported rarely. We describe a 59-year-old woman with inverted Meckel's diverticulum located at the distal ileum simulating a benign tumor. Computed tomography showed a small mass with a central area of low fat density, and appearance not described previously.

The effects of cholinergic agents on morphine-induced circling behavior in the intact mouse.

The effects of morphine on locomotor activity in mice was studied. It was shown that morphine in this species induces circling, a dose-dependent, stereotyped behavior. At high doses of morphine, mice engaged virtually exclusively in circling uninterrupted by other activities. The effect was modified by muscarinic agents. Blockade of muscarinic receptors with atropine potentiated circling while the muscarinic agonist, oxotremorine, attenuated it. The mixed muscarinic/nicotinic cholinergic agonist, physostigmine, had no effect on this behavior.

Motor innervation of the smooth muscle of the rat seminal vesicle.

Frequency-related isovolumetric contractions of the rat seminal vesicle elicited with transmural electrical stimulation were blocked by tetrodotoxin but unaffected by hexamethonium. The postganglionic motor innervation of the rat seminal vesicle is purely excitatory and contains both an adrenergic and a cholinergic component which are excited simultaneously during transmural stimulation. Contractions elicited by adrenergic nerve stimulation were mediated by norepinephrine acting via alpha adrenoceptors, i.e., 1) responses of untreated vesicles to transmural stimulation and to exogenous norepinephrine were antagonized by phentolamine and potentiated by cocaine, 2) pretreatment of animals with reserpine or 6-hydroxydopamine produced a marked depletion of tissue norepinephrine concentration and reduced the responses to transmural stimulation to a level which resembled that of untreated organs in the presence of phentolamine, 3) the residual responses of vesicles from pretreated rats were not modified by phentolamine or cocaine, and 4) responses to tyramine in untreated organs were antagonized by phentolamine but not by cocaine and were observed in organs from reserpine-pretreated rats only after repletion with exogenous norepinephrine. Responses elicited by cholinergic nerve stimulation were mediated by acetylcholine through muscarinic receptors, i.e., 1) responses of untreated vesicles to transmural stimulation and to exogenous acetylcholine were antagonized by atropine, 2) the residual responses to transmural stimulation of vesicles from animals pretreated with reserpine of 6-hydroxydopamine were nearly abolished by atropine and 3) physostigmine potentiated and prolonged the responses of organs from untreated and reserpine-pretreatd animals to transmural stimulation; these effects of physostigmine were abolished by atropine.

The beta adrenergic receptors of chromatophores of the frog, Rana pipiens.

The isolated skin of Rana pipiens was found to be a suitable model for the quantitative study of chromatophore beta adrenergic receptors uninfluenced by prejunctional phenomena. Cumulative concentration-response curves for adrenergic agonists were obtained in preparations in which effective alpha adrenergic blockade had been produced with phenoxybenzamine. The beta adrenergic agonists darkened the preparation, as did melanocyte-stimulating hormone, but the maximum effects differed. The maximum of the l-isoproterenol cumulative concentration-response curve was approximately 50% less than that of melanocyte-stimulating hormone, while the maxima for l-epinephrine and l-norepinephrine were significantly less than that for isoproterenol. Microscopic examination revealed a qualitative difference: while maximal darkening produced by melanocyte-stimulating hormone was associated with maximal changes in both interspot melanophores and iridophores, maximal adrenergic-induced darkening was associated with maximal iridophore granule concentration only. No qualitative differences could be observed in the darkening caused by the three adrenergic agonists. The beta adrenergic potencies of l-norepinephrine and l-isoproterenol relative to l-epinephrine were determined by four-point bioassay. Isoproterenol was found to be 138 times as potent as epinephrine, while norepinephrine was 4 times as potent. Similarly, antagonism of isoproterenol-induced darkening of phenoxybenzamine-pretreated skin samples by the beta adrenergic blocking agents dl-propranolol, dl-sotalol, dl-practolol, l-butoxamine and d-butoxamine was studied, and their KB and pA2 values, respectively, were found to be: dl-propranolol (1.44 X 10(-8)M, 7.81); dl-sotalol (7.25 X 10(-8)M, 7.23); l-butoxamine (6.92 X 10(-6)M, 5.10); dl-practolol (1.91 X 10(-5)M, 4.96); d-butoxamine (no activity). Comparison of the potency ratios and pA2 values cited above with similar parameters obtained by other investigators in several mammalian tissues suggests that there is wide variation among beta adrenergic receptors.