Biomedical subjects
Publications and source records attributed to J M Loeb.
In two patients with thyroiditis caused by Coccidioides immitis, presented thyroid symptoms and findings were characteristic of subacute thyroiditis. Fine needle aspiration biopsy of the thyroid proved useful in establishing the diagnosis of coccidioidomycosis. This is the first report of coccidioidomycosis presenting as thyroiditis.
The adrenergic mechanisms involved in the sinus tachycardia which follows the termination of vagal stimulation ("postvagal tachycardia") were studied in the anesthetized dog. The following results were obtained. Postvagal tachycardia: 1) is not affected by ventricular or atrial drive; 2) is enhanced by the application of either norepinephrine or dopamine on the sinus node area; 3) is increased in magnitude and duration by the catecholamine uptake blockers desipramine and phenoxybenzamine; 4) is significantly reduced by beta blockade with propranolol; 5) is not affected by alpha blockade with phentolamine or dopaminergic blockade with haloperidol; 6) is not affected by Disulfiram, a drug which inhibits dopamine beta-hydroxylase and thereby increases endogenous dopamine; 7) rises more slowly to a smaller peak after bretylium; and 8) is enhanced by phenoxybenzamine, but not by desipramine, after destruction of sympathetic nerves by 6-hydroxydopamine. It is concluded that release of catecholamines by vagally liberated acetylcholine is involved in postvagal tachycardia. The released catecholamine acts on beta but not alpha or dopamine receptors. Catecholamines released from sympathetic nerves may account for an initial component in postvagal tachycardia, but catecholamine(s) released from extraneuronal stores account for most of postvagal tachycardia.
The role of acetylcholine (ACh) in the sinus tachycardia which follows vagal stimulation ('postvagal tachycardia') was investigated in anesthetized dogs. The stimulation of either vagus was followed by postvagal tachycardia. The bradycardia induced by local application of ACh to the sinus node was followed by sinus tachycardia while local application of methacholine (a predominantly muscarinic agonist) induced only bradycardia. Atropine potentiated the postvagal tachycardia in low doses and blocked it in high doses. The conclusion drawn is that postvagal tachycardia is caused by the release of ACh by either vagus acting on a nicotinic receptor.
beta-estradiol was administered to mice continuously by diffusion from a silastic tube that was implanted subcutaneously at 4 weeks of age. Four to 6 weeks of estrogen administration caused a substantial reduction in natural killer cell activity in the spleens from mice of either sex. Androgen (5alpha-dihydrotestosterone) did not. Castration of male or female mice did not affect natural killing and did not alter the effect of beta-estradiol. Estradiol did not affect natural killing in vitro and the loss of natural killing was not due to a soluble or a cellular suppressor of natural killing. The effects of estradiol were not dependent on the thymus, since estradiol reduced natural killing in mice that had been neonatally thymectomized. After removal of the estrogen implant, natural killing recovered over a period of 8 weeks. The loss of natural killing may reflect a loss of bone marrow secondary to estrogen-induced osteosclerosis.