Research Protocol For A Pilot Study. The Effect Of ST (36) And Ren12 In The Control Of Hyperglycemia In Diabetic Patients

These acupunture points stimulated with EA have shown their hypoglycemic effect in animal models. One of the main mechanisms by which this effect is supported is the regulation of the hypothalamic-pituitary-adrenal axis, regulating the secretion of adrenal cortical hormone.

Rescue and Nursing of Acute Severe Viral Myocarditis in Children

<p><strong>Objective: </strong>To explore clinical rescue and nursing measures for children with acute severe viral myocarditis. <strong>Method: </strong>Patients in the hospital were immediately given positive anti-heart failure, anti-shock therapy and correct treatment of arrhythmia. Large doses of gamma globulin, adrenal cortical hormone, pulse therapy, direct current cardioversion, vitamin C, oxygen inhalation, ECG and other treatments were given. <strong>Results</strong><strong>: </strong>58 cases were rescued successfully and the prognosis was good. However, there were 3 cases of patients with severe myocardial damage, ECG, ventricular fibrillation, and 1 invalid death. <strong>Conclusion: </strong>In the treatment of acute severe viral myocarditis of children, timely, accurate and safe implementation of various rescue measures is the key to improving the success rate.</p>

Physiological effects of endogenous ouabain: control of intracellular Ca2+ stores and cell responsiveness

Ouabain is a well-known compound but a newly discovered adrenal cortical hormone that plays a role in cell Na+ regulation and in whole body salt and water balance. Ouabain may also be a paracrine hormone and may be secreted by some central nervous system neurons as well as by other types of cells. This article focuses on the cellular mechanisms that underlie the physiological (and pathophysiological) effects of ouabain. Ouabain directly inhibits the plasmalemmal Na+ pump in a variety of cell types. Low ouabain concentrations cause, in the steady state, a modest rise in the cytosolic Na+ concentration but only a minimal decline in membrane potential. All Na+ gradient-dependent processes may thereby be affected, albeit to only a small extent. Most important, however, is the secondary redistribution of Ca2+, mediated by Na(+)-Ca2+ exchange, that should slightly increase the cytosolic free Ca2+ concentration ([Ca2+]cyt). As a result of Ca2+ sequestration in intracellular stores [the endoplasmic and/or sarcoplasmic reticulum (ER/SR)], however, a new steady state is achieved with a slightly increased [Ca2+]cyt but a substantially augmented Ca2+ store; thus the ER/SR effectively acts as a Ca2+ amplifier. This extra stored Ca2+ is then available for mobilization whenever the cells are activated. Cytosolic Ca2+ is a key signaling mechanism in virtually all cells: it controls numerous physiological processes such as contraction, secretion, and excitability. Thus ouabain may modulate cell responsiveness via its influence on ER/SR Ca2+ stores. With these principles in mind, we examine evidence that endogenous ouabain may play a role in numerous physiological and pathophysiological processes associated with altered fluid and electrolyte metabolism and deviations from the normal blood pressure-blood volume relationship. We discuss the possible participation of ouabain in the regulation of vascular tone and then consider the putative role of ouabain in several forms of hypertension, congestive heart failure, thyroid and adrenocortical dysfunction, and diabetes mellitus, as well as in the adaptation to high altitude.

ADRENAL CORTICAL HORMONES AND RESISTANCE TO HISTAMINE STRESS IN THE INFANT RAT

ABSTRACT The adrenal gland corticosterone concentration in the infant rat is similar to that found in the intact unstressed normal adult. 1–2 day old rats did not respond to histamine administration with an increase in adrenal cortical hormone content while adults exhibited the expected increase. The 90 minute dose-mortality relationship for histamine was determined on these stress-non-responsive infant rats. Prior treatment with cortisone, cortisol, corticosterone or ACTH did not significantly influence the number of deaths occurring at a given dose of histamine. These results are compatible with the hypothesis that, in the otherwise normal animal, the abrupt secretion of ACTH and the adrenal cortical hormones in response to acute stress may not contribute stress resistance to contemporaneous insults, at least to those allied to histamine administration.