'tissue' pressure to the 'jugular' tube during pump flow produced the typical pressures found in the jugular vein in giraffe. Constriction of the lowest, 'jugular cuff', portion of the 'jugular' limb showed that the cuff may augment the orthostatic reflex during head raising. Except when all tubes were rigid, pressures were unaffected by a siphon.We conclude that mean arterial blood pressure in giraffes is a consequence of the hydrostatic pressure generated by the column of blood in the neck, that tissue pressure around the collapsible jugular vein produces the known jugular pressures, and that a siphon does not assist flow through the cranial circulation.
Although agonist-induced desensitization of adrenergic receptors has been previously demonstrated, the regulation of adrenergic receptors during acute psychological stress has not been investigated in humans. We studied 30 first year medical students during final examination week and one month earlier. Platelet alpha 2 receptor binding was measured using 3H-yohimbine and leukocyte beta 2 receptor binding was measured with 125I-CYP (Iodocyanopindolol). During final examination week, platelet alpha 2-receptor binding affinity was significantly reduced, while levels of plasma catecholamines and reported anxiety were significantly increased, compared with the earlier period. Students showing the greatest increases in plasma norepinephrine and in reported anxiety also demonstrated the greatest reductions in alpha 2 receptor binding affinity. These data show that acute psychological stress can produce adrenergic receptor desensitization, possibly through increased levels of circulating norepinephrine.
We have previously demonstrated that the vasospastic attacks of Raynaud's disease can be induced despite blockade of efferent digital nerves and that feedback-induced vasodilation is mediated through a non-neural, beta-adrenergic mechanism. Here, we sought to determine the role of sympathetic activity, as measured by plasma epinephrine and norepinephrine, during finger temperature feedback and autogenic training. Thirty-one female patients with idiopathic Raynaud's disease were randomly assigned to receive finger temperature feedback or autogenic training over 28 days. Half of each group began and finished training during the follicular phase of the menstrual cycle, the other half during the luteal phase. During training, significant temperature elevations were shown by feedback patients but not by autogenic patients. There were no significant effects for norepinephrine and epinephrine for either group. Cycle phase did not interact with training effects or with catecholamines. These findings do not support the role of decreased sympathetic activation in behavioral treatments for Raynaud's disease.
Thirty-nine normal volunteers of both sexes were randomly assigned to receive 8 sessions of temperature biofeedback or autogenic training to increase finger temperature. Temperature biofeedback subjects produced significant elevations in finger temperature during training, whereas those who received autogenic training did not. Temperature feedback subjects had significantly higher heart rates and diastolic blood pressures during training compared to autogenic subjects. There were no significant changes or group differences in plasma catecholamine levels. These data do not support the hypothesis that feedback-induced vasodilation is accompanied by decreased sympathetic activation in normal populations, when only temperature biofeedback is employed.
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