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Results for “VASOMOTOR SYSTEM”

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At least 217 records · Page 12Linked to original sources
PubMed1980

Microwaves induce peripheral vasodilation squirrel monkeys.

Vasomotor activity in cutaneous tail veins was indexed by changes in local skin temperature during exposure of the whole body to 12.3-centimeter continuous microwaves. At an ambient temperature (26 degrees C) just below that at which tail vessels normally vasodilate, criterion dilation was initiated by 5-minute exposures to a microwave power density of 8 milliwatts per square centimeter. This intensity deposits energy equivalent to approximately 20 percent of the monkey's resting metabolic rate but produces no observable change in deep body temperature. Intensity increments of 3 to 4 milliwatts per square centimeter for 1 degree C reductions in ambient temperature below 26 degrees C produced identical responses. That no vasodilation occurred during infrared exposures of equivalent power density suggests that noncutaneous thermosensitive structures may mediate microwave activation of thermoregulatory responses in the peripheral vasomotor system.

Animals↗
PubMed1985

Acute haemodynamic effects of nifedipine at rest and during maximal exercise in patients with chronic cor pulmonale.

The pulmonary hypertension of cor pulmonale can be reversed by sustained correction of hypoxia but continuous oxygen treatment poses problems in clinical practice. Alternative methods of relieving pulmonary vasoconstriction have therefore been explored. Eight patients with chronic cor pulmonale (five of them men) were studied to measure the haemodynamic effects of the calcium antagonist nifedipine, both at rest and on maximal, symptom limited exercise. The mean duration of exercise was unchanged by nifedipine (7.8 (SD 3.3) compared with 7.3(3.1) min). Cardiac output rose from 5.2(1.5) l min-1 to 8.6(3.3) 1 min-1 on exercise. Nifedipine increased resting cardiac output by 26%, but did not influence maximal exercise output. It did not significantly alter resting mean pulmonary artery pressure but reduced the level during exercise from 67(15) to 52(11) mm Hg. Nifedipine lowered resting pulmonary vascular resistance (PVR) by 32% and exercise PVR by 28%. It reduced supine mean systemic arterial pressure by 17%, standing pressure by 22%, and pressure at the maximal exercise level by 20%. Nifedipine lowered supine systemic vascular resistance (SVR) by 35%, standing SVR by 28%, and exercise SVR by 20%. Haemodynamic changes were achieved without adverse symptoms, alteration in arterial PO2, or impairment of calculated oxygen delivery. Nifedipine therefore reduced both pulmonary and systemic vasomotor tone at rest and during exercise. It did not alter exercise tolerance, which is probably limited by underlying respiratory disease. It seems possible therefore that nifedipine could delay the development of cor pulmonale, although this hypothesis remains to be tested.

Adult↗
PubMed2005

Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans.

Skin sympathetic nerve activity (SSNA) exhibits low- and high-frequency spectral components in normothermic subjects. However, spectral characteristics of SSNA in heat-stressed subjects are unknown. Because the main components of the integrated SSNA during heat stress (sudomotor/vasodilator activities) are different from those during normothermia and cooling (vasoconstrictor activity), we hypothesize that spectral characteristics of SSNA in heat-stressed subjects will be different from those in subjects subjected to normothermia or cooling. In 17 healthy subjects, SSNA, electrocardiogram, arterial blood pressure (via Finapres), respiratory activity, and skin blood flow were recorded during normothermia and heat stress. In 7 of the 17 subjects, these variables were also recorded during cooling. Spectral characteristics of integrated SSNA, R-R interval, beat-by-beat mean blood pressure, skin blood flow variability, and respiratory excursions were assessed. Heat stress and cooling significantly increased total SSNA. SSNA spectral power in the low-frequency (0.03-0.15 Hz), high-frequency (0.15-0.45 Hz), and very-high-frequency (0.45-2.5 Hz) regions was significantly elevated by heat stress and cooling. Interestingly, heat stress caused a greater relative increase of SSNA spectral power within the 0.45- to 2.5-Hz region than in the other spectral ranges; cooling did not show this effect. Differences in the SSNA spectral distribution between normothermia/cooling and heat stress may reflect different characteristics of central modulation of vasoconstrictor and sudomotor/vasodilator activities.

Action Potentials↗
PubMed1981

A vasoconstrictor cardiogenic chemoreflex induced by prostaglandin F2 alpha.

Systemic and skeletal muscle vascular responses to intracardiac prostaglandin F2 alpha (PGF2 alpha) were studied in anesthetized dogs. Resistance changes in a vascularly isolated but innervated reservoir-perfused gracilis muscle could occur only neurogenically. Injection of PGF2 alpha or serotonin (5-HT) raised systemic arterial blood pressure (BP) and caused reflex increases in gracilis muscle perfusion pressure (GMPP) that were abolished by alpha-adrenergic blockade. These changes in GMPP are opposite to the expected baroreceptor responses to an increase in BP. Subepicardial local anesthesia attenuated both delta BP and delta GMPP to 5-HT but only the delta GMPP to PGF2 alpha. Changes in BP and GMPP to 5-HT were reduced by vagotomy but not by stellate ganglionectomy. Conversely, stellate ganglionectomy significantly reduced the delta GMPP to PGF2 alpha but not the delta BP. Vagotomy affected neither delta BP nor delta GMPP following PGF2 alpha. Thus, while PGF2 alpha and 5-HT produce reflex vasoconstriction in gracilis muscle that is mediated through sympathetic efferent nerves and initiated by cardiogenic reflexes, apparently PGF2 alpha does so through sympathetic afferent and 5-HT through vagal afferent pathways. Further, since the systemic pressor response to PGF2 alpha persisted after stellatectomy, vagotomy, or local anesthesia, it is independent of the sympathetic cardiogenic chemoreflex.

Animals↗
PubMed1987

Effect of AVP on pressor responses to peripheral sympathetic stimulation in the rat.

Studies were carried out to determine whether arginine vasopressin (AVP) could modulate pressor responses to peripheral sympathetic stimulation or potentiate systemic norepinephrine (NE) vasoconstrictor effects. The effects of graded 30-min infusions of AVP (0.02, 0.2, and 2.0 ng X kg-1 X min-1) on the pressor responses to either electrical stimulation of spinal sympathetic outflow or NE injection (0.1, 0.5, and 1.0 micrograms/kg) were determined in central nervous system-ablated rats. Spinal stimulation with increasing frequency (0.25, 0.5, and 1.0 Hz, n = 8) at a constant voltage (20 V) or increasing voltage (8, 10, 15, and 20 V, n = 6) at a constant frequency (1 Hz) elicited significant stimulus-response relationships in mean arterial pressure (MAP). Similarly, NE increased MAP in a dose-related manner. AVP had no significant effect (P less than 0.05) on pressor responses to increasing frequency or voltage stimulation or to NE injection. We conclude that pressor responses to sympathetic stimulation in the rat are not modulated by actions of AVP to inhibit peripheral sympathetic ganglionic transmission or potentiate NE vasoconstrictor effects.

Animals↗