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Results for “VASOMOTOR SYSTEM”

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At least 127 records · Page 7Linked to original sources
PubMed1983

Immunohistochemical characterization of reactive and neoplastic mast cells.

Mast cells are connective tissue elements likened to unicellular endocrine organs because of the wide diversity of physiologic and pathologic events associated with the secretion of biologically active compounds. Using an immunoperoxidase method (PAP), we studied tissue from patients with benign and malignant systemic mastocytosis and with a variety of reactive conditions. The following immunoreactive antigens were identified in mast cells: a heparinlike compound or compounds (HLC), prostaglandin, serotonin, and fibronectin. HLC is constantly present, staining mast cells in a granular fashion from most lesions. Serotonin and prostaglandin stain in a diffuse cytoplasmic manner in occasional lesions. Fibronectin is found in a surface location in selected cases. We found no clear association between the immunoreactivity of one compound in mast cells and one clinical symptom, e.g., HCL with bleeding, prostaglandin, or serotonin with systemic vasomotor activity or fibronectin with increased tissue fibrosis. However, patients with localized and systemic disease had symptoms that might have been attributed to more than one compound. Only occasional patients with reactive conditions showed such symptoms. The presence of these compounds, either alone or in combination, did not separate benign from malignant conditions. Other cells within selected tissues also stained with the antibodies tested. Despite the lack of exclusivity, these antibodies are useful in identifying mast cells within tissue sections and may have a role in the study of mast cell constituents.

Animals↗
PubMed1997

Clinical neurophysiology laboratory tests to assess the nociceptive system in humans.

This paper presents some currently available neurophysiological tools that are helpful in the clinical setting to evaluate and document neuropathic disturbances that may be associated with pain. The specific tests described in this discussion are quantitative sensory tests (QSTs), autonomic tests (ATs), microneurography (MCNG), and laser evoked potentials (LEPs). Quantitative sensory testing of the nociceptive system includes the thermal stimulation (TST) and current perception threshold (CPT) tests. The ATs applicable to some patients with pain are sudomotor and vasomotor tests. The quantitative sudomotor axon reflex test (QSART), resting sweat output (RSO), and sympathetic skin response (SSR) are the tests for sudomotor involvement. The vasomotor system is tested by measuring skin temperature (surface thermistor or thermography) at rest and, in some cases, after provocative maneuvers. In addition, MCNG (intraneural recording of single nerve fibers or fascicles of nerves) allows examiners to look directly at muscle and skin sympathetic efferent output in normal subjects without pain or with experimental pain and in patients with neuropathic pain. This technique also provides a means of studying the physiology of primary afferent fibers in persons with neurogenic pain. Recent development of LEPs that incorporate the use of painful infrared laser-induced stimuli allow selective study of the nociceptive system, both the central and peripheral portions.

Algorithms↗
PubMed2000

The cardiovascular responses of the red-eared slider (Trachemys scripta) acclimated to either 22 or 5 degrees C. II. Effects of anoxia on adrenergic and cholinergic control.

Cardiovascular control in cold-acclimated freshwater turtles during chronic anoxic exposure is not well understood. We tested the hypothesis that the observed bradycardia in Trachemys scripta results from increased cholinergic inhibitory tone and reduced sympathetic activity. Cardiovascular status was measured in vivo in turtles acclimated to either 22 degrees C or 5 degrees C and either acutely exposed (6 h) to anoxia at 22 degrees C or chronically exposed (22 days) to anoxia at 5 degrees C. In 22 degrees C-acclimated turtles, injection of the cholinergic antagonist atropine induced a significant tachycardia under both normoxic and anoxic conditions. However, in 5 degrees C-acclimated turtles, atropine injection had little effect on heart rate. Therefore, cholinergic control of heart rate was suppressed during cold acclimation; instead, temperature effects are more important in bringing about bradycardia, while the intrinsic effects of anoxia and acidosis are probably important during chronic anoxia. Injection of adrenaline caused a pressor response through increased systemic resistance at both acclimation temperatures. This response was blunted by acute and chronic anoxic exposure, suggesting that systemic vasomotor control was altered independently of acclimation temperature. This anoxic blunting may be related in part to the anoxia-induced increase in systemic resistance. Injection of nadolol after atropine decreased systemic cardiac output. The tonic beta-adrenergic cardiac stimulation was attenuated by acute and chronic anoxic exposure. Some of this attenuation of beta-adrenergic control could be attributed to the 39-40 % reduction in cell surface beta-adrenoreceptor density in the ventricles of these turtles that accompanied acute and chronic anoxic exposure. In conclusion and contrary to our original hypothesis, cholinergic and adrenergic control of the cardiovascular system in turtles was attenuated under cold anoxic conditions, perhaps assisting in the depressed physiological state of these animals.

Acid-Base Equilibrium↗
PubMed1989

Closed loop control of human body temperature: results from a one-dimensional model.

A one-dimensional model of human thermo-regulation is used to solve a variety of basic problems in determining an adequate structure of the controller for metabolic heat production, skin blood flow and sweat production. Assuming one integrated central and one integrated peripheral afferent signal the controller parameters are evaluated by analysis of the control performance. Based on a validation by experimental results this allows the determination of a first optimized set of values for controller gains and weight of skin temperature feedback. Furthermore we analyse the effect of inhomogeneous distribution of heat production and blood flow, the influence of body fat content, of controller gains, of weight of skin temperature feedback and of depth of peripheral receptors on the dynamic performance. Increase of peripheral blood flow in particular evokes essentially both an increase of energy requirement in the cold and a quicker system response. Differing rates of increase of metabolic heat production are the consequence of differing body fat content. The weight of skin temperature feedback can be limited to 5...20%, because values outside this range evoke dynamic responses incompatible with the experiments. The actual value can only be determined if there is a correct assumption for the depth of the skin receptors. The use of measured superficial skin temperatures brings about an underestimation of the peripheral afferent signal. Of the controller gains it is primarily the gain of the metabolic controller which affects the dynamic response of the system. The experimental fact of a delayed onset of sweat production after a transition from cold to heat is the consequence of a high gain of the vasomotor system.

Adipose Tissue↗
PubMed1990

Effects of prolonged hypoxia on adenylate cyclase activity and beta-adrenergic receptors in pulmonary and systemic arteries of the rat.

Prolonged hypoxia causes pulmonary hypertension but no change in systemic vasomotor tone. In an effort to define the mechanisms involved, we determined the effects of 3 and 7 days of hypoxia on adenylate cyclase activity and beta-adrenergic receptor binding characteristics in pulmonary and systemic arteries in an adult rat model of hypoxic pulmonary vasoconstriction produced by hypobaria. Basal and stimulated adenylate cyclase activity were measured in crude membrane preparations by radioimmunoassay for cyclic AMP. Basal enzyme activity in pulmonary arteries did not change with hypoxia, whereas in systemic arteries it increased 3.5- and 5.3-fold following 3 and 7 days of hypoxia, respectively. GTP-stimulated activity in pulmonary arteries also did not change, but in systemic arteries it increased 7.1- and 5.5-fold. Isoproterenol-stimulated activity in pulmonary arteries was decreased to 49% of control-stimulated activity following 3 days but was similar to control-stimulated activity after 7 days of hypoxia; in systemic arteries it increased 5.6- and 4.6-fold. Sodium fluoride-stimulated activity in pulmonary arteries was unchanged, whereas in systemic arteries it increased 3.8- and 5.3-fold. In contrast, forskolin-stimulated activity, which also was not altered in pulmonary arteries, was increased by only 85% and 71% in systemic arteries. beta-Adrenergic receptors were studied with [125I]iodocyanopindolol. Seven days of hypoxia decreased receptor density by 37% and 57% in the pulmonary and systemic arteries, respectively. Receptor affinity for agonists was not altered. Thus, despite downregulation of beta-adrenergic receptors in both artery types, prolonged hypoxia has no sustained effect on adenylate cyclase activity in pulmonary arteries, whereas enzyme activity in systemic arteries is markedly increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1977

Cardiopulmonary baroreflexes: effects of pulmonary congestion and edema.

Systemic vasodepressor reflexes were initiated in pump-oxygenator perfused dogs by separately pressurizing the pulmonary vessels and the left cardiac chambers. Pulmonary vascular pressurization caused transient systemic vasodilation of a magnitude proportional to stimulus pressure over the range 0-65 cmH2O. The sensitivity of this reflex was sigificantly less than that of the left heart baroreflex. Mild pulmonary edema produced by a period of sustained congestion, and moderate edema, caused by sustained congestion in the presence of alloxan, had no discernible effect on systemic vasomotor tone or on subsequent pulmonary vascular baroreflexes. By comparison of these results with earlier studies in similar preparations I concluded that pulmonary arterial baroreflexes could alone produce the response obtained by pressurizing the entire pulmonary vascular bed. Although it was anticipated that type-J, irritant, and stretch receptors would be affected by congestion, no systemic vascular effects attributable to them were seen.

Animals↗
PubMed1998

Regulation of autonomic nervous system in space and magnetic storms.

Variations in the earth's magnetic field and magnetic storms are known to be a risk factor for the development of cardiovascular disorders. The main "targets" for geomagnetic perturbations are the central nervous system and the neural regulation of vascular tone and heart rate variability. This paper presents the data about effect of geomagnetic fluctuations on human body in space. As a method for research the analysis of heart rate variability was used, which allows evaluating the state of the sympathetic and parasympathetic parts of the autonomic nervous system, vasomotor center and subcortical neural centers activity. Heart rate variability data were analyzed for 30 cosmonauts at the 2nd day of space flight on transport spaceship Soyuz (32nd orbit). There were formed three groups of cosmonauts: without magnetic storm (n=9), on a day with magnetic storm (n=12) and 1-2 days after magnetic storm (n=9). The present study was the first to demonstrate a specific impact of geomagnetic perturbations on the system of autonomic circulatory control in cosmonauts during space flight. The increasing of highest nervous centers activity was shown for group with magnetic storms, which was more significant on 1-2 days after magnetic storm. The use of discriminate analysis allowed to classify indicated three groups with 88% precision. Canonical variables are suggested to be used as criterions for evaluation of specific and non-specific components of cardiovascular reactions to geomagnetic perturbations. The applied aspect of the findings from the present study should be emphasized. They show, in particular, the need to supplement the medical monitoring of cosmonauts with predictions of probable geomagnetic perturbations in view of the prevention of unfavorable states appearances if the adverse reactions to geomagnetic perturbations are added to the tension experienced by regulatory systems during various stresses situations (such as work in the open space).

Adult↗
PubMed1999

Cardiovascular autonomic dysfunction in multiple sclerosis: correlation with orthostatic intolerance.

Autonomic dysfunction is frequently observed in patients with multiple sclerosis (MS), but clinical studies disagree on the frequency and type of abnormalities in autonomic function tests. Orthostatic dizziness (OD) has been reported in up to 49% of patients, but the pathophysiological mechanisms are poorly understood. This study investigated cardiovascular reflex tests and their association with OD in patients with MS in order to examine the hypothesis that the sympathetic nervous system is specifically involved in these patients. Forty patients with clinically active relapsing-remitting (n = 27) and secondary progressive MS (n = 13), aged 35.0+/-8.5 years, were studied by parasympathetic (heart rate responses to the Valsalva maneuver, deep breathing, and active change in posture) and sympathetic function tests (blood pressure responses to active change in posture and sustained handgrip), and by spectral analysis of heart rate variability during rest and during standing. Results were compared to those obtained in 24 healthy volunteers, aged 29.4+/-7.2 years. A standardized questionnaire was used to evaluate symptoms of orthostatic intolerance. Abnormal responses on at least one cardiovascular reflex test were observed in 40% of MS patients, compared to 17% of the control group, with a statistically significant involvement of the sympathetic vasomotor system. Orthostatic intolerance was reported in 50% of patients (controls: 14%, P<0.006). Subgroup comparison of patients with and without OD suggests that orthostatic intolerance results from impaired sympathetic vasoconstriction. These results provide further evidence that the sympathetic nervous system is involved in patients with MS.

Adult↗