Rate Of Vasoconstriction Research Articles

Relationship between maximum oxygen uptake and peripheral vasoconstriction in a cold environment

BackgroundVarious individual characteristics affect environmental adaptability of a human. The present study evaluates the relationship between physical fitness and peripheral vasoconstriction in a cold environment.MethodsSeven healthy male students (aged 22.0 years) participated in this study. Cold exposure tests consisted of supine rest for 60 min at 28 °C followed by 90 min at 10 °C. Rectal and skin temperatures at seven sites, oxygen consumption, and the diameter of a finger vein were measured during the experiment. Metabolic heat production, skin heat conductance, and the rate of vasoconstriction were calculated. Individual maximum oxygen consumption, a direct index of aerobic fitness, was measured on the day following the cold exposure test.ResultsDecreases in temperature of the hand negatively correlated with the changes in rectal temperature. Maximum oxygen consumption and the rate of vasoconstriction are positively correlated. Furthermore, pairs of the following three factors are also significantly correlated: rate of metabolic heat production, skin heat conductance, and the rate of vasoconstriction.ConclusionThe results of this study suggested that the capacity for peripheral vasoconstriction can be improved by physical exercise. Furthermore, when exposed to a cold environment, fitter individuals could maintain metabolic heat production at the resting metabolic level of a thermoneutral condition, as they correspondingly lost less heat.

Discussion of “Core cooling and thermal responses during whole-head, facial, and dorsal immersion in 17 °C water”

1. The rate of oesophageal temperature reduction and the heat loss from the head were less in the second 30 min of cooling than in the first 30 min. This was despite no increase in metabolic rate and a lessening in the rate of vasoconstriction (going by the slope of fingertip blood flow and the change in fingertip temperature). Is the extent of vasoconstriction (even though the rate was lessening) sufficient to explain the reduced rate of oesophageal temperature reduction and heat loss in the second 30 min? Or is there something else going on which slowed up the heat loss? 2. With regard to the core cooling increase with facial compared to dorsal immersion, could some of the difference also be attributable to airway heat loss? With facial cooling, presumably part of the snorkel tubing passed through the water which may have meant that the inspired air was cooler than in the facial cooling condition where perhaps none of the snorkel tubing was in the water.

Coronary Artery Endothelial Dysfunction Associated With Sleep Apnea

There is little information about coronary artery endothelial dysfunction in patients with sleep apnea. We evaluated relation between severity of sleep apnea and coronary artery endothelial dysfunction. In all, 26 patients without significant coronary stenoses were enrolled. Endothelial function was estimated by measuring coronary vasoreactivity in response to acetylcholine infusion (10(-7) mol/L) into coronary arteries. Vasoconstriction rate was defined as ([lumen diameter after isosorbide dinitrate injection - lumen diameter after acetylcholine injection]/lumen diameter after isosorbide dinitrate injection × 100). Vasoconstriction rate was calculated at each major coronary artery and the highest value was used for that patient. Overnight sleep study was performed and the apnea-hypopnea index (AHI) was calculated as the mean number of apneas and hypopneas per hour of sleep. There was significant correlation between AHI and vasoconstriction rate (P = .04). There is significant correlation between severity of sleep apnea and endothelial function of coronary arteries.

Core cooling and thermal responses during whole-head, facial, and dorsal immersion in 17 °C water

This study isolated the effects of dorsal, facial, and whole-head immersion in 17 degrees C water on peripheral vasoconstriction and the rate of body core cooling. Seven male subjects were studied in thermoneutral air (approximately 28 degrees C). On 3 separate days, they lay prone or supine on a bed with their heads inserted through the side of an adjustable immersion tank. Following 10 min of baseline measurements, the water level was raised such that the water immersed the dorsum, face, or whole head, with the immersion period lasting 60 min. During the first 30 min, the core (esophageal) cooling rate increased from dorsum (0.29 ± 0.2 degrees C h-1) to face (0.47 ± 0.1 degrees C h-1) to whole head (0.69 ± 0.2 degrees C h(-1)) (p < 0.001); cooling rates were similar during the final 30 min (mean, 0.16 ± 0.1 degrees C h(-1)). During the first 30 min, fingertip blood flow (laser Doppler flux as percent of baseline) decreased faster in whole-head immersion (114 ± 52% h(-1)) than in either facial (51 ± 47% h-1) or dorsal (41 ± 55% h(-1)) immersion (p < 0.03); rates of flow decrease were similar during minutes 30 to 60 (mean, 22.5 ± 19% h(-1)). Total head heat loss over 60 min was significantly different between whole-head (120.5 ± 13 kJ), facial (86.8 ± 17 kJ), and dorsal (46.0 ± 11 kJ) immersion (p < 0.001). The rate of core cooling, relative to head heat loss, was similar in all conditions (mean, 0.0037 ± 0.001 degree C kJ(-1)). Although the whole head elicited a higher rate of vasoconstriction, the face did not elicit more vasoconstriction than the dorsum. Rather, the progressive increase in core cooling from dorsal to facial to whole-head immersion simply correlates with increased heat loss.

Reflex vascular responses from aortic arch, carotid sinus and coronary baroreceptors in the anaesthetized dog.

In chloralose-anaesthetized dogs, pressure applied to coronary, carotid and aortic baroreceptors were changed independently and the resulting reflex vascular responses were determined. Increases in pressure to each group of baroreceptors resulted in reflex vasodilatation; the maximal responses to distension of carotid and coronary baroreceptors were significantly larger than those to aortic receptors, but not different from each other. Increases in pressure in all three regions induced maximal responses at similar times from the onset of the pressure stimulus. However, the time for recovery of vascular resistance following a decrease in baroreceptor pressure differed. Vasoconstriction following a period of coronary hypertension occurred slowly, requiring 70 s for 90% of the response to develop. This was significantly longer than the corresponding times for carotid and aortic receptors (about 28 s). The rate of vasoconstriction in response to coronary baroreceptor unloading was influenced by the period for which the pressure stimulus was applied and vasoconstriction was even slower when the pressure stimulus had been maintained for 8 min. The mechanism responsible for delaying the vasoconstriction following a period of coronary hypertension is not known, but this effect may have important implications for the control of arterial blood pressure.