Vasoconstriction Threshold Research Articles

Thermoregulatory vasoconstriction during propofol/nitrous oxide anesthesia in humans: threshold and oxyhemoglobin saturation.

To determine the thermoregulatory effects of propofol and nitrous oxide, we measured the threshold for peripheral vasoconstriction in seven volunteers over a total of 13 study days. We also evaluated the effect of vasoconstriction on oxyhemoglobin saturation (SpO2). Anesthesia was induced with an intravenous bolus dose of propofol (2 mg/kg), followed by an infusion of 180 micrograms.kg-1 x min-1 for 15 min, and maintained with 60% nitrous oxide and propofol (80-160 micrograms.kg-1 x min-1). Central and skin surface temperatures and SpO2 (using two different pulse oximeters) were measured continuously; plasma propofol concentrations and arterial PO2 were measured at 15-min intervals. Volunteers were cooled with a circulating water blanket until definitive peripheral vasoconstriction was detected. The tympanic membrane temperature triggering vasoconstriction was considered the thermoregulatory threshold. Vasoconstriction developed on seven study days during propofol/nitrous oxide anesthesia at a central temperature of 33.3 +/- 1.0 degrees C (mean +/- SD) and plasma propofol concentration of 3.9 +/- 1.1 micrograms/mL. The thresholds during anesthesia were significantly lower than those during the control period (36.7 +/- 0.3 degrees C), but the correlation between plasma propofol concentrations and vasoconstriction thresholds was poor. On the remaining six study days, vasoconstriction did not develop despite central temperatures ranging from 32.1 to 32.7 degrees C. Corresponding propofol concentrations were 4.1-10.9 micrograms/mL. These data suggest that anesthesia with propofol, in typical clinical concentrations, and 60% nitrous oxide substantially inhibits thermoregulatory vasoconstriction. Vasoconstriction increased SpO2 by approximately 2% without a significant concomitant change in PO2. The observed increase in SpO2 probably reflects decreased transmission of arterial pulsations to venous blood in the finger.

Painful Stimulation Minimally Increases the Thermoregulatory Threshold for Vasoconstriction During Enflurane Anesthesia

Painful Stimulation Minimally Increases the Thermoregulatory Threshold for Vasoconstriction During Enflurane Anesthesia

Sweating Threshold During Isoflurane Anesthesia in Humans

Isoflurane anesthesia in humans markedly decreases the threshold temperature triggering peripheral thermoregulatory vasoconstriction (i.e., central temperature triggering vasoconstriction). However, it is not known whether the sweating threshold remains unchanged (e.g., near 37 degrees C), decreases along with the vasoconstriction threshold, or increases during anesthetic administration. Accordingly, the hypothesis that isoflurane anesthesia increases the thermoregulatory threshold for sweating was tested. Forehead sweating was evaluated in five healthy patients given isoflurane anesthesia. The sweating threshold was prospectively defined as the distal esophageal temperature at which significant sweating was first observed. Sweating was observed in each patient at a mean central temperature of 38.3 +/- 0.3 degrees C and an end-tidal isoflurane concentration of 1.1% +/- 0.2%. The interthreshold range (difference between vasoconstriction and sweating thresholds) without anesthesia is approximately 0.5 degrees C; isoflurane anesthesia increases this range to approximately 4 degrees C.

The Thermoregulatory Threshold is Inversely Proportional to Isoflurane Concentration

This study tested the hypothesis that the threshold for thermoregulatory vasoconstriction is lowered as isoflurane concentration increases, but the intensity of vasoconstriction, once triggered, is well preserved during isoflurane anesthesia. The thermoregulatory threshold was prospectively defined as the central temperature at which vasoconstriction occurred, and significant vasoconstriction was defined as a skin-surface temperature gradient (forearm-fingertip) greater than or equal to 4 degrees C. The threshold for thermoregulatory vasoconstriction and the intensity of vasoconstriction, measured as maximum skin-temperature gradient, was determined in six unpremedicated patients electively donating a kidney during isoflurane anesthesia, and in four healthy, awake volunteers. All anesthetized patients were deliberately cooled and became hypothermic. Vasoconstriction occurred in five of six at central temperatures between 35.3 and 32.4 degrees C, at end-tidal isoflurane concentrations between 0.74 and 1.65%. The patient who did not vasoconstrict received the highest isoflurane concentration (approximately 2.5%) and reached a central temperature of 31 degrees C. Unanesthetized volunteers also were exposed to cold and each vasoconstricted at a temperature near 37 degrees C. The threshold for thermoregulatory cutaneous vasoconstriction was inversely correlated with anesthetic dose, the thermoregulatory threshold decreasing approximately 3 degrees C/% isoflurane concentration. There were no statistically significant differences between maximum skin-surface temperature gradients in awake volunteers and patients given isoflurane, or between any of the groups when patients from previous studies given halothane or nitrous oxide/fentanyl anesthesia were included in the comparison. These data indicate that the intensity of vasoconstriction, once triggered, is similar during several different types of anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in cold- and heat-defence following electrolytic lesions of raphe nuclei in the guinea-pig.

In conscious guinea-pigs the effects of electrolytic lesions of the nucleus raphe magnus (NRM) and of adjacent areas in the lower brainstem on cold- and heat-defence were studied. Changes in core temperature, heat production and heat loss effectors as well as their threshold temperatures were compared in the same animals before and after lesioning. As an additional index of heat loss, ear skin temperature and a derived parameter--vasomotor index--were also measured. Three days after NRM lesion the fall in core temperature evoked by an exposure to 14-15 degrees C was smaller than before lesion, furthermore the body temperature threshold for shivering increased. Cold-induced heat production was also higher following NRM lesions. Lesions outside the NRM or sham-operation did not influence cold-defence. After NRM lesion heat-defence was also improved; the rise in core temperature elicited by an exposure to 36-37 degrees C was smaller and the body temperature threshold for ear skin vasoconstriction during recovery from hyperthermia decreased. No change in respiratory evaporative heat loss could be observed after NRM lesion. Lesions outside the NRM or sham-operation did not influence heat-defence. An attempt has been made to explain the observed improvements in cold- and heat-defence by discussing relevant data on mechanisms in central temperature control.

Vascular reactivity is increased in rat lungs injured with alpha-naphthylthiourea.

We investigated the effects of lung injury due to alpha-naphthylthiourea (ANTU) on pulmonary vascular reactivity. Rats were treated with ANTU (10 mg/kg ip) or the vehicle Tween 80. Four hours later, lungs from ANTU-treated rats had increased wet-to-dry weight ratios, bronchial lavage protein concentrations, and perivascular edema. To test vascular reactivity, lungs were isolated and perfused with blood at constant flow rate, while mean pulmonary arterial pressure was monitored. ANTU-treated lungs vasoconstricted earlier than Tween-treated lungs in response to severe airway hypoxia (fractional inspired O2 0%). ANTU-treated lungs vasoconstricted in response to 10% O2, while Tween-treated lungs failed to respond to 10% O2, indicating that the threshold for hypoxic vasoconstriction was decreased by ANTU. ANTU also decreased the threshold for and increased the magnitude of angiotensin II pressor responses, indicating that the increased vasoreactivity was not specific for hypoxia. Addition of meclofenamate to perfusates increased the rate and magnitude of responses to 0% O2 in Tween-treated lungs, but did not change the responses of ANTU-treated lungs. Light microscopy of ANTU-treated lungs showed no pulmonary arterial obstruction, and electron microscopy revealed mild capillary endothelial cell injury. We conclude that enhanced pulmonary vascular reactivity accompanies the increased-permeability pulmonary edema caused by ANTU. A similar increase in vasoreactivity might contribute to pulmonary hypertension observed in patients with the adult respiratory distress syndrome.

Hospital noise--levels and potential health hazards.

Abstract Hospital noise levels were measured in infant incubators, recovery room and two rooms of an acute-care unit. Sources of the noise were noted, and 24-hour measurements were made. The average noise levels were as follows: 57.7 dB(A) and 74.5 dB (linear) for the incubators; 65.6 dB(A) and 80.0 dB (linear) at patients' heads; 57.2 dB(A) and 69.8 dB (linear) for the recovery room; and for the acute care unit 60.1 dB(A) and 73.3dB (linear) for room 1 and 55.8 dB(A)and 68.1 dB (linear) for room 2. In the recovery room and acute-care unit noise levels were correlated with number of hospital staff. On the basis of present knowledge of the physiologic effects of noise, these noise levels probably stimulate the hypophyseal-adrenocortical axis of patients, exceed the noise threshold for peripheral vasoconstriction, pose a threat to hearing in patients receiving aminoglycosidic antibiotics and are incompatible with sleep. (N Engl J Med 289:774–781, 1973)

Comparison of thermoregulatory function in men and women.

Comparison of thermoregulatory function in men and women.

Partitional calorimetric studies of responses of man to thermal transients.

Partitional calorimetric studies of responses of man to thermal transients.

Potentiation of the vasoconstrictor action of topical norepinephrine on the human bulbar conjuctival vessels after topical application of certain adrenocortical hormones.

ABSTRACT Studies were undertaken to estimate whether adrenocortical steroids can directly potentiate the vasoconstrictor activity of norepinephrine in the intact human being and whether this property is shared equally by various adrenal steroids. Most of the 21 subjects were in good health; 5 had migraine. Under direct visualization with a slit-lamp microscope the bulbar conjunctival capillary beds were inspected for basal activity and measurement of the thresholds for vasoconstriction following topically administered serial dilutions of norepinephrine. A 2.5 per cent ophthalmic suspension of either cortisone, hydrocortisone, Δ1-cortisone, compound A, compound S or DCA was then instilled into one eye and basal activity and norepinephrine thresholds estimated again fifteen minutes later. The other eye served as control. It was demonstrated that hydrocortisone and cortisone consistently induced a threefold increase in sensitivity to norepinephrine, and Δ1-cortisone induced a tenfold increase. Compounds A an...