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PubMed1988

Regulation of immune-aggregate-stimulated hepatic glycogenolysis and vasoconstriction by vicinal dithiols.

Evidence suggesting that vicinal dithiols regulate immune-aggregate-induced vasoconstriction and glycogenolysis in the perfused rat liver was obtained. Phenylarsine oxide (PhAsO) and other tervalent organic arsenicals inhibited in a dose-dependent manner hepatic glycogenolysis, vasoconstriction, Ca2+ mobilization and the stimulated O2 consumption caused by immune-aggregate infusion. Polar tervalent and quinquivalent arsenicals were less effective than hydrophobic arsenicals. Prior infusion of Fc- but not Fab-fragments of IgG prevented partially immune-aggregate-stimulated hepatic metabolism, suggesting that immune aggregates elicit hepatic metabolic responses through Fc gamma receptors. The inhibitory action of PhAsO on immune-aggregate-stimulated hepatic glycogenolysis was unique; inhibition of glycogenolysis was not observed when phenylephrine, isoprenaline or glucagon was used as a stimulant. Although PhAsO might be expected to sequester cellular thiols, no significant change in the oxidation-reduction state of the major cellular thiol, glutathione, was found during PhAsO infusion. In addition, PhAsO exerted its effects without producing changes in hepatic adenine nucleotides and cyclic AMP. Evidence suggesting the involvement of vicinal dithiols was obtained through thiol-competition experiments using mono- and di-thiols. PhAsO inhibition of IgG-aggregate-stimulated hepatic vasoconstriction and glycogenolysis was reversed significantly by infusion of 2,3-dimercaptopropan-1-ol at 3-fold molar excess, whereas 2-mercaptoethanol at 40-fold molar excess was ineffective. The results of the present study provide evidence documenting the participation of vicinal dithiols during the coupling of hepatic immune-aggregate clearance by Kupffer cells with vasoconstriction of the hepatic vasculature (e.g. endothelial cells) and glycogenolysis (e.g. parenchymal cells).

Adenine Nucleotides↗
PubMed1979

Pattern A personality and noise-induced vasoconstriction.

A perplexing question about noise-induced hearing loss is why some persons seem to be more affected by high intensity noise than others. Hawkins (1971) has shown noise-induced vasoconstriction to be implicated in noise-induced hearing loss in animals as evidenced by vascular changes within the inner ear and he asks the question: Are these changes caused by the noise itself or mediated by the autonomic nervous system (ANS)? Our research employed a plethysmograph to measure ANS mediated vasoconstriction during noise exposure. The subjects were stress prone males and females (Pattern A) whose behavior in noise was compared to non-stress prone males and females (Pattern B). The results indicated Pattern A males showed marked vasoconstriction in the presence of noise whereas Pattern B males did not. Pattern A females performed very much like Pattern A males with no statistical difference between these two groups. However, Pattern B females demonstrated a significant increase in vasoconstriction in the presence of noise and in this respect Pattern B females are different from Pattern B males. This difference possibly resulted from the use of a test to assess personality type which was intended for use with male subjects. The authors conclude there is strong evidence to suggest that being prone to stress in the presence of noise is a contributing factor to noise-induced hearing loss.

Adolescent↗
PubMed1996

Vasoconstriction in active calf persists after discontinuation of combined exercise with high-intensity elbow flexion.

The present study aimed to determine whether vasoconstriction in active calf occurring during combined exercise diminished or persisted when added low- and high-intensity elbow flexion exercise ceased and single leg exercise continued. Six active women (mean age, 21.2 years) participated in this study. During 10-min plantar flexion exercise at 10% of maximum voluntary contraction (MVC), elbow flexion exercise at 10% MVC was added over the 3rd and 4th min. Calf blood flow did not change significantly upon superimposition and cessation of this elbow flexion exercise. However, when elbow flexion exercise at 50% MVC was added during the 7th and 8th min, calf blood flow above the resting value (2.23 +/- 0.23 mL 100 mL-1 min-1) decreased significantly (P < 0.05) from 6.72 +/- 0.87 (6th min) to 5.14 +/- 1.36 mL 100 mL-1 min-1 after 2 min of combined exercise and was accompanied by a similar change in the non-exercising calf blood flow value. The vascular conductance of the exercising calf decreased significantly (P < 0.01) from 6.48 +/- 1.08 (6th min) to 3.11 +/- 1.27 mL 100 mL-1 min-1 mmHg-1 at the end of the 2nd min of combined plantar flexion exercise with elbow flexion exercise at 50% MVC. After elbow flexion exercise at 50% MVC was discontinued and plantar flexion exercise at 10% MVC alone was performed, the vascular conductance in the exercising calf remained significantly low for the next 2 min. These results indicate that the vasoconstriction induced by adding high-intensity arm exercise is persistent, suggesting a major contribution of metabo-receptor-mediated vasoconstriction rather than central command- and mechano-receptor-mediated vasoconstriction.

Adult↗
PubMed1997

The cGMP pathway is not responsible for the blunted hypoxic vasoconstriction in rat lungs after altitude exposure.

To examine the contribution of the cyclic guanosine monophosphate (cGMP) pathway in changes in pulmonary vasoconstriction during the initial days of altitude exposure, we tested the effects of LY83583 (an inhibitor of guanylate cyclase activation) and those of N(G)-monomethyl-L-arginine (an inhibitor of nitric oxide synthesis) on airway hypoxia- (3% O2) and angiotensin II- (AII, 0.2 microg) induced vasoconstrictions in lungs from the rats exposed to either moderate altitude (MA, 570 torr) or high altitude (HA, 430 torr) At 2 days' exposure, hypoxic response was significantly blunted compared with the response in low-altitude (LA, 710 torr) lungs in an altitude-dependent manner. At 7 days' exposure, the response was recovered fully in MA lungs but partially in HA lungs. AII response was not significantly blunted at 2 days' exposure, but was significantly augmented in an altitude-dependent manner at 7 days' exposure. LY83583 (10 micromol L(-1)) potentiated both responses in LA lungs but did not significantly potentiate either response in any altitude-exposed lungs. N(G)-monomethyl-L-arginine (10 micromol L(-1)) potentiated both responses in LA lungs but did not significantly potentiate either response in HA lungs at 2 days' and 7 days' exposure. Thus the cGMP pathway is not responsible for either the change in hypoxic vasoconstriction or the change in AII vasoconstriction in rat lungs during the initial 7 days of altitude exposure.

Altitude↗
PubMed2001

Sympathetic skin vasoconstriction--further evaluation using laser Doppler techniques.

The aim of this study was to quantify the reflex sympathetic vasoconstriction in skin at different depths. Twenty healthy subjects were studied. Finger skin blood flow was measured using laser Doppler perfusion imaging (LDPI) and laser Doppler perfusion monitoring (LDPM). In LDPM, a probe with fibres separated 0.25 mm (deep) and 0.14 mm (superficial) from the illuminating fibre was used. Local heating (40 degrees C) was achieved with a Peltier element, and reflex vasoconstriction induced by immersion of the contra-lateral hand and forearm for 3 min in water at 15 degrees C. The change in skin blood flow was measured and a vasoconstriction index (VAC: cooling/before cooling) calculated. VAC indices of LDPI, LDPM-0.25 and LDPM-0.14 were 0.60, 0.59 and 0.60, respectively. The two components of the LDPM perfusion value, blood cell velocity and concentration, were studied separately. Their contributions in LDPM-0.25 were roughly the same, whereas the velocity component dominated in LDPM-0.14, although their relative responses in the two channels were similar. We conclude that sympathetic skin vasoconstriction does not significantly differ in two compartments, as probed with fibres separated by 0.25 and 0.14 mm. Blood cell velocity is influenced in a proportional way, as is concentration.

Adult↗
PubMed2002

Oestrogen attenuates coronary vasoconstriction after angioplasty: role of endothelin-1.

BACKGROUND AND AIMS: There were controversies as to whether endothelin-1 is released after coronary angioplasty. We sought to determine whether endothelin-1 is released after coronary angioplasty and whether oestrogen administration can affect coronary vasomotor tone by reducing endothelin-1 concentrations. METHODS: The study was designed to prospectively investigate 24 consecutive patients scheduled for elective coronary angioplasty. Patients were randomized into two groups according to whether they did not (group 1, n = 12) or did (group 2, n = 12) have intracoronary treatment with oestrogen. Quantitative coronary angiography was monitored at baseline, immediately after successful angioplasty, and 15 min after the last deflation. Blood samples for measuring the levels of endothelin-1 were drawn from the ascending aorta and the coronary sinus simultaneously before angioplasty and 15 min after balloon dilatation. RESULTS: The diameters of the coronary artery at the dilated segments were significantly reduced 15 min after dilation compared with those immediately after dilation in group 1 from 3.20 +/- 0.22 to 2.30 +/- 0.23 mm (P < 0.001), respectively. The vasoconstriction was significantly blunted in group 2. The endothelin-1 levels from the coronary sinus rose significantly, by 29%, 15 min after angioplasty in group 1, which was attenuated after administering oestrogen. Significant correlation was found between the changes of coronary vasomotion of the dilated segment and endothelin-1 levels (r = 0.70, P = 0.01). CONCLUSION: Endothelin-1 is released into the coronary circulation after angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction. The vasoconstriction is attenuated by oestrogen by reducing the endothelin-1 levels. This finding provided a new strategy to treat coronary vasoconstriction after angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed2002

Coupling of c-Src to large conductance voltage- and Ca2+-activated K+ channels as a new mechanism of agonist-induced vasoconstriction.

The voltage-dependent and Ca(2+)-activated K(+) channel (MaxiK, BK) and the cellular proto-oncogene pp60(c-Src) (c-Src) are abundant proteins in vascular smooth muscle. The role of MaxiK channels as a vasorelaxing force is well established, but their role in vasoconstriction is unclear. Because Src participates in regulating vasoconstriction, we investigated whether c-Src inhibits MaxiK as a mechanism for agonist-induced vasoconstriction. Functional experiments in human and rat show that inhibitors of Src (Lavendustin A, PP2) but not inactive compounds (Lavendustin B, PP3) induce a pronounced relaxation of coronary or aortic smooth muscle precontracted with 5-hydroxytriptamine, phenylephrine, or Angiotensin II. Iberiotoxin, a MaxiK blocker, antagonizes the relaxation induced by Lavendustin A or PP2, indicating that c-Src inhibits the Iberiotoxin-sensitive component, likely MaxiK channels. In agreement, coronary muscle MaxiK currents were enhanced by Lavendustin A. To investigate the molecular mechanism of c-Src action on MaxiK channels, we transiently expressed its alpha subunit, hSlo, with or without c-Src in HEK293T cells. The voltage sensitivity of hSlo was right-shifted by approximately 16 mV. hSlo inhibition by c-Src is due to channel direct phosphorylation because: (i) excised patches exposed to protein tyrosine phosphatase (CD45) resulted in a partial reversal of the inhibitory effect by approximately 10 mV, and (ii) immunoprecipitated hSlo channels were recognized by an anti-phosphotyrosine Ab. Furthermore, coexpression of hSlo and c-Src demonstrate a striking colocalization in HEK293T cells. We propose that MaxiK channels via direct c-Src-dependent phosphorylation play a significant role supporting vasoconstriction after activation of G protein-coupled receptors by vasoactive substances and neurotransmitters.

Angiotensin II↗
PubMed1995

Endothelin 1 mediates ex vivo coronary vasoconstriction caused by exogenous and endogenous cytokines.

Treatment of rats with cytokines has been associated with an increase in the circulating levels of endothelin 1 (ET-1). Here we show that administration of tumor necrosis factor alpha (TNF-alpha; 4 micrograms.kg-1) to anesthetized rats caused within 15 min a strong elevation in the circulating levels of ET-1. This was associated with a striking coronary vasoconstriction in hearts from these animals when they were removed and perfused in vitro by the Langendorff technique. This vasoconstriction was largely overcome by treatment with either the endothelin type A (ETA) receptor antagonist FR 139317 or antibody against ET-1. Furthermore, it was mimicked by in vivo exposure to exogenous ET-1. Endogenously produced TNF-alpha may also cause such a coronary vasoconstriction, for treatment with interleukin 2 (600 micrograms.kg-1) produced an increase in coronary perfusion pressure that correlated with the increases in circulating TNF-alpha. This coronary vasoconstriction was substantially reversed by treatment either with antibody against TNF-alpha or with FR 139317. We suggest, therefore, that cytokine-driven changes in the production of ET-1 are key events in the development of vascular pathologies.

Animals↗
PubMed1998

Impaired metabolic modulation of alpha-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle.

The neuronal isoform of nitric oxide synthase (nNOS) is highly expressed in mammalian skeletal muscle, but its functional role has not been defined. NO has been implicated in the local metabolic regulation of blood flow in contracting skeletal muscle in part by antagonizing sympathetic vasoconstriction. We therefore hypothesized that nNOS in skeletal muscle is the source of the NO mediating the inhibition of sympathetic vasoconstriction in contracting muscle. In the mdx mouse, a model of Duchenne muscular dystrophy in which dystrophin deficiency results in greatly reduced expression of nNOS in skeletal muscle, we found that the normal ability of skeletal muscle contraction to attenuate alpha-adrenergic vasoconstriction is defective. Similar results were obtained in mutant mice that lack the gene encoding nNOS. Together these data suggest a specific role for nNOS in the local metabolic inhibition of alpha-adrenergic vasoconstriction in active skeletal muscle.

Animals↗
PubMed2000

Adp-ribosyl cyclase and cyclic ADP-ribose hydrolase act as a redox sensor. a primary role for cyclic ADP-ribose in hypoxic pulmonary vasoconstriction.

Hypoxic pulmonary vasoconstriction is unique to pulmonary arteries and serves to match lung perfusion to ventilation. However, in disease states this process can promote hypoxic pulmonary hypertension. Hypoxic pulmonary vasoconstriction is associated with increased NADH levels in pulmonary artery smooth muscle and with intracellular Ca(2+) release from ryanodine-sensitive stores. Because cyclic ADP-ribose (cADPR) regulates ryanodine receptors and is synthesized from beta-NAD(+), we investigated the regulation by beta-NADH of cADPR synthesis and metabolism and the role of cADPR in hypoxic pulmonary vasoconstriction. Significantly higher rates of cADPR synthesis occurred in smooth muscle homogenates of pulmonary arteries, compared with homogenates of systemic arteries. When the beta-NAD(+):beta-NADH ratio was reduced, the net amount of cADPR accumulated increased. This was due, at least in part, to the inhibition of cADPR hydrolase by beta-NADH. Furthermore, hypoxia induced a 10-fold increase in cADPR levels in pulmonary artery smooth muscle, and a membrane-permeant cADPR antagonist, 8-bromo-cADPR, abolished hypoxic pulmonary vasoconstriction in pulmonary artery rings. We propose that the cellular redox state may be coupled via an increase in beta-NADH levels to enhanced cADPR synthesis, activation of ryanodine receptors, and sarcoplasmic reticulum Ca(2+) release. This redox-sensing pathway may offer new therapeutic targets for hypoxic pulmonary hypertension.

ADP-ribosyl Cyclase↗
PubMed1988

Presence of a serum vasoconstrictive factor following unilateral nephrectomy.

Experimental hypertension is often associated with decreased renal mass and/or impediments to normal renal compensatory growth. This has led to the hypothesis that the renal growth factor (renotropin) is also a vasoconstrictor responsible for elevated blood pressure. Unilateral nephrectomy (uni) is the most popular mechanism to investigate compensatory renal growth. Accordingly, we examined the vasoconstrictive potential of rat sera following uni in order to compare it with serum renotropic activity. Compared to sham-operated (sham) rat sera, uni sera obtained at 24 hours after operation, a point in time when renotropic activity is highest, stimulated the constriction of isolated rat aortic rings significantly more than sham sera, and in a dose-dependent fashion. By paired analysis, the differences in constriction between uni and sham sera were significant at all doses examined. Unlike those obtained at 24 hours, uni sera did not show this response 48 hours, 1 week and 2 weeks after operation, simulating the temporal course of renotropin found in sera after uni. The uni serum factor was not influenced by dialysis suggesting that its molecular weight exceeds 6,000 daltons and that the vasoconstrictive response was not due to electrolyte differences between uni and sham sera. Vasoconstrictive activity was retained after serum passage through Affi-gel blue to remove albumin and after serum was heated in boiling water for 5 minutes. We conclude that a heat resistant serum vasoconstrictive factor with a molecular weight greater than 6,000 daltons arises shortly after uni but disappears once the remaining kidney begins to undergo a physiological compensatory growth response.

Animals↗
PubMed1989

Comparison of pulse oximeters: effects of vasoconstriction and venous engorgement.

The effects of cold-induced vasoconstriction and venous occlusion on the detection of induced hypoxaemia by four pulse oximeters were examined in 10 volunteers. In three further subjects vasoconstriction was maintained until at least one instrument failed to detect the induced hypoxaemia. Time taken to detect hypoxaemia was increased for all instruments to between two and three times the instrument's own control value for both vasoconstriction and venous engorgement (P less than 0.01). There was highly significant variation in detected minimum saturation between the instruments (P less than 0.001). One instrument failed to detect the full extent of desaturation under the experimental conditions and was more likely to fail completely to detect desaturation than the other test instruments when influenced by vasoconstriction (P less than 0.05). Significant impairment in the performance of all the instruments tested occurred in the presence of normal pulse signals. The duration of detected reductions in oxygen saturation was not significantly affected.

Blood Circulation↗
PubMed1995

Perioperative plasma endothelin-1 concentrations and vasoconstriction during prolonged plastic surgical procedures.

The role of endothelin-1, a potent vasoconstrictor released by vascular endothelium, in the vasoconstriction that develops after prolonged operations is not clear. This study was performed in order to determine if there was any relationship between endothelin-1 and the degree of vasoconstriction during prolonged plastic surgery. Plasma concentrations of endothelin-1, skin-forearm temperature gradient (Tgrad), rectal temperature, mean arterial pressure (MAP) and heart rate (HR) were measured at nine predetermined times before, during and after operation in nine women undergoing breast reconstruction with a pedicled transverse rectus abdominis musculocutaneous flap. Development of cutaneous or fat necrosis of the flap was assessed clinically and with ultrasound. Concentrations of endothelin-1 before induction were increased (median 8.9 (25-75% quartiles 5.5-12.5) pg ml-1). During operation they were approximately 3 pg ml-1 and after operation approximately 5 pg ml-1. Tgrad was approximately 4 degrees C before induction and after operation, indicating marked vasoconstriction; during operation it was about zero, indicating vasodilatation. There was a statistically significant correlation between endothelin-1 concentrations and Tgrad (Spearman non-linear correlation) (r = 0.32, P = 0.004) and between endothelin-1 and MAP (r = 0.25, P = 0.02), but not between endothelin-1 and HR or development of minor cutaneous or fat necrosis of the flap (five patients). We conclude that increased plasma concentration of endothelin-1 is associated with the extent of peripheral vasoconstriction.

Adult↗
PubMed1977

Failure of saralasin acetate, a competitive inhibitor of angiotensin II, to diminish alveolar hypoxic vasoconstriction in the dog.

The role of angiotensin II in the pulmonary vasoconstriction induced by alveolar hypoxia was investigated with the competitive inhibitor of angiotensin, saralasin acetate. Unilateral alveolar hypoxia was induced in dogs by ventilation of one lung with 100% N2 through a double lumened endotracheal cannula while maintaining adequate systemic oxygenation by ventilating the other lung with 1oo% O2. Pulmonary perfusion was monitored with 133Xe and external detectors. In 8 dogs perfusion to the test lung on room air before N2 ventilation was 49.2% (SEM +/- 3.8) of total lung perfusion. After 7 min of nitrogen ventilation, perfusion to that lung was 35.6% (SEM +/- 2.9) of cardiac output (P less than 0.001), a reduction of 27.5% (SEM +/- 2.4). After infusion of 6--24 microgram.kg-1/min of saralasin acetate, beginning 2 min before the alveolar hypoxic challenge and continuing through it, unilateral alveolar hypoxia continued to reduce perfusion to that lung by 28.8% (P = 0.6 from control). In 2 dogs a higher infusion of 60 microgram.kg-1/min failed to reduce the alveolar hypoxic vasoconstriction and in 2 dogs a 15 min infusion of 6 microgram.kg-1 of saralasin acetate before alveolar hypoxia and continuing through it, still failed to inhibit alveolar hypoxic vasoconstriction. Thus, no role was demonstrated for angiotensin II in acute alveolar hypoxic vasoconstriction of the dog.

Angiotensin II↗
PubMed2006

Norepinephrine-induced vasoconstriction results in decreased blood volume in dialysis patients.

BACKGROUND: Hypotension during haemodialysis results from an inadequate cardiovascular response to ultrafiltration-induced hypovolaemia. It has been suggested that plasma volume could be increased as a result of systemic vasoconstriction. METHODS: We studied the effect of a norepinephrine (NOR) infusion (30 min), compared with no infusion, on relative blood volume (RBV) in six haemodialysis patients. During infusion we measured RBV, systolic blood pressure (SAP), heart rate (HR), stroke volume index (SI), total peripheral resistance (TPRI), ejection fraction (EF), inferior vena cava diameter (VCD) and core temperature. RESULTS: At the end of the NOR infusion, we observed a significant increase in TPRI (47+/-47% vs 4+/-17%; P<0.01) and SAP (27+/-12% vs 0+/-8%; P<0.01). Norepinephrine-induced vasoconstriction resulted in a significant decrease in RBV (-9+/-3% vs 0+/-1%; P<0.01). No significant changes were seen in SI (-4+/-21% vs 0+/-8%), HR (-5+/-19% vs -4+/-5%), EF (7+/-14% vs -2+/-10%), VCD or temperature. CONCLUSIONS: We conclude that norepinephrine-induced vasoconstriction results in a decrease in RBV. This indicates that improved haemodynamic stability during haemodialysis through vasoconstriction can be accompanied by a decrease in RBV and that part of the variability in blood volume may be due to changes in arterial tone. Such changes must be taken into account if RBV measurements are used to improve the haemodynamic tolerance of dialysis.

Blood Volume↗
PubMed1998

Tramadol reduces the sweating, vasoconstriction, and shivering thresholds.

UNLABELLED: The analgesic tramadol inhibits the neuronal reuptake of norepinephrine and 5-hydroxytryptamine, facilitates 5-hydroxytryptamine release, and activates mu-opioid receptors. Each of these actions is likely to influence thermoregulatory control. We therefore tested the hypothesis that tramadol inhibits thermoregulatory control. Eight volunteers were evaluated on four study days, on which they received no drugs, tramadol 125 mg, tramadol 250 mg, and tramadol 250 mg with naloxone, respectively. Skin and core temperatures were gradually increased until sweating was observed and then decreased until vasoconstriction and shivering were detected. The core temperature triggering each response defined its threshold. Tramadol decreased the sweating threshold by -1.03 +/- 0.67 degrees C microgram-1.mL (r2 = 0.90 +/- 0.12). Tramadol also decreased the vasoconstriction threshold by -3.0 +/- 4.0 degrees C microgram-1.mL (r2 = 0.94 +/- 0.98) and the shivering threshold by -4.2 +/- 4.0 degrees C microgram-1.mL(r2 = 0.98 +/- 0.98). The sweating to vasoconstriction interthreshold range nearly doubled from 0.3 +/- 0.4 degree C to 0.7 +/- 0.6 degree C during the administration of large-dose tramadol (P = 0.04). The addition of naloxone only partially reversed the thermoregulatory effects of tramadol. The thermoregulatory effects of tramadol thus most resemble those of midazolam, another drug that slightly decreases the thresholds triggering all three major autonomic thermoregulatory defenses. In this respect, both drugs reduce the "setpoint" rather than produce a generalized impairment of thermoregulatory control. Nonetheless, tramadol nearly doubled the interthreshold range at a concentration near 200 ng/mL. This indicates that tramadol slightly decreases the precision of thermoregulatory control in addition to reducing the setpoint. IMPLICATIONS: The authors evaluated the effects of the analgesic tramadol on the three major thermoregulatory responses: sweating, vasoconstriction, and shivering. Tramadol had only slight thermoregulatory effects. Its use is thus unlikely to provoke hypothermia or to facilitate fever.

Adult↗
PubMed1992

Painful stimulation minimally increases the thermoregulatory threshold for vasoconstriction during enflurane anesthesia in humans.

Generalized autonomic stimulation enhances hemodynamic responses and may, in a similar fashion, facilitate thermoregulatory responses. We thus tested the hypothesis that painful stimulation increases the central temperature threshold for vasoconstriction during general anesthesia. Healthy volunteers were anesthetized with 1.3% end-tidal enflurane on 2 separate days. On 1 day (randomly assigned), painful stimulation was produced by tetanic electrical stimulation. On the other day, electrical stimulation was not given. Significant thermoregulatory vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. The distal esophageal temperature triggering significant vasoconstriction was considered the thermoregulatory threshold. The threshold was 35.5 +/- 0.8 degrees C during electrical stimulation and 35.1 +/- 0.6 degrees C without stimulation (P = 0.050, 95% confidence interval for the difference = 0-0.7 degree C). These data suggest that thresholds determined in nonsurgical volunteers will be slightly (but not clinically significantly) less than those in operative patients. Similarly, intraoperative vasoconstriction thresholds likely will be slightly less when surgical pain is prevented by simultaneous regional or local analgesia.

Adult↗
PubMed1993

Clonidine comparably decreases the thermoregulatory thresholds for vasoconstriction and shivering in humans.

BACKGROUND: Clonidine stops postoperative shivering, but its underlying mechanism of action is unknown. Clonidine may impair central control of thermoregulation or act on peripheral receptors. Accordingly, the authors tested the hypothesis that clonidine reduces both the vasoconstriction and shivering thresholds, a pattern consistent with central thermoregulatory impairment. METHODS: Seven healthy volunteers participated in the study. Thermoregulatory vasoconstriction was evaluated using forearm minus fingertip, skin-temperature gradients; values exceeding 4 degrees C were considered to be significant vasoconstriction. Systemic oxygen consumption (VO2) was measured with a canopy system. In addition, shivering was qualitatively evaluated using a simple scale, graduated from 0 (no shivering) to 2 (intense shivering). The tympanic membrane temperatures triggering significant vasoconstriction and grade 1 shivering were considered to be the thresholds for the two thermoregulatory responses. Measurements were performed after a 10-min steady state period and during cooling by central venous infusion of Ringer's lactate solution at 4 degrees C. Each subject was evaluated at two sessions, separated by at least 48 h. They were randomly and blindly assigned to received either an intravenous bolus of 75 micrograms clonidine or a placebo before cooling. When the shivering score equaled 2, 75 micrograms clonidine was injected intravenously, and repeated if necessary, to completely stop shivering.

Adult↗