Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vasoconstriction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2000

[Control mechanisms of renal functions: effects of cardiovascular drugs on vasoconstrictive and antinatriuretic stimuli in the in vivo kidney].

The kidney contributes to cardiovascular homeostasis through Na+ and water excretion and renin secretion. Changes in renal functions, therefore, have a close relationship to pathophysiology of cardiovascular diseases and to drug efficacy for them. The functions of the kidney are controlled by the sympathetic nervous system and various kinds of humoral factors and by their complicated interactions. Studies in the intact and working kidney in vivo have been providing physiologically significant information on the renal functions and drug actions. This review, by demonstrating data obtained in our laboratory with experiments in anesthetized dogs in vivo, refers mainly to the neural control of renal functions and renal actions of atrial natriuretic peptide (ANP) and an adenylate cyclase activator NKH477, either of which could be used for the treatment of congestive heart failure. Electrical stimulation of the renal nerves, which could mimic the events during elevation of renal sympathetic nerve activity, induces frequency-dependent renal norepinephrine release, renal vasoconstriction, antinatriuresis and renin secretion. ANP causes potent natriuresis and suppresses the nerve stimulation-induced renin secretion and renal vasoconstriction without affecting the norepinephrine release. Effects of ANP on other vasoconstrictive and antinatriuretic stimuli such as angiotensin II and endothelin are also demonstrated. Renal actions of NKH477 had been unknown, but we revealed that NKH477 elevates renal cAMP level and causes vasodilation and natriuresis. NKH477 also suppresses the nerve stimulation-induced renal vasoconstriction, and thereby blunts the antinatriuresis. The renal actions of these drugs clarified in our study may contribute to their curative effects on congestive heart failure.

Angiotensin II↗
PubMed2004

Training enhances vascular relaxation after chemotherapy-induced vasoconstriction.

PURPOSE: Although evidence is accumulating that suggests regular moderate physical activity improves physiological and psychological well-being of cancer patients undergoing chemotherapy, the mechanisms involved remain unclear. Therefore, the purpose of this study was to determine if exercise training improves endothelium-dependent vasodilation after exposure to the chemotherapeutic agent 5-fluorouracil (5-FU). METHODS: Rats were injected with N-methyl-N-nitrosourea (MNU) and assigned to either exercise (EX; treadmill running, 20-25 m.min(-1) grade, 30 min.d(-1), 5 d.wk(-1) for 8 wk) or sedentary (SED) groups. After the exercise training period, aortic rings were obtained and used to assess contractile and relaxation characteristics. In addition, endothelial nitric oxide synthase (eNOS) protein content and eNOS enzyme activity was determined. RESULTS: Exercise training resulted in increased maximal endothelium-dependent vasorelaxation to acetylcholine (ACh, 1 x 10(-5) M) (SED, 56 +/- 3%; exercise, 71 +/- 5%; P < 0.05) after norepinephrine-induced (1 x 10(-7) M) vasoconstriction. Exposure of aortic rings from each group to increasing concentrations of 5-FU (7 x 10(-5) x 10 M(-3)) resulted in vasoconstriction. Rings obtained from exercise-trained animals demonstrated enhanced vasorelaxation to ACh (1 x 10(-5) M) after 5-FU-induced vasoconstriction compared with rings obtained from SED animals (P < 0.05). In addition, exercise training enhanced eNOS protein content and eNOS activity. CONCLUSION: Exercise training enhances endothelium-dependent vasorelaxation after 5-FU-induced vasoconstriction, and this may be due, at least in part, to an increase in aortic eNOS protein content and activity. Such exercise-induced adaptations may help alleviate chemotherapy-related fatigue observed in cancer patients.

Animals↗
PubMed1983

Estimated affinity of isoproterenol to cardiac chronotropic beta-receptor and of phenylephrine to vasoconstrictive alpha-receptor of the systemic resistance vessels in human borderline hypertension.

There has been yet no report, to our knowledge, which clarified the affinity ("sensitivity") of catecholamines to cardiac chronotropic beta-adrenergic receptor or to vasoconstrictive alpha-adrenergic receptor of skeletal muscle resistance vessels in human borderline hypertension (BHT), using an analysis of the kinetics of the drug-receptor interaction. In the first half of this study, isoproterenol (ISO) infusion test was performed on "normal" subjects (n = 12) and subjects with BHT (n = 10). Dose-response relation was obtained in terms of various doses of ISO and the increments of heart rate (deltaHR) produced by ISO. In the latter half of this study, phenylephrine (PHE) infusion test was carried out in the series of "normal" subjects (n = 5) and subjects with BHT (n = 6), a partly different series from the first series of subjects. Dose-response relation, again, was obtained in terms of various doses of PHE and the increments of total peripheral resistance (deltaTPR) produced by PHE. These relations were displayed on Lineweaver-Burk's plot and the "affinity" of ISO to cardiac chronotropic beta-receptor or that of PHE to vasoconstrictive alpha-receptor of skeletal muscle resistance vessels was estimated, graphically, assuming that 1) drugs were diluted by a volume of body fluid equal to the blood volume which was actually measured in each individual and 2) this concentration of drugs existed around the receptor site, i.e., there was no significant individual variations in terms of the metabolism and the distribution of the drugs. Estimated "affinity" of ISO to cardiac chronotropic beta-receptor was 0.168 +/- 0.014 x 10(4) ml X ug-1 (mean +/- SE, n = 10) in patients with BHT, while it was 0.170 +/- 0.015 x 10(4) (n = 12) in "normal" subjects. Estimated "affinity" of PHE to vasoconstrictive alpha-receptor of skeletal muscle resistance vessels was 0.171 +/- 0.011 x 10(2) ml X ug-1 (n = 6) in patients with BHT, while it was 0.183 +/- 0.012 x 10(2) (n = 5) in "normal" subjects. It is concluded from these data, almost fairly, that there is no difference in terms of the estimated "affinity" of ISO to cardiac chronotropic beta-receptor or that of PHE to vasoconstrictive alpha-receptor between "normal" subjects and patients with BHT. It was also found, in PHE infusion tests, that the plasma adrenaline concentration was significantly higher in patients with BHT than in "normal" subjects, at least at two points of time in the test: a) immediately before PHE infusion, when every individual appeared to be considerably restful and b) at the end of 1-2 min after the completion of the infusion of the largest dose of PHE used.

Adult↗
PubMed1995

Distal vasoconstriction following coronary angioplasty--comparison of emergent and elective PTCA.

To examine the occurrence of distal vasoconstriction following primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction, quantitative coronary angiography was performed during and after acute myocardial infarction. An assessment of coronary artery vasoconstriction was made in patients undergoing primary and elective PTCA. The primary PTCA group was subdivided into two groups based on initial antegrade flow characteristics: group 1 (TIMI grade flow 0/1) and group 2 (TIMI grade flow 2/3). All balloon angioplasties were performed during continuous administration of nitrates. There was no significant difference with relation to lesion diameter, lesion stenosis, or diameter of the left circumflex coronary artery between the acute and chronic phase in both groups. The distal diameter, however, was smaller during the acute phase than in the chronic phase in both groups (1.7 +/- 0.5 vs 2.0 +/- 0.4 mm, p < 0.001; 2.0 +/- 0.4 vs 2.2 +/- 0.3 mm, p < 0.05, respectively). The percent vasoconstrictive response of the distal segment was greater in the primary PTCA group than in the elective PTCA group (11.2 +/- 18.1 vs -1.9 +/- 7.1%, p < 0.0001, respectively). In conclusion, nitrate-resistant coronary artery vasoconstriction following primary PTCA occurs distal to the site of balloon dilation.

Aged↗
PubMed2005

Differences in alpha 1-adrenoceptor subtype-mediated vasoconstriction by tyramine and nerve stimulation in canine splenic artery.

This study was designed to clarify the alpha(1)-adrenoceptor subtypes mediating the vasoconstrictor response to tyramine in isolated and perfused canine splenic artery. It was shown that tyramine potentiated the nerve stimulation-induced second peaked vasoconstriction that was readily suppressed by prazosin treatment. A bolus injection of tyramine (0.01-0.3 micromol) caused a vasoconstriction in a dose-related manner. The tyramine-induced vasoconstriction was inhibited by WB 4101 (10 and 100 nM), an alpha(1A)-and alpha(1D)-adrenoceptor antagonist, in a concentration-related manner. Neither BMY 7378 (100 nM), a selective alpha(1D)-adrenoceptor antagonist, nor chloroethylclonidine (60 microM), an alpha(1B)- and alpha(1D)-adrenoceptor antagonist, affected the tyramine-induced response. The results indicate that the noradrenaline released by tyramine may diffuse to the extrajunctional cleft, and thus it activates the extrajunctional alpha(1A)-adrenoceptors, because nerve stimulation-evoked second peaked vasoconstrictions were markedly inhibited by chloroethylclonidine but not by WB 4101.

Adrenergic Fibers↗
PubMed1992

Vasoconstriction by angiographic contrast media in isolated canine arteries.

To study the mechanism of the pain produced by contrast media (CM) in peripheral arteriography, we examined the direct effects of low concentrations (1.85-100 mg I/ml) of CM (diatrizoate, iopamidol, ioxaglate, and iotrolan) on helically cut strips of canine blood vessels taken from six different regions. We found that: (a) low concentrations of CM induced vasoconstriction. (b) This occurred immediately after the application of CM and produced sustained constriction. (c) The constriction produced in arteries was dose-dependent. (d) The production and intensity of constriction in the arterial strips differed as follows: cranial mesenteric artery > renal artery > femoral artery > common carotid artery > thoracic aorta > coronary artery. The effects of the CM were, in order of magnitude: diatrizoate > iopamidol > ioxaglate > iotrolan. Differences between CM corresponded with the differences in osmolality of the CM solutions. (e) Low concentrations of meglumine and mannitol also produced vasoconstriction. (f) Constriction caused by all drug samples used was reversible, but the process of relaxation to the original tension was much slower in CM-treated arterial strips than in the other strips. From these results, we confirmed that the incidence and degree of vasoconstriction produced by all drug samples used in this experiment depended on solution osmolality, rather than on chemotoxicity or ionicity. We discuss the physiological mechanism of these results and stress the importance of CM hyperosmolality in vasoconstriction and vascular pain production.

Animals↗
PubMed2005

Redox activation of intracellular calcium release channels (ryanodine receptors) in the sustained phase of hypoxia-induced pulmonary vasoconstriction.

Hypoxia-induced pulmonary vasoconstriction (HPV) is an important adaptive process that remains incompletely understood. In preconstricted rat pulmonary arteries (inner diameter, 250 to 400 microm), hypoxia (pO2 approximately 10 mm Hg) induces an initial transient phase and a more slowly developing sustained phase of vasoconstriction. Since the release of calcium ions (Ca2+) from intracellular stores by redox-sensitive intracellular Ca2+ release channels known as ryanodine receptors (RyRs) in pulmonary arterial smooth-muscle cells (PASMCs) may play a role in HPV, and considerable evidence now supports that levels of reactive oxygen species (ROS) are paradoxically increased in PASMC under hypoxia, we investigated whether redox activation of RyRs by ROS may transduce HPV. By reverse transcriptase-polymerase chain reaction, we found that all three RyR isoforms are expressed in rat pulmonary arteries and in PASMCs. The sustained phase, but not the transient phase, of HPV can be prevented by pretreating pulmonary arteries with RyR inhibitors ryanodine (200 micromol/L) or dantrolene (50 micromol/L). The addition of dantrolene, ryanodine or the thiol-reducing agent dithiothreitol (1 mmol/L) during the sustained phase of HPV reversed the hypoxic vasoconstriction. In contrast, the superoxide scavenger nitroblue tetrazolium (500 nmol/L) prevented further hypoxic pulmonary vasoconstriction during the sustained phase of HPV but did not reverse it. Taken together, our data suggest that redox activation of RyRs by ROS has an important role in transducing the sustained contraction of pulmonary arteries under hypoxia.

Animals↗
PubMed1997

Effect of theophylline on hypoxic pulmonary vasoconstriction in awake rats.

Whether or not theophylline inhibits hypoxic pulmonary vasoconstriction in vivo still remains uncertain. We therefore studied the effect of theophylline on hypoxic pulmonary vasoconstriction in awake rats. Two days before hemodynamic measurement, indwelling catheters were placed. Animals were divided into three groups; Group-H (20 mg/kg of theophylline), Group-L (8 mg/kg of theophylline), Group-S (saline). At the day of hemodynamic measurement, animals breathed 21% and 10% O2 gas. [{Pulmonary vascular resistance (PVR) during 10% O2-PVR during 21% O2}/PVR during 21% O2] x 100 was termed as hypoxic pulmonary vasoconstriction (HPV). The first HPV measurement was followed without drug administration and then the second HPV measurement was performed with theophylline or saline infusion. Post-theophylline HPV was divided by pre-theophylline HPV to normalize individual variation. Ratio of post-theophylline HPV to pre-theophylline HPV was 0.49 +/- 0.10, 0.77 +/- 0.23, 1.06 +/- 0.33 in Group -H, -L, -S, respectively (means +/- S.E.M). Ratio of post-theophylline HPV to pre-theophylline HPV was significantly less in Group-H than in Group-S. This result suggests that theophylline used in the present study (18.6-26.9 micrograms/ml) attenuates hypoxic pulmonary vasoconstriction in the unanesthetized rat.

Animals↗
PubMed2001

Renal cortical vasoconstriction contributes to development of salt-sensitive hypertension after angiotensin II exposure.

Rats that are administered angiotensin II (AngII) for 2 wk develop persistent salt-sensitive hypertension, which can be prevented by the immunosuppressor mycophenolate mofetil (MMF) given during the AngII infusion. This study examined the contribution of glomerular hemodynamics (GFR dynamics) in the post-AngII hypertensive response to a high-salt diet (HSD) and the effect of MMF treatment. During AngII administration, rats developed severe hypertension (systolic BP [SBP], 185 +/- 3.9 mmHg), proteinuria, afferent and efferent vasoconstriction, and glomerular hypertension. Rats that received AngII+MMF showed similar responses to AngII; however, they developed lower proteinuria (P < 0.05). At 2 wk, AngII was withdrawn and SBP returned toward normal. Rats were then placed on an HSD (4% NaCl), resulting in a progressive increase in SBP (155 +/- 8.2 mmHg at week 1 and 163 +/- 4.5 mmHg at week 5). GFR dynamic alterations persisted after AngII was stopped, i.e., afferent and efferent vasoconstriction, decreased glomerular plasma flow and single-nephron GFR, and lower ultrafiltration coefficient. These changes correlated with the thickening of the afferent arteriole and with focal tubulointerstitial injury. In the AngII+MMF group, SBP remained unchanged throughout the HSD period (146 +/- 2.3 mmHg at week 1 and 148 +/- 4.4 mmHg at week 5) in association with less afferent arteriolar thickening and tubulointerstitial injury. Single-nephron GFR, glomerular plasma flow, efferent resistance, and ultrafiltration coefficient returned to normal with a significant reduction in afferent resistance. These results suggest a critical role of cortical vasoconstriction in salt-sensitive hypertension. The MMF-induced prevention of these changes suggests that immune mechanisms are involved in the vasoconstrictive response.

Angiotensin II↗
PubMed1992

Exaggerated sensitivity to NE-induced vasoconstriction in IDDM patients with microalbuminuria. Possible etiology and diagnostic implications.

Increased urinary albumin excretion rate (AER) in the microalbuminuric phase of diabetic nephropathy has been attributed to intraglomerular hypertension. This could be caused by constriction of efferent glomerular arterioles, which carry alpha-adrenoceptors. We tested the hypothesis that insulin-dependent diabetes mellitus (IDDM) patients with microalbuminuria are hypersensitive to vasoconstriction induced by norepinephrine (NE). We studied 15 IDDM patients with microalbuminuria (AER 32-295 mg/24 h), 13 IDDM patients with normal AER (5-24 mg/24 h), and 9 nondiabetic subjects (AER 8-22 mg/24 h). All were normotensive. NE-induced vasoconstriction was measured in dorsal hand veins, which carry alpha-receptors similar to those of glomerular efferent arterioles. Vein diameter was measured with a linear displacement probe during a stepped NE infusion (1-32 ng/min) into the vein, and venoconstriction was expressed as a percentage of the maximum passively distended venous diameter. Microalbuminuric IDDM patients exhibited significantly greater vasoconstriction (P less than 0.005) at all NE infusion rates than both other groups. The NE infusion rate producing 50% of maximal venoconstriction (ED50) in the microalbuminuric IDDM group (median 1.1 ng/min, range 0.2-25.2 ng/min) was significantly less than in both the normoalbuminuric IDDM group (median 12.5 ng/min, range 4.9-40.5 ng/min, P = 0.00007) and the nondiabetic group (median 17.7 ng/min, range 5.9-42.2 ng/min, P = 0.0003). Dose-response curves and ED50 did not differ significantly between normalbuminuric IDDM and nondiabetic groups. IDDM patients with microalbuminuria are hypersensitive to NE-induced vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Assessment of vasoconstrictive potential of D-lysergic acid using an isolated bovine lateral saphenous vein bioassay.

Vasoconstriction has been associated with several symptoms of fescue toxicosis thought to be alkaloid induced. Lysergic acid, an ergot alkaloid, has been proposed as a toxic component of endophyte-infected tall fescue. The objective of this study was to examine the vasoconstrictive potential of D-lysergic acid using a bovine lateral (cranial branch) saphenous vein bioassay. Before testing lysergic acid, validation of the bovine lateral saphenous vein bioassay for use with a multimyograph apparatus was conducted using a dose-response to norepinephrine to evaluate the effects of limb of origin (right vs. left) and overnight storage on vessel contractile response. Segments (2 to 3 cm) of the cranial branch of the lateral saphenous vein were collected from healthy mixed breed cattle (n = 12 and n = 7 for the lysergic acid and norepinephrine experiments, respectively) at local abattoirs. Tissue was placed in modified Krebs-Henseleit, oxygenated buffer and kept on ice or stored at 2 to 8 degrees C until used. Veins were trimmed of excess fat and connective tissue, sliced into 2- to 3-mm sections, and suspended in a myograph chamber containing 5 mL of oxygenated Krebs-Henseleit buffer (95% O2, 5% CO2; pH = 7.4; 37 degrees C). Tissue was allowed to equilibrate at 1 g of tension for 90 min before initiation of treatment additions. Increasing doses of norepinephrine (1 x 10(-8) to 5 x 10(-4) M) or lysergic acid (1 x 10(-11) to 1 x 10(-4) M) were administered every 15 min after buffer replacement. Data were normalized as a percentage of the contractile response induced by a reference dose of norepinephrine. Veins from both left and right limbs demonstrated contractions in a dose-dependent manner (P < 0.01) but did not differ between limbs. There were no differences in dose-response to norepinephrine between tissue tested the day of dissection and tissue tested 24 h later. Exposure of vein segments to increasing concentrations of lysergic acid did not result in an appreciable contractile response until the addition of 1 x 10(-4) M lysergic acid (15.6 +/- 2.3% of the 1 x 10(-4) M norepinephrine response). These data indicate that only highly elevated concentrations of lysergic acid result in vasoconstriction. Thus, in relation to the symptoms associated with vasoconstriction, lysergic acid may only play a minor role in the manifestation of fescue toxicosis.

Animals↗
PubMed1981

Vasoconstriction and d-amphetamine-induced hypothermia.

The hypothermic effect of d-amphetamine was investigated in rats in which vasoconstriction or vasodilation was induced by pharmacological agents: aramine as vasoconstrictor and neprasol as vasodilator. The d-amphetamine-induced hypothermia was enhanced by both drugs among rats kept at 4 degrees C, and both drugs were unable to modify the d-amphetamine-induced hypothermia. These results indicate that although vasoconstriction and vasodilation play a major role in thermoregulation, d-amphetamine-induced hypothermia is not mediated peripherally by vasoconstriction. Since changes in basal metabolic rate, motor activity, food intake and vasoconstriction are not the peripheral mechanisms by which d-amphetamine induced hypothermia, the mechanisms is still unknown.

Animals↗
PubMed1994

Role of angiotensin II in renal vasoconstriction with acute hypoxemia and hypercapnic acidosis in conscious dogs.

To evaluate the role of renin-angiotensin in the renal vasoconstriction with combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied eight conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 mEq/24 h x 4 days). The animals were studied during combined acute hypoxemia and hypercapnic acidosis (PaO2 34 +/- 1 mm Hg, PaCo2 57 +/- 1 mm Hg, pH 7.20 +/- 0.01) preceded by 80 min of acute hypoxemia (PaO2 34 +/- 1 mm Hg) during: (a) intrarenal infusion of vehicle (n = 8); or (b) intrarenal administration of the angiotensin II antagonist [Sar1,Ala8]-AII, 70 ng kg-1 min-1 (n = 8). The combination of acute hypoxemia and hypercapnic acidosis resulted in diminished effective renal plasma flow and increased renal vascular resistance during intrarenal vehicle infusion. Intrarenal [Sar1,Ala8]-AII did not abolish the renal vasoconstriction in the initial 20 min of this combined blood gas derangement but resulted in a more prompt return of the renal vascular variables toward control levels with continuation of the blood gas derangement for an additional 20 min, suggesting a role for angiotensin in renal vasoconstriction. These observations suggest that while renin-angiotensin may not mediate the initial renal vasoconstriction in the first 20 min of combined acute hypoxemia and hypercapnic acidosis, in uninephrectomized conscious dogs, it attenuates the spontaneous recovery of renal hemodynamic variables to baseline as the blood gas derangement continues.

Acidosis, Respiratory↗
PubMed1999

Modulatory effect of blood cells on hypoxic vasoconstriction response and nitric oxide release in rat lungs.

In this study, we investigated the modulatory effects of different types of blood cells on hypoxic pulmonary vasoconstrictive (HPV) response and nitric oxide (NO) release in isolated rat lungs. The lungs were perfused at a constant flow with physiologic saline solution (PSS). The changes in pulmonary arterial pressure (PAP) and NO release were observed. Two hypoxic challenges with a 5% CO2-95% N2 gas mixture were carried out in each experiment. Hypoxia induced pulmonary vasoconstriction, as reflected by an increase in PAP (0.88 +/- 0.22 cmH2O). At the same time, NO (342.9 +/- 78.3 mv) release from the lungs was also increased. Addition of white blood cells (WBCs, 0.70 to 0.88 x 10(5)/mL), platelets (1.48 to 1.96 x 10(5)/mL), or red blood cells (RBCs, 4.6 to 6.6 x 10(5)/mL) into the perfusate produced different effects on PAP and NO changes. WBCs decreased the pulmonary vasoconstriction response and this was accompanied by an increase in NO release. Platelets had no significant effects on either PAP or NO. RBCs significantly potentiated the PAP increase and attenuated the NO release. The results indicate that NO release during hypoxia tends to offset pulmonary vasoconstriction and that NO release and HPV response are modulated by different cell elements.

Animals↗
PubMed2000

[Involvement of nitrogen oxide in the cerebral vasoconstriction during respiration with high pressure oxygen].

High pressure oxygen evokes a cerebral vasoconstriction and diminishes cerebral blood flow with the aid of mechanisms which are not yet sufficiently studied. We were checking a hypothesis that the hyperbaric oxygen (HBO2) inactivates cerebral nitrogen oxide (NO), interrupts its basal relaxing effect, and evokes a vasoconstriction. In our experiments, HBO2 decreased cerebral blood flow depending on the pressure. Inhibiting the NO-synthase weakened basal vasorelaxation in breathing with atmosphere air and eliminated the vasoconstriction in exposure to the HBO2. Inactivation of O2 prevented the HBO2-induced vasoconstriction. The data obtained reveal that diminishing of cerebral blood flow in HBO is related to the NO inactivation and weakening of its basal vasorelaxing effect. Possible mechanisms of the NO inactivation may involve its reaction with oxygen and superoxide anion which lead to diminishing of the tissue NO concentration and weakening of its vasorelaxing effect.

Anesthesia↗
PubMed1992

Limited heat transfer between thermal compartments during rewarming in vasoconstricted patients.

Thermoregulatory vasoconstriction may serve to separate and limit heat transfer between peripheral and central thermal compartments, in effect providing a thermal buffer for central temperature. We hypothesized that thermoregulatory vasoconstriction would limit heat transfer to the central compartment in patients warmed cutaneously. Hypothermic patients (central temperatures < 35 degrees C) recovering from surgery were randomly assigned to receive forced-air warming (n = 6) or warmed cotton blankets (n = 6). The forced-air warmer delivers approximately 50 W of heat, compared to a heat loss of approximately 50 W with warmed cotton blankets. Despite a significantly greater increase in mean skin-surface temperature with forced-air warming, central temperature in the two groups did not significantly differ. All patients vasoconstricted and there was no difference in oxygen consumption between groups. These data confirm that thermoregulatory vasoconstriction limits heat transfer from peripheral to central thermal compartments and impedes skin surface warming of the body core.

Blood Pressure↗
PubMed1992

[Effect of halothane on the peripheral cutaneous vasoconstriction and shivering induced by internal body cooling in rabbits].

Although suppression of thermoregulatory mechanisms by anesthetics is generally assumed, the extent to which thermoregulatory responses are active during general anesthesia is not known. To evaluate the effect of anesthetics on thermoregulation, we investigated the threshold body core temperatures to induce peripheral cutaneous vasoconstriction and shivering in spontaneously breathing rabbits. Rabbits are anesthetized with halothane at 0.05, 0.2 and 0.4 MAC (minimum alveolar concentration). Internal whole body cooling was performed by perfusing the cool water through an intestinal U-shaped thermode placed in the colon. Core (esophagus) and peripheral (ear) temperatures were measured with thermistors. The esophageal temperatures at the beginning of peripheral cutaneous vasoconstriction and shivering induced by internal whole body cooling were determined. Peripheral cutaneous vasoconstriction was not significantly affected by halothane. However, the incidence of shivering was significantly decreased by halothane dose-dependently. Threshold of shivering (37.3 +/- 0.8 degrees C) was significantly lower than that of peripheral cutaneous vasoconstriction (38.9 +/- 1.1 degrees C). We conclude that the halothane can exert an influence on shivering.

Animals↗
PubMedDate not supplied

Nitric oxide effect on 5-hydroxytryptamine-induced vasoconstrictions of isolated smooth muscle.

The aim of the present study was to investigate a nitric oxide (NO) involvement in the mediation of a 5-HT-induced vasoconstriction response in the rat portal vein in vitro. Isolated rat portal vein segments were placed in organ baths for isometric force measurement. 5-HT (3 x 10(-8) M-3 x 10(-4) contracted portal vein preparations (EC50 = 7 x 10(-7) M) in a concentration-dependent manner. The vasoconstriction induced by 5-HT was significantly increased in endothelium-denuded vessels. Pretreatment with Nomega-nitro-L-arginine methyl ester (L-NAME 100 microM) enhanced the contractive response to 5-HT either in intact or endothelium-denuded vessels. However, ketanserin (0.1 microM) abolished 5-HT-induced vasoconstrictions (EC50 = 4.6 x 10(-8) M). Furthermore, a non-selective 5-HT(1B/D) receptor agonist, sumatriptan (1 x 10(-10) M-1 x 10(-5) M), induced a reduction of spontaneous rhythmic contractions also in endothelium-intact vessels. However, 5-HT- induced vasoconstriction was unaffected by propranolol (10 microM). The data support the hypothesis of the existence of serotonergic innervations modulating the contractility of vascular smooth muscle. These findings are consistent with the hypothesis that the vasoconstrictor activity of 5-HT in smooth muscle was mediated by activation of 5-HT(1B/D) and 5-HT(2B) receptor subtypes involving the endothelium-dependent mechanism.

Animals↗