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PubMed1998

The effect of prolonged inhaled nitric oxide on pulmonary vasoconstriction in rats.

UNLABELLED: Down-regulation of the endogenous nitric oxide (NO) pathway may explain rebound pulmonary hypertension after discontinuation of inhaled NO. We determined whether the prolonged administration of inhaled NO increases pulmonary vasoconstriction, which may occur from decreased endogenous NO. Rats were placed in normoxic (N; 21% O2) or hypoxic (H; 10% O2) chambers with or without inhaled NO (20 ppm) for 1 or 3 wk. Immediately after or 24 h after discontinuation of NO, vasoconstrictive responses were determined in isolated lungs to acute hypoxia (HPV; 0% O2 for 6 min), angiotensin II (0.05 microg), and the thromboxane analog U-46619 in the presence and absence of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 100 microM). Inhaled NO did not alter HPV or angiotensin II vasoconstriction in the N group immediately after or 24 h after discontinuation of NO. In the H group, inhaled NO decreased HPV but had no effect on the angiotensin II vasoconstriction compared with H alone. Inhaled NO did not alter the response to L-NAME. Inhaled NO did not alter, whereas L-NAME significantly decreased, the dose of U-46619 required to increase the pulmonary pressure by 10 mm Hg. In conclusion, prolonged inhaled NO decreased or did not alter HPV and did not alter vasoconstriction secondary to angiotensin II, U-46619, or L-NAME in N and H rats. These results suggest that prolonged inhaled NO does not increase pulmonary vasoconstriction, as would be expected from down-regulation of endogenous NO. IMPLICATIONS: High pulmonary pressure has been observed clinically after discontinuation of inhaled NO. This rat study suggests that 1-3 wk of inhaled NO does not increase pulmonary vasoconstriction, as would be expected from decreasing the endogenous vasodilator NO.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Barbiturate anesthetics inhibit thromboxane-, potassium-, but not angiotensin-induced pulmonary vasoconstriction.

Administration of the oxidant lipid peroxide tertiary butyl hydroperoxide (t-bu-OOH) in the isolated rabbit lung leads to acute pulmonary vasoconstriction, which is caused by the synthesis of thromboxane. The inhalational anesthetics, halothane, nitrous oxide, and cyclopropane, markedly enhance t-bu-OOH-induced pulmonary vasoconstriction and thromboxane production. The effects of the intravenous (iv) barbiturates thiopental and pentobarbital on t-bu-OOH-induced vasoconstriction were studied. Thiopental completely and pentobarbital partially blocked t-bu-OOH-induced vasoconstriction. Thiopental inhibited t-bu-OOH-induced synthesis of thromboxane and prostacyclin but pentobarbital did not. This inhibitory action of thiopental may be due to its antioxidant properties because similar inhibition has been observed of t-bu-OOH-induced thromboxane production with the antioxidants, vitamin E, or butylated hydroxylanisole. Thiopental and pentobarbital also inhibited the vasoconstriction induced by a thromboxane analog, epoxymethano prostaglandin H2 (U46619). Finally, both barbiturates partially inhibited the pulmonary vasoconstriction caused by potassium chloride, which requires calcium entry, but they did not inhibit the constriction caused by angiotensin II, which does not require calcium entry. These results suggest that pentobarbital and thiopental may block pulmonary vasoconstriction by inhibiting calcium entry.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Thermoregulatory thresholds for vasoconstriction in pediatric patients anesthetized with halothane or halothane and caudal bupivacaine.

The thermoregulatory threshold for vasoconstriction has been studied in infants and children given isoflurane, but not in those given halothane anesthesia. More importantly, the effect of vasoconstriction on central temperature in pediatric patients remains unknown. Also unknown is the effect of caudal analgesia on vasoconstriction thresholds. Accordingly, in the first portion of this study, we determined the central thermoregulatory threshold in 23 infants and children given approximately 0.6% halothane and caudal anesthesia for abdominal surgery. Patients were prospectively assigned to one of four weight groups: 5-10, 10-20, 20-30, and 30-50 kg. The threshold was considered the central temperature triggering peripheral vasoconstriction, and significant vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. Thresholds were similar (approximately 35.7 degrees C) in each study group, suggesting that thermoregulatory responses to halothane anesthesia are similar in infants and children of differing weights. However, they were higher than expected based on the previously reported thresholds in pediatric patients given isoflurane anesthesia. After peripheral vasoconstriction, central temperature continued to decrease in patients weighing more than 30 kg but remained constant or increased slightly in the others. These data suggest that thermoregulatory responses are more effective in infants and small children than in bigger children or adults. In the second part of this study we evaluated the effect of caudal analgesia on the thermoregulatory threshold for vasoconstriction. Children undergoing hypospadias repair were anesthetized with halothane (0.9%) and oxygen. Following induction, they were randomly assigned to caudal analgesia (n = 7) or penile nerve block (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Caudal↗
PubMed1993

The threshold for thermoregulatory vasoconstriction during nitrous oxide/isoflurane anesthesia is lower in elderly than in young patients.

BACKGROUND: Thermoregulatory vasoconstriction minimizes further core hypothermia during anesthesia. Elderly patients become more hypothermic during surgery than do younger patients, and take longer to rewarm postoperatively. These data indicate that perianesthetic thermoregulatory responses may be especially impaired in the elderly. Accordingly, the authors tested the hypothesis that the thermoregulatory threshold for vasoconstriction during nitrous oxide/isoflurane anesthesia is reduced more in elderly than in young patients. METHODS: The authors studied 12 young patients aged 30-50 yr and 12 elderly patients aged 60-80 yr. All were undergoing major orthopedic or open abdominal surgery. Anesthesia was induced with thiopental and fentanyl, and maintained only with nitrous oxide (70%) and isoflurane (0.6-0.8%). Core temperature was measured in the distal esophagus. Fingertip vasoconstriction was evaluated using forearm minus fingertip, skin-temperature gradients. A gradient of 4 degrees C identified significant vasoconstriction, and the core temperature triggering vasoconstriction identified the thermoregulatory threshold. RESULTS: The vasoconstriction threshold was significantly less in the elderly patients (33.9 +/- 0.6 degree C) than in the younger ones (35.1 +/- 0.3 degrees C) (P < 0.01). The gender distribution, weight, and height of the elderly and young patients did not differ significantly. The end-tidal isoflurane concentration at the time of vasoconstriction did not differ significantly in the two groups. CONCLUSIONS: These data indicate that thermoregulatory responses in the elderly are initiated at temperatures approximately 1.2 degrees C less than that in younger patients. Thus, it is likely that elderly surgical patients become more hypothermic than do younger patients, at least in part, because they fail to trigger protective thermoregulatory responses.

Adult↗
PubMed1999

Selective iNOS inhibition attenuates acetylcholine- and bradykinin-induced vasoconstriction in lipopolysaccharide-exposed rat lungs.

BACKGROUND: Nonselective nitric oxide synthase (NOS) inhibition has detrimental effects in sepsis because of inhibition of the physiologically important endothelial NOS (eNOS). The authors hypothesized that selective inducible NOS (iNOS) inhibition would maintain eNOS vasodilation but prevent acetylcholine- and bradykinin-mediated vasoconstriction caused by lipopolysaccharide-induced endothelial dysfunction. METHODS: Rats were administered intraperitoneal lipopolysaccharide (15 mg/kg) with and without the selective iNOS inhibitors L-N6-(1-iminoethyl)-lysine (L-NIL, 3 mg/kg), dexamethasone (1 mg/kg), or the nonselective NOS inhibitor Nomega-nitro-L-arginine methylester (L-NAME, 5 mg/kg). Six hours later, the lungs were isolated and pulmonary vasoreactivity was assessed with hypoxic vasoconstrictions (3% O2), acetylcholine (1 microg), Biochemical Engineering, and bradykinin (3 microg). In additional lipopolysaccharide experiments, L-NIL (10 microM) or 4-Diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 100 microM), a selective muscarinic M3 antagonist, was added into the perfusate. RESULTS: Exhaled nitric oxide was higher in the lipopolysaccharide group (37.7+/-17.8 ppb) compared with the control group (0.4+/-0.7 ppb). L-NIL and dexamethasone decreased exhaled nitric oxide in lipopolysaccharide rats by 83 and 79%, respectively, whereas L-NAME had no effect. In control lungs, L-NAME significantly decreased acetylcholine- and bradykinin-induced vasodilation by 75% and increased hypoxic vasoconstrictions, whereas L-NIL and dexamethasone had no effect. In lipopolysaccharide lungs, acetylcholine and bradykinin both transiently increased the pulmonary artery pressure by 8.4+/-2.0 mmHg and 35.3+/-11.7 mmHg, respectively, immediately after vasodilation. L-NIL and dexamethasone both attenuated this vasoconstriction by 70%, whereas L-NAME did not. The acetylcholine vasoconstriction was dose-dependent (0.01-1.0 microg), unaffected by L-NIL added to the perfusate, and abolished by 4-DAMP. CONCLUSIONS: In isolated perfused lungs, acetylcholine and bradykinin caused vasoconstriction in lipopolysaccharide-treated rats. This vasoconstriction was attenuated by administration of the iNOS inhibitor L-NIL but not with L-NAME. Furthermore, L-NIL administered with lipopolysaccharide preserved endothelium nitric oxide-dependent vasodilation, whereas L-NAME did not.

Acetylcholine↗
PubMed2003

Systemically administered alpha2-agonist-induced peripheral vasoconstriction in humans.

BACKGROUND: alpha(2)-Adrenoceptors mediate both sympatholytic and vasoconstrictive hemodynamic effects. The goal of this study was to profile the peripheral vasoconstrictive effects of a selective alpha(2)-adrenoceptor agonist in isolation from the sympatholytic effects it also induces. METHODS: The authors administered increasing plasma target concentrations of dexmedetomidine (0.075, 0.15, 0.3, and 0.6 ng/mL) or saline placebo to healthy young volunteers in whom the sympatholytic effects of the drug were attenuated in one of two ways: general anesthesia (propofol-alfentanil-nitrous oxide) or axillary brachial plexus block. Measurements were made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmitted through a finger (LTF) and hemodynamic variables. Measurements made before and during the four steps of infusion were compared by repeated-measures ANOVA. RESULTS: In anesthetized volunteers, all concentrations of dexmedetomidine increased LTF (vasoconstriction) and systolic blood pressure (P < 0.001 for both), whereas placebo did not. In awake volunteers, all concentrations decreased systolic blood pressure (P < 0.001). Concentrations of 0.15, 0.3, and 0.6 ng/mL decreased LTF (vasodilation) in the neurally intact hand; in contrast, the same concentrations increased LTF (vasoconstriction) in the sympathectomized hand (P < 0.001 for both). CONCLUSIONS: The results of this study are the first to characterize the lower end of the dose-response curve for vasoconstriction induced by dexmedetomidine. By denervating the vascular bed of interest or by decreasing sympathetic nervous system activity, the authors were able to observe vasoconstriction induced by a systemically administered alpha(2)-agonist with minimal interference from the sympatholytic effects of the drug.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1993

Endothelin-1 does not mediate acute hypoxic pulmonary vasoconstriction in the intact newborn lamb.

The mechanisms by which acute alveolar hypoxia induces pulmonary vasoconstriction remain unclear. Previous studies suggest that hypoxia-induced vasoconstriction is endothelium-dependent and is associated with the release of endothelin-1 (ET-1), a potent vasoactive paracrine hormone produced by vascular endothelial cells. The vasoconstrictive effects of ET-1 are likely to be mediated by ETA receptors located on vascular smooth-muscle cells. BQ-123 is a selective ETA receptor antagonist. To determine the role of ET-1 and ETA receptors on resting tone and hypoxic pulmonary vasoconstriction, we studied the effects of ET-1 and BQ-123 at rest and during hypoxia-induced pulmonary vasoconstriction in 12 intact newborn lambs (< 1 week old). At rest, the intrapulmonary infusion of BQ-123 did not change resting pulmonary arterial pressure but completely blocked the rapid increase in pulmonary artery pressure produced by high doses of ET-1 (2,000 ng/kg) (23.0 +/- 10.8% versus -12.6 +/- 27.5%; p < 0.05). During mechanical ventilation there was no difference in the increase in mean pulmonary arterial pressure and pulmonary vascular resistance induced by alveolar hypoxia before and after BQ-123 (34.0 +/- 8.9% versus 30.5 +/- 10.9% and 25.3 +/- 11.6% versus 35.2 +/- 22.4%). This study suggests that the pulmonary vasoconstrictive effects of ET-1 are mediated by ETA receptors and that ET-1 does not mediate acute hypoxic pulmonary vasoconstriction in intact newborn lambs.

Acute Disease↗
PubMed1997

Mechanism of resistance to alpha-adrenergic receptor antagonists of renal nerve stimulation-induced vasoconstriction at low frequencies.

To determine why renal vasoconstriction elicited by periarterial nerve stimulation (RNS) at lower frequencies (< 4 Hz) is resistant to alpha-adrenergic receptor blockade in the rat kidney, we reevaluated the effect of alpha-receptor antagonists on the vasoconstrictor response to norepinephrine (NE) and to RNS and on the release of adrenergic transmitter. The alpha-receptor antagonist prazosin (PZ) at 0.2 and 7 nM reduced the vasoconstrictor response to NE, and 2.4 microM PZ abolished it. PZ (0.2 or 7 nM) reduced RNS-induced vasoconstriction without altering the fractional tritium overflow. PZ (2.4 microM) enhanced fractional tritium overflow and reduced the vasoconstrictor response to RNS at 2-10 Hz, but not at 0.5 or 1 Hz. The effect of 0.2 nM PZ to reduce RNS-induced vasoconstriction was reversed by increasing the concentration to 2.4 microM. Corynanthine (COR; 2.6 microM), a preferential alpha-receptor blocker, or phenoxybenzamine (PBZ; 30 nM) abolished the vasoconstrictor response to NE but only partially reduced response to RNS and enhanced the fractional tritium overflow. Rauwolscine (RW; 2.5 nM), a preferential alpha 2-receptor antagonist, did not alter the vasoconstrictor response to NE but potentiated RNS-induced vasoconstriction and fractional tritium overflow. RW (7.7 microM) inhibited NE-induced vasoconstriction but potentiated the vasoconstrictor response to RNS and fractional tritium overflow. PZ (7 nM) abolished the potentiation by RW and reduced the vasoconstrictor response to RNS. These data suggest that a component of RNS-induced vasoconstriction in the rat kidney is attributable to co-release of a nonadrenergic transmitter with NE. The diminished effect of alpha-receptor antagonists at higher concentrations (e.g., PZ 2.4 microM) to reduce RNS-induced vasoconstriction is caused by their prejunctional action to enhance co-release of the nonadrenergic transmitter.

Adrenergic Antagonists↗
PubMed1998

Nitric oxide mediates contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle.

1. Sympathetic vasoconstriction is attenuated by metabolic events in contracting rat skeletal muscle, in part by activation of ATP-sensitive potassium (KATP) channels. However, the specific metabolites in contracting muscle that open KATP channels are not known. We therefore asked if contraction-induced attenuation of sympathetic vasoconstriction is mediated by the endogenous vasodilators nitric oxide (NO), adenosine, or prostaglandins PGI2 or PGF2, all of which are putative KATP channel openers. 2. In anaesthetized rats, hindlimb contraction alone significantly attenuated the vasoconstrictor responses to lumbar sympathetic nerve stimulation. Inhibition of NO synthase with N-nitro-L-arginine methyl ester (L-NAME, 5 mg kg-1, i.v.) partially reversed this effect of contraction, resulting in enhanced sympathetic vasoconstriction in contracting hindlimb. Subsequent treatment with the KATP channel blocker glibenclamide (20 mg kg-1, i.v.) had no further effect on sympathetic vasoconstriction in contracting hindlimb. 3. This effect of L-NAME to partially reverse contraction-induced attenuation of sympathetic vasoconstriction was not replicated by D-NAME (5 mg kg-1, i.v.) or angiotensin II (12.5 ng kg-1 min-1, i.v.), the latter used as a hypertensive control. 4. Adenosine receptor blockade with 8-(p-sulphophenyl)theophylline (10 mg kg-1, i.v.) or cyclooxygenase inhibition with indomethacin (5 mg kg-1, i.v.) had no effect on contraction-induced attenuation of sympathetic vasoconstriction. 5. These results suggest that NO plays an important role in the precise regulation of blood flow in exercising skeletal muscles by opposing sympathetic vasoconstriction. Although the underlying mechanism is not known, it may involve NO-induced activation of vascular KATP channels.

Adenosine↗
PubMed1985

Noradrenaline and adenosine triphosphate as co-transmitters of neurogenic vasoconstriction in rabbit mesenteric artery.

The largest rami caecales of the ileocolic artery, which is a branch of the mesenteric artery, were perfused at a constant rate of flow. Either vasoconstriction (as an increase in perfusion pressure) or the release of previously incorporated [3H]-noradrenaline was measured. Noradrenaline and ATP, but not carbachol, serotonin, adenosine, Arg-vasopressin and neuropeptide Y, caused marked vasoconstriction. When the sympathetic vasoconstrictor axons in the arterial wall were stimulated by electrical field pulses (either 5 pulses at 10 Hz or 100 pulses at 5 Hz; 0.3 ms pulse width, 200 mA current strength), the ensuing vasoconstriction was at best slightly reduced by phentolamine, prazosin and phenoxybenzamine. The response to 100 pulses, 5 Hz was even enhanced by phentolamine and yohimbine. All antagonists except yohimbine blocked the effect of exogenous noradrenaline. Prazosin did not change the effect of exogenous ATP. alpha,beta-Methylene-ATP (3-15 mumol/l) elicited transient vasoconstriction. Subsequently, responses to ATP as well as to electrical stimulation were reduced and recovered slowly. The response to noradrenaline was not changed. That part of the electrically induced vasoconstriction that remained after alpha,beta-methylene-ATP was almost abolished by phentolamine or prazosin. Pre-treatment of the animals with reserpine decreased but did not prevent the electrically evoked contraction of their arteries. The reserpine-resistant response was not changed by prazosin but was abolished by alpha,beta-methylene-ATP. The vasoconstriction elicited by electrical pulses was not affected by atropine or methysergide but was entirely blocked by tetrodotoxin, guanethidine or exposure to 6-hydroxydopamine. In arteries pre-incubated with [3H]-noradrenaline, electrical stimulation (100 pulses at 5 Hz) increased the outflow of tritium. The evoked overflow was blocked by tetrodotoxin, not changed by alpha,beta-methylene-ATP (9 mumol/l) or prazosin, and enhanced by phentolamine, phenoxybenzamine and yohimbine. We conclude that, in the branch of the mesenteric artery examined, both noradrenaline and ATP or a closely related compound transmit information from sympathetic neurones to smooth muscle. An alpha-adrenoceptor antagonist can reduce neurogenic vasoconstriction by blockade of post-junctional alpha-(probably alpha 1) receptors, reserpine by selective depletion of noradrenaline, and alpha,beta-methylene-ATP by desensitization of the post-junctional ATP (probably P2) receptor mechanism. Noradrenaline and ATP appear to be released from the same neurone. In addition, prejunctional alpha 2-adrenergic autoinhibition of transmitter release operates in the artery. alp

Adenosine Triphosphate↗
PubMed2003

Inhibition of alpha-adrenergic vasoconstriction in exercising human thigh muscles.

The mechanisms underlying metabolic inhibition of sympathetic responses within exercising skeletal muscle remain incompletely understood. The aim of the present study was to test whether alpha(2)-adrenoreceptor-mediated vasoconstriction was more sensitive to metabolic inhibition than alpha(1)-vasoconstriction during dynamic knee-extensor exercise. We studied healthy volunteers using two protocols: (1) wide dose ranges of the alpha-adrenoreceptor agonists phenylephrine (PE, alpha(1) selective) and BHT-933 (BHT, alpha(2) selective) were administered intra-arterially at rest and during 27 W knee-extensor exercise (n= 13); (2) flow-adjusted doses of PE (0.3 microg kg(-1) l(-1)) and BHT (15 microg kg(-1) l(-1)) were administered at rest and during ramped exercise (7 W to 37 W; n= 10). Ultrasound Doppler and thermodilution techniques provided direct measurements of femoral blood flow (FBF). PE (0.8 microg kg(-1)) and BHT (40 microg kg(-1)) produced comparable maximal reductions in FBF at rest (-58 +/- 6 versus-64 +/- 4%). Despite increasing the doses, PE (1.6 microg kg(-1) min(-1)) and BHT (80 microg kg(-1) min(-1)) caused significantly smaller changes in FBF during 27 W exercise (-13 +/- 4 versus-3 +/- 5%). During ramped exercise, significant vasoconstriction at lower intensities (7 and 17 W) was seen following PE (-16 +/- 5 and -16 +/- 4%), but not BHT (-2 +/- 4 and -4 +/- 5%). At the highest intensity (37 W), FBF was not significantly changed by either drug. Collectively, these data demonstrate metabolic inhibition of alpha-adrenergic vasoconstriction in large postural muscles of healthy humans. Both alpha(1)- and alpha(2)-adrenoreceptor agonists produce comparable vasoconstriction in the resting leg, and dynamic thigh exercise attenuates alpha(1)- and alpha(2)-mediated vasoconstriction similarly. However, alpha(2)-mediated vasoconstriction appears more sensitive to metabolic inhibition, because alpha(2) is completely inhibited even at low workloads, whereas alpha(1) becomes progressively inhibited with increasing workloads.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2007

17beta-Estradiol modulates vasoconstriction induced by endothelin-1 following trauma-hemorrhage.

Although endothelin-1 (ET-1) induces vasoconstriction, it remains unknown whether 17beta-estradiol (E(2)) treatment following trauma-hemorrhage alters these ET-1-induced vasoconstrictive effects. In addition, the role of the specific estrogen receptor (ER) subtypes (ER-alpha and ER-beta) and the endothelium-localized downstream mechanisms of actions of E(2) remain unclear. We hypothesized that E(2) attenuates increased ET-1-induced vasoconstriction following trauma-hemorrhage via an ER-beta-mediated pathway. To study this, aortic rings were isolated from male Sprague-Dawley rats following trauma-hemorrhage with or without E(2) treatment, and alterations in tension were determined in vitro. Dose-response curves to ET-1 were determined, and the vasoactive properties of E(2), propylpyrazole triol (PPT, ER-alpha agonist), and diarylpropionitrile (DPN, ER-beta agonist) were determined. The results showed that trauma-hemorrhage significantly increased ET-1-induced vasoconstriction; however, administration of E(2) normalized ET-1-induced vasoconstriction in trauma-hemorrhage vessels to the sham-operated control level. The ER-beta agonist DPN counteracted ET-1-induced vasoconstriction, whereas the ER-alpha agonist PPT was ineffective. Moreover, the vasorelaxing effects of E(2) were not observed in endothelium-denuded aortic rings or by pretreatment of the rings with a nitric oxide (NO) synthase inhibitor. Cyclooxygenase inhibition with indomethacin had no effect on the action of E(2). Thus, E(2) administration attenuates ET-1-induced vasoconstriction following trauma-hemorrhage via an ER-beta-mediated pathway that is dependent on endothelium-derived NO synthesis.

Animals↗
PubMed1997

Alpha-adrenergic vasoconstriction reduces systolic retrograde coronary blood flow.

There is a paradoxical alpha-adrenoceptor-mediated coronary vasoconstriction whenever there is adrenergic activation of the heart, as during cardiovascular reflexes or exercise. A previous study demonstrated that this paradoxical vasoconstriction helps maintain blood flow to the vulnerable inner layer of the left ventricular wall during exercise, but the mechanism for this effect was not elucidated. The purpose of the present investigation was to test the hypothesis that alpha-adrenoceptor-mediated vasoconstriction lessens the to-and-fro oscillation of blood flow that occurs in the coronary arterial tree during systole and diastole. Septal coronary artery blood velocity was measured in anesthetized open-chest dogs with a 20-MHz pulsed Doppler velocimeter. Systolic retrograde velocity and diastolic forward velocity were compared during norepinephrine infusion before and after alpha-adrenoceptor blockade with phenoxybenzamine. Systolic aortic pressure was held constant by aortic banding; heart rate was controlled by pacing at 80, 140, and 200 beats/min; and maximum left ventricular dP/dt was unchanged by alpha-blockade. At each pacing rate, systolic retrograde velocity was significantly greater after alpha-blockade, indicating that alpha-vasoconstriction reduced systolic retrograde flow by changing coronary vascular impedance. Transmural blood flow was measured with microspheres in a second group of dogs during the same experimental conditions, and flow to the inner layer of the left ventricle was diminished by alpha-adrenoceptor blockade at a heart rate of 250 beats/min, demonstrating a beneficial effect of alpha-vasoconstriction. In conclusion, adrenergic alpha-adrenoceptor-mediated coronary vasoconstriction reduces systolic retrograde coronary flow during norepinephrine infusion. This lessens to-and-fro flow oscillation in the coronary circulation and probably is the mechanism whereby alpha-vasoconstriction helps maintain blood flow to the inner layer of the left ventricle during exercise.

Adipose Tissue↗
PubMed1997

Uterine arterial vasoconstrictions mediated by ovarian nerves in virgin and postpartum rats.

In most mammals, including humans, pregnancy results in the loss of most uterine vasomotor fibers. These experiments determined whether, despite this denervation, sympathetic nerves mediated uterine vasoconstrictions in the rat 24 h after delivery. Both virgin and uniparous postpartum rats were anesthetized with urethan. Femoral vessels were cannulated for measurement of arterial pressure and intravenous administration of fluids and drugs. Blood flow was measured in a uterine artery after ligation of all anastomotic ovarian vessels. Electrical stimulation of ovarian nerve efferents elicited frequency-dependent uterine vasoconstrictions in both virgin and postpartum rats. Vasoconstrictions in postpartum rats were not significantly different from those observed in virgins. In both virgin and postpartum rats, neurogenic vasoconstrictions were reduced by combined alpha 1- and alpha 2-adrenergic blockade. We conclude that the uterine branches of the ovarian nerve mediate adrenergic uterine vasoconstrictions. In the largely denervated uterus of the postpartum rat, these vasoconstrictions may be mediated by surviving innervation of the uterine artery and its major branches. Sympathetic vasoconstriction acting at these sites would constitute an effective defense against postpartum hemorrhage.

Adrenergic Antagonists↗
PubMed1991

Effects of glucose on hypoxic vasoconstriction in isolated ferret lungs.

To characterize the effects of glucose on the pulmonary vascular response to anoxia and hypoxia, isolated ferret lungs were ventilated with 28% O2 and 5% CO2 and perfused at constant flow (100 ml.kg-1.min-1). Perfusate glucose concentrations were allowed to fall spontaneously to less than 1 mM (low glucose) or were controlled at 5-6 mM (normal glucose) or 12-17 mM (high glucose). At 60, 120, and 180 min of perfusion, the inspired O2 tension (PIO2) was reduced to 0, 10, or 30 Torr for 30 min, and vasomotor responses were quantified by continuous measurement of pulmonary arterial pressure. At PIO2 of 0 Torr, the response consisted of an early phase of transient intense vasoconstriction and a late phase of sustained slight vasoconstriction. High glucose markedly potentiated the magnitude of late-phase vasoconstriction with each successive anoxic exposure. This effect was not reproduced in normal glucose lungs and was not caused by a change in perfusate osmolarity, an action on blood cells, or an altered ability of pulmonary vascular smooth muscle to contract. At PIO2 of 10 Torr, high glucose not only potentiated late-phase vasoconstriction but also slowed the onset of early-phase vasoconstriction. At PIO2 of 30 Torr, high glucose had no effect on vasomotor responses, which were characterized by a slowly developing sustained vasoconstriction. Our results suggest that the vascular response of isolated ferret lungs to severe hypoxia consisted of separate early and late phases of vasoconstriction. This biphasic response may have resulted from two distinct vasoconstrictor mechanisms or from modulation of a single vasoconstrictor mechanism by a secondary vasodilator influence.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Topical retinoic acid does not alter the vasoconstrictive properties of topical corticosteroids in humans.

Dermo-epidermal atrophy is one of the main side effects of long-term treatment with topical corticosteroids. Retinoic acid may prevent and even reverse these effects in animals. Extension of this concept to therapy in humans implies that several studies have been performed; among others, it has to be established that treatment with topical retinoic acid does not interfere with the anti-inflammatory action of topical corticosteroids. The present study on the cutaneous vasoconstriction test comprised two different double-blind approaches: (i) vasoconstriction tests with betamethasone dipropionate (Diprolene) and clobetasone butyrate (Emovate) were carried out on skin that had previously been treated for 10 days with retinoic acid 0.01, 0.025 or 0.05% (or excipient); (ii) vasoconstriction tests with a combination of triamcinolone acetonide 0.1% and retinoic acid 0.025% were compared with triamcinolone acetonide 0.1% alone. Pretreatment for 10 days with retinoic acid did not alter the vasoconstriction induced by corticosteroids: no decrease or increase in the vasoconstriction score was observed, whether the skin had been previously treated with retinoic acid or with excipient. The vasoconstriction scores obtained with a combination of retinoic acid and triamcinolone acetonide were identical with those obtained with the steroid alone. This study indicates that retinoic acid does not inhibit the vasoconstriction induced by topical corticosteroids and suggests that the anti-inflammatory effect of the latter should be maintained in association with retinoic acid.

Administration, Topical↗
PubMed1991

Intracoronary thrombus formation causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease.

BACKGROUND: Experimental studies have demonstrated that intracoronary platelet aggregation and thrombus formation may induce marked vasoconstriction of epicardial arteries with endothelial injury. METHODS AND RESULTS: To examine the effects of intracoronary thrombus formation on coronary vasomotor tone of human epicardial arteries in vivo, we studied 15 patients who developed intracoronary thrombi adherent to the guide wire during balloon dilatation. Epicardial artery luminal area was evaluated by quantitative coronary angiography proximal and distal to the site of intracoronary thrombus formation and in a reference vessel before and after thrombus formation as well as after intracoronary injection of 0.2-0.3 mg nitroglycerin. All artery segments distal to the site of thrombus formation showed vasoconstriction with a luminal area reduction of -27.4 +/- 17.1% (p less than 0.001), whereas proximal vessel segments and reference vessels not manipulated during percutaneous transluminal coronary angioplasty did not demonstrate any significant luminal area changes during thrombus formation. Angiographic measurements after advancing the guide wire with the adherent thrombus (performed in six of the 15 patients) revealed in all patients that vasoconstriction did develop at a new site distal to the thrombus persistence of the initial vasoconstriction now residing proximal to the thrombus. Thus, there was a sequential association between thrombus formation and subsequent distal vasoconstriction. Intracoronary injection of nitroglycerin abolished the thrombus-induced vasoconstriction. No significant luminal area changes were observed in 20 patients without angiographic evidence of intracoronary thrombus formation. CONCLUSIONS: Intracoronary thrombus formation during percutaneous transluminal coronary angioplasty causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease. Although caution must be advised in the extrapolation of this phenomenon, which was observed in a manipulated artery during coronary angioplasty, the vasoconstrictor response to intracoronary thrombus formation in vivo may play an important role in the dynamic mechanisms of acute coronary heart disease syndromes.

Angiography↗
PubMed1997

Attenuation of neurogenic vasoconstriction by nitric oxide in hindlimb microvascular beds of the rat in vivo.

There is evidence that sympathetic nerve activity leads to endothelium-derived nitric oxide release, which in turn attenuates neurogenic vasoconstriction. Here we tested in vivo (1) whether the magnitude of the vasoconstriction induced by N(G)-nitro-L-arginine methyl ester given systemically is altered when ongoing sympathetic activity is abolished by sectioning the lumbar sympathetic trunk, and (2) whether hindlimb sympathetic vasoconstriction elicited by electrical stimulation of the lumbar sympathetic trunk is enhanced after inhibition of nitric oxide synthesis. Blood flow in the microvascular beds of hairless skin and skeletal muscle of the rat hindlimb was measured with laser Doppler flowmetry. Sectioning the lumbar sympathetic trunk resulted in an increase of blood flow in both tissues, indicating that tonic neurogenic vasoconstriction was abolished. Inhibition of nitric oxide synthesis resulted in vasoconstriction in both vascular beds. This vasoconstriction was more pronounced after abolition of sympathetic activity than with intact sympathetic supply in skin but was smaller in skeletal muscle. The vasoconstriction elicited by graded electrical stimulation of the centrally sectioned lumbar sympathetic trunk with frequencies less than 5 Hz was significantly enhanced after blockade of nitric oxide in skeletal muscle but not in skin microvasculature. These findings suggest that under physiological conditions, sympathetic nerve impulses directly promote the release of nitric oxide in skeletal muscle but not in cutaneous blood vessels. Therefore, basal nitric oxide release is probably in part dependent on sympathetic activity in skeletal muscle, whereas it appears to be mainly due to flow-dependent shear stress in hairless skin microvasculature.

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