PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Vasoconstriction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1994

Vasoconstriction with norepinephrine causes less forearm insulin resistance than a reflex sympathetic vasoconstriction.

We used the insulin-perfused human forearm model to assess the effects of vasoconstriction induced with norepinephrine on the extraction of glucose in the forearm in two groups of healthy young volunteers. The norepinephrine findings were compared with a previously studied group in which vasoconstriction has been caused by reflex activation of the sympathetic nervous system. The aim of the study was to determine the relative importance of hemodynamic and receptor-mediated mechanisms of insulin resistance. Plasma insulin, arterial and venous glucose samples, and forearm blood flow were measured at 10-minute intervals during a 30-minute baseline, a 60-minute intra-arterial insulin infusion, and during 30 minutes of insulin infusion plus vasoconstriction. Group 1 (n = 14) had physiological vasoconstriction induced by inflation of bilateral thigh cuffs to 40 mm Hg to cause pooling of blood in the lower extremities and reflex vasoconstriction in the forearm; group 2 (n = 8) had intra-arterial infusion of norepinephrine to achieve the same degree of vasoconstriction as seen with inflation of thigh cuffs in group 1. Subjects in group 3 (n = 7) had infusion of intra-arterial norepinephrine to achieve a twofold increase in physiological vasoconstriction. With a physiological decrease in forearm blood flow (group 1), there was a 19% decrease in forearm blood flow resulting in a 23% reduction in glucose uptake in the forearm (P < .03). The same degree of reduction in forearm blood flow with a predominantly alpha-adrenergic agonist, norepinephrine (group 2), causes much less insulin resistance (a decrease in utilization of 13%) (P < .04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Contrast medium-induced vasoconstrictions. An investigation of the vasoconstrictive action of iohexol in isolated rabbit coronary arteries.

Angiographic contrast media (CM) may cause both vasodilatation and vasoconstriction. This study evaluates a contrast medium-induced vasoconstriction that occurs when isolated arteries are exposed directly to a CM. Segments of rabbit coronary arteries were mounted in tissue baths containing buffer solution. During the experiments the buffer solution was exchanged with iohexol iso-osmolar with plasma, which caused a temporary vasoconstriction of the vessel segments. The constriction did not depend on the degree of oxygenation of iohexol. The endothelium was not involved in the vasoconstriction. Prazosin slightly decreased the vasoconstriction and a small part of the constriction might thus depend on liberation of norepinephrine by iohexol. The constriction was totally inhibited by the calcium antagonist nifedipine, while it was augmented by addition of low concentrations of KCl to ihoexol. It is concluded that the otherwise safe CM iohexol causes vasoconstriction in vitro by depolarizing the smooth muscle cells and the nerve terminals in the vessel wall.

Animals↗
PubMed1992

Calcium antagonists block angiotensin II-mediated vasoconstriction in humans: comparison with their effect on phenylephrine-induced vasoconstriction.

Calcium antagonists are known to decrease peripheral vascular resistance in vivo in humans. The mechanism of this vascular relaxation has not been clearly elucidated. Vascular tone is maintained by several endogenous neurohumoral systems including sympathetic nervous system activity and angiotensin II. We compared and contrasted the capacity of calcium antagonist drugs to prevent angiotensin II and phenylephrine-induced alpha-1 adrenergic vasoconstriction using brachial artery infusion and measurement of forearm blood flow by strain gauge plethysmography. In a dose-dependent manner, calcium antagonists blocked angiotensin II-induced vasoconstriction. The rank order of this blockade was nifedipine greater than verapamil greater than diltiazem. Nifedipine and verapamil, but not diltiazem blocked alpha-1 adrenergic (phenylephrine-induced) vasoconstriction. At 7.64 and 19.1 micrograms/min infusion rates for nifedipine and verapamil, respectively, they abolished the angiotensin II effect; however, the phenylephrine effect was incompletely blocked. Calcium antagonist-induced vascular relaxation in vivo in humans is in part explained by their capacity to block angiotensin II-mediated vasoconstriction. In addition, two calcium antagonists (nifedipine and verapamil) may inhibit alpha-1 adrenergic vasoconstriction.

Adult↗
PubMed1990

Failure of nitroglycerin and diltiazem to reduce platelet-mediated vasoconstriction in dogs with coronary artery stenosis and endothelial injury: further evidence for thromboxane A2 and serotonin as mediators of coronary artery vasoconstriction in vivo.

This study was designed to test the efficacy of nitroglycerin and diltiazem in inhibiting in vivo platelet aggregation and reducing platelet-mediated vasoconstriction in a canine model of coronary artery stenosis and endothelial injury. Coronary artery diameter was measured in vivo by means of ultrasonic crystals sutured on the left anterior descending coronary artery (LAD) immediately distal to an external constrictor (LAD1), 1 cm below (LAD2), and on the left circumflex coronary artery. Coronary diameter was continuously measured before, during cyclic flow variations (progressive declines in blood flow followed by sudden restorations of flow due to recurrent intracoronary platelet aggregation), during cyclic flow variations and intravenous infusion of nitroglycerin (5 micrograms/kg per min) or diltiazem (15 micrograms/kg per min), and after cyclic flow variations were abolished by administration of LY53857, a serotonin receptor antagonist (n = 7), or SQ29548, a thromboxane A2 receptor antagonist (n = 7). During control cyclic flow variations, at the nadir of coronary flow (6% to 11% of the nonstenosed values), LAD1 cross-sectional area decreased by 43 +/- 8% and 44 +/- 3% in the two groups of dogs subsequently treated with LY53857 and SQ29548, respectively. Neither nitroglycerin nor diltiazem caused changes in cyclic flow variation frequency or severity. Furthermore, neither drug significantly reduced the vasoconstriction associated with cyclic flow variations, whereas they significantly increased circumflex artery cross-sectional area. In contrast, LY53857 and SQ29548 were very effective in abolishing cyclic flow variations and the coronary vasoconstriction related to them. Five additional dogs received an intracoronary infusion of nitroglycerin (21 +/- 5 micrograms/kg per min) and later diltiazem (15 micrograms/kg per min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Vasoconstrictions mediated by an endothelium-derived vasoconstricting factor (EDCF).

To enlighten the role of endothelium in the generation of vasospasms we examined vascular tone after reduction of oxygen supply in dependence on endothelial function in isolated vessels (rabbit aorta abdominalis, pig coronary, and pulmonary artery). Therefore, after ligation of all side branches, vessel segments, prepared either with or without endothelium, were cannulated and arranged in two systems (with two segments each) in a serial manner (system I: endothelium-denuded vessel followed by an endothelium-denuded segment) and perfused with Tyrode's solution (constant flow 20 ml/min). Pressure gradient over each segment was continuously measured. Endothelial function was checked by perfusion with 1 mumol/l actetylholine after precontraction with 0.1 mumol/l norepinephrine, thereby inducing an EDRF mediated vasodilation (greater than 70%) indicating normal endothelial function. After 2 h equilibration with Tyrode's solution the preparations of rabbit aorta abdominalis were perfused for 30 min with oxygen-deprived medium (reduction from 95% O2 and 5% CO2 to 95% N2 and 5% CO2) and a marked long lasting (60 min) increase in pressure gradient (indicating vasoconstriction) was observed in those endothelium-denuded vessel segments which were mounted distal to a normal vessel with an intact endothelium. This contraction could be inhibited by pretreatment with either 1 mumol/l dexamethasone. 1 mumol/l indomethacine or 10 mumol/l methylene blue or attenuated by the TXA2-antagonist BM 17133 (5 mumol/l) but not by radical scavengers as superoxid dismutase or by inhibition of the lipoxygenase by nordihydroguaretic acid. From these results it is concluded that endothelium releases a vasoconstricting factor (EDCF) at pO2 values beneath 550 mm Hg. This EDCF seems to depend on phospholipase A2 and cyclooxygenase, but because of the long-lasting effect it is probably no prostanoid itself, especially not TXA2.

Animals↗
PubMed1988

Atrial natriuretic peptide reverses afferent arteriolar vasoconstriction and potentiates efferent arteriolar vasoconstriction in the isolated perfused rat kidney.

The intrarenal sites of action of atrial natriuretic peptide (ANP) have not been resolved fully. Although ANP relaxes in vitro preparations of smooth muscle and exerts profound effects on renal hemodynamics, the effects of ANP on resistance vessels remain a subject of controversy. In the present study, we utilized an in vitro perfused hydronephrotic rat kidney model to assess directly the actions of ANP on renal microvessels during norepinephrine (NE)-induced renal vasoconstriction. Perfusion pressure was maintained constant, and perfusate flow to the kidney was monitored while the afferent arteriole (AA) and efferent arteriole (EA) were visualized using videomicroscopy. Renal AA and EA diameters were measured by computer-assisted image analysis. NE (0.3 microM) decreased renal perfusate flow from 11.8 +/- 1.7 (S.E.) to 5.8 +/- 1.2 ml/min (P less than .005), decreased AA diameter from 20.2 +/- 0.7 to 14.3 +/- 0.8 mu (P less than .005) and decreased EA diameter from 18.6 +/- 1.2 to 15.1 +/- 1.2 mu (P less than .005). ANP (human ANF-(4-28), anaritide, Wyeth) completely reversed the NE-induced AA vasoconstriction with an IC50 of 9.3 +/- 5.6 nM. In contrast, ANP caused a further decrease in EA diameter at concentrations up to 10(-8) M, and elicited a slight dilation of the EA at 10(-7) M. In normal rat kidneys perfused under identical conditions, NE decreased renal perfusate flow, glomerular filtration rate and filtration fraction. ANP increased glomerular filtration rate and filtration fraction above control levels, with maximal effects at 10(-8) M.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

[Reflexphotometric determinations of vasoconstriction after topical application of steroids. IV. Time slope of vasoconstriction and reactive vasodilatation (author's transl)].

In this study a reflex photometrical technique has been used to examine local steroid induced vasoreactions. When applied but once, steroids cause a maximum vasoconstriction between 8 and 16 h after beginning the test. Followed by a 32 h period, the phase of vasoconstriction is succeeded by a dilatation of dermis blood vessels. It appears, that the stronger the vasocontriction, the smaller the degree of vasodilatation.

Administration, Topical↗
PubMed1999

Mechanisms of melatonin-induced vasoconstriction in the rat tail artery: a paradigm of weak vasoconstriction.

1. Vasoconstrictor effects of melatonin were examined in isolated rat tail arteries mounted either in an isometric myograph or as cannulated pressurized segments. Melatonin failed by itself to mediate observable responses but preactivation of the arteries with vasopressin (AVP) reliably uncovered vasoconstriction responses to melatonin with maxima about 50% of maximum contraction. Further experiments were conducted with AVP preactivation to 5-10% of the maximum contraction. 2. Responses to melatonin consisted of steady contractions with superimposed oscillations which were large and irregular in isometric but small in isobaric preparations. Nifedipine (0.3 microM) reduced the responses and abolished the oscillations. Charybdotoxin (30 nM) increased the magnitude of the oscillations with no change in the maximum response. 3. Forskolin (0.6 microM) pretreatment increased the responses to melatonin compared to control and sodium nitroprusside (1 microM) treated tissues. The AVP concentration required for preactivation was 10 fold higher than control in both the forskolin and nitroprusside treated groups. 4. In isometrically-mounted arteries treated with nifedipine, melatonin receptor agonists had the potency order 2-iodomelatonin > melatonin > S20098 > GR196429, and the MT2-selective antagonist luzindole antagonized the effects of melatonin with a low pK(B) of 6.1+/-0.1. 5. It is concluded that melatonin elicits contraction of the rat tail artery via an mt1 or mt1-like receptor that couples via inhibition of adenylate cyclase and opening of L-type calcium channels. Calcium channels and charybdotoxin-sensitive K channels may be recruited into the responses via myogenic activation rather than being coupled directly to the melatonin receptors. 6. It is proposed that the requirement of preactivation for overt vasoconstrictor responses to melatonin results from the low effector reserve of the melatonin receptors together with the tail artery having threshold inertia. Potentiative interactions between melatonin and other vasoconstrictor stimuli probably also result from the threshold inertia. A simple model is presented and a general framework for consideration of interactions between weak vasoconstrictor agonists and other vasoconstrictor stimuli is discussed.

Acetamides↗
PubMed2001

Hypoxic vasoconstriction of cyclostome systemic vessels: the antecedent of hypoxic pulmonary vasoconstriction?

Hypoxic vasoconstriction (HV) is an intrinsic response of mammalian pulmonary vascular smooth muscle (VSM). In the present study, HV was examined by myography of vessel rings from three primitive vertebrates: New Zealand hagfish (NZH), Pacific hagfish (PH), and sea lamprey (SL). Hypoxia dilated pre-gill arteries (ventral aorta, afferent branchial) from all species, whereas it contracted systemic arteries [dorsal aorta (DA), efferent branchial, celiacomesenteric]. DA HV was reproducible over several days, and it could be sustained in NZH for 8 h without adverse effects. Tension was proportional to PO(2), and half-maximal HV was obtained at PO(2) (mmHg) of 4.7 +/- 0. 2 (NZH), 0.8 +/- 0.1 (PH), and 10.7 +/- 1.9 (SL). HV did not require preconditioning (preexisting contractile stimulus) and was unaffected by elevated extracellular potassium (200 mM NZH; 80 mM SL); removal of the endothelium (NZH); or inhibitors of cyclooxygenase, lipoxygenase, cytochrome P-450 or antagonists of alpha-adrenergic, muscarinic, nicotinic, purinergic, or serotoninergic receptors. These results show that HV is an intrinsic feature of systemic VSM in cyclostomes and suggest that HV has been in the repertoire of VSM responses, since the origin of vertebrates. The exceptionally hardy HV in cyclostome DA may provide a useful model with which to examine both the phylogeny and mechanisms of this response.

Animals↗
PubMed1976

[Reflexphotometric determinations of vasoconstriction after topical application of steroids. V. Vasoconstriction phaenomenon and tachyphylaxis after repeated steroid application (author's transl)].

On the basis of reflexphotometrical vasoconstriction tests it is demonstrated, that the intensity of vasoreactions caused by a first topical application of steroids, diminishes rapidly after repeated applications, until there is no response of vessels to a new application. This phaenomenon is know as tachyphylaxis and has been found in all tested glucocorticoids.

Administration, Topical↗
PubMed1999

5-Hydroxytryptamine(1F) receptors do not participate in vasoconstriction: lack of vasoconstriction to LY344864, a selective serotonin(1F) receptor agonist in rabbit saphenous vein.

Recently, several novel approaches to the treatment of migraine have been advanced, including selective 5-hydroxytryptamine (or serotonin) 1B/1D (5-HT(1B/1D)) receptor agonists such as sumatriptan and 5-HT(1F) receptor agonists such as LY344864. Many 5-HT(1B/1D) receptor agonists have been identified based on their ability to produce cerebral vascular contraction, whereas LY344864 was identified as an inhibitor of trigeminal nerve-mediated dural extravasation. In our study, several triptan derivatives were compared with LY344864 for their ability to contract the rabbit saphenous vein, a tissue used in the preclinical identification of sumatriptan-related agonists. Sumatriptan, zolmitriptan, rizatriptan, and naratriptan all contracted the rabbit saphenous vein from baseline tone, whereas LY344864 in concentrations up to 10(-4) M did not contract the rabbit saphenous vein. Furthermore, vascular contractions to sumatriptan were markedly augmented in the presence of prostaglandin F(2alpha) (PGF(2alpha)). However, even in the presence of PGF(2alpha) (3 x 10(-7) M), LY344864 did not contract the rabbit saphenous vein in concentrations well in excess of its 5-HT(1F) receptor affinity (pK(i) = 8.2). Only when concentrations exceeded those likely to activate 5-HT(1B) and 5-HT(1D) receptors (>10(-5) M) did modest contractile responses occur in the presence of PGF(2alpha). Use of these serotonergic agonists revealed a significant correlation between the contractile potency in the rabbit saphenous vein and the affinities of these agonists at 5-HT(1B) and 5-HT(1D) receptors, although contractile agonist potencies were not quantitatively similar to 5-HT(1B) or 5-HT(1D) receptor affinities. In contrast, no significant correlation existed between the contractile potencies of these serotonergic agonists in the rabbit saphenous vein and their affinity at 5-HT(1F) receptors. These data support the contention that activation of 5-HT(1F) receptors will not result in vascular contractile effects.

Animals↗
PubMed1995

Desflurane reduces the gain of thermoregulatory arteriovenous shunt vasoconstriction in humans.

BACKGROUND: Thermoregulatory responses, such as arteriovenous shunt vasoconstriction, provide substantial protection against core hypothermia. A response can be characterized by its threshold (core temperature triggering response), gain (rate at which response intensity increases, once triggered), and maximum response intensity. Reduced gain decreases the efficacy of a thermoregulatory response at a given threshold because response intensity will increase more slowly than usual. The effects of general anesthesia on the gain of arteriovenous shunt vasoconstriction have not been reported. Accordingly, we tested the hypothesis that desflurane decreases the gain of centrally mediated vasoconstriction. METHODS: We studied seven healthy male volunteers. Each was studied twice: (1) desflurane (end-tidal concentration 0.4 minimum alveolar concentration); and (2) control (no anesthesia). Mean skin and fingertip temperatures were controlled at 35.5 degrees C throughout the study. Core temperature was reduced at a rate of 1.5 degrees C/h by central venous infusion of cold fluid. Fingertip arteriovenous shunt flow was measured using venous occlusion volume plethysmography at 1-min intervals. Flow was also evaluated using the perfusion index and laser Doppler flowmetry. Vasoconstriction thresholds were calculated as the core temperatures triggering fingertip flows of 1.0 ml/min (beginning of vasoconstriction) and 0.25 ml/min (intense vasoconstriction). The gain of vasoconstriction was considered to be the slope of the fingertip flow versus core temperature regression within the linear range from 1.0 ml/min to 0.15 ml/min. The minimum observed flow was considered maximum vasoconstriction intensity. Data are presented as means +/- SD; P < 0.01 was considered statistically significant. RESULTS: The vasoconstriction threshold (when defined using a flow of 1.0 ml/min) was reduced from 36.8 +/- 0.3 degrees C to 35.6 +/- 0.3 degrees C by desflurane anesthesia (P < 0.01). Desflurane reduced the gain of vasoconstriction by a factor of three, from 2.4 to 0.8 ml.min-1.degrees C-1 (P < 0.01). Gains, as determined by the perfusion index and laser Doppler flowmetry, were likewise reduced (P < 0.01). The threshold on the control day was only 0.2 +/- 0.1 degrees C less when significant vasoconstriction was defined as a flow of 0.25 ml/min rather than 1.0 ml/min. Because gain was reduced, however, the threshold during desflurane administration was 0.8 +/- 0.2 degrees C less when significant vasoconstriction was defined by a flow of 0.25 ml/min. Minimum flows were comparable and near zero with and without anesthesia. CONCLUSIONS: The threshold reduction (1.2 degrees C/0.4 minimum alveolar concentration) was similar to that observed previously during isoflurane anesthesia. Similarly, it is established already that maximum vasoconstriction intensity is comparable with and without isoflurane anesthesia. However, the data also indicate that even relatively low desflurane concentrations markedly reduce the gain of vasoconstriction. It is likely that reduced gain (i.e., slow onset of vasoconstriction) contributes to core hypothermia in some surgical patients.

Adult↗