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PubMed1985

The effect of prostacyclin on angiotensin II-induced placental vasoconstriction.

Significant alterations in vascular responsiveness to angiotensin II have been documented during pregnancy. We have observed that prostacyclin, a potent vasodilating prostaglandin, does not dilate the ovine placental vasculature. However, we thought it might modulate the placental vasoconstriction produced by angiotensin II. Regional blood flows and resistances were measured by the radioactive microsphere technique in six near-term sheep. Blood flows were measured in the control condition and 15 minutes after beginning an infusion of angiotensin II at 5 micrograms/min (T1). Additional measurements were made 15 minutes after the addition of 50 micrograms/min of prostacyclin to the angiotensin II infusate (T2) and 15 minutes after withdrawing prostacyclin from the angiotensin II infusion (T3). Mean arterial pressure rose in response to angiotensin II and decreased significantly with prostacyclin administration. The renal and uterine nonplacental vascular beds showed the expected vasoconstriction in response to angiotensin II, which was then reversed to control levels by prostacyclin infusion. Unexpectedly, prostacyclin did not reverse the angiotensin II vasoconstriction in the placenta but further increased resistance (p less than 0.03). Placental resistance changed from 0.33 +/- 0.04 peripheral resistance units in the control condition to 0.42 +/- 0.06 peripheral resistance units for T1 (p less than 0.03), and prostacyclin infusion further increased placental resistance to 0.63 +/- 0.10 peripheral resistance units for T2 (p less than 0.03). We conclude that the placental vascular response to prostacyclin is different from that of other organs and that prostacyclin does not dilate, but further constricts the placenta in the near-term sheep with angiotensin II-induced systemic vasoconstriction.

Angiotensin II↗
PubMed1989

Fetoplacental vascular responses to prostacyclin after thromboxane-induced vasoconstriction.

The vasodilator prostacyclin is produced by fetal tissues and may serve to protect umbilical blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by a thromboxane mimic (U-46619). Fetal regional blood flow was measured by the radioactive microsphere technique in six unanesthetized, near-term ovine fetuses. Measurements were made in the control period, again 20 minutes after a fetal infusion of U-46619 was begun, and finally 20 minutes after prostacyclin was added to the U-46619 infusion. Mean arterial pressure rose significantly in response to U-46619 (38 +/- 1 to 51 +/- 2 mm Hg, p less than 0.01) and returned to baseline after prostacyclin (42 +/- 2 mm Hg). Renal resistance was increased from 0.16 +/- 0.01 to 0.22 +/- 0.01 mm Hg.ml-1.min.100 gm-1 (p less than 0.05) by U-46619 and decreased significantly (p less than 0.05) below baseline by addition of prostacyclin (0.10 +/- 0.02 mm Hg.ml-1.min.100 gm-1). Placental resistance also increased significantly (p less than 0.03) in response to U-46619 (from 0.15 +/- 0.01 to 0.21 +/- 0.01 mm Hg.ml-1.min.kg-1 fetal weight) but was further increased to 0.29 +/- 0.03 mm Hg.ml-1.min.kg-1 fetal weight by the addition of prostacyclin. Umbilical placental blood flow decreased significantly (p less than 0.03) when prostacyclin was added to U-46619 (315 +/- 40 to 195 +/- 30 ml.min-1.kg-1 fetal weight). Whereas U-46619 had no effect on fetal arterial blood gases, the addition of prostacyclin resulted in significant fetal acidosis (p less than 0.03). We conclude that thromboxane mimic causes fetal hypertension and renal and placental vasoconstriction. Prostacyclin reverses hypertension and renal vasoconstriction but, unexpectedly, worsens fetal placental vasoconstriction produced by thromboxane. It is likely that the observed fetal acidosis is a result of compromised placental function.

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

Hypoxic pulmonary vasoconstriction is enhanced by inhibition of the synthesis of an endothelium derived relaxing factor.

Inhibition of the synthesis of endothelium derived relaxing factor by NG-monomethyl-L-arginine, a competitive inhibitor of the synthesis of nitric oxide from L-arginine, enhances hypoxic pulmonary vasoconstriction in pulmonary artery rings and isolated, Krebs albumin perfused rat lungs. L-arginine rapidly reduces hypoxic vasoconstriction, particularly in lungs treated with NG-monomethyl-L-arginine. Following administration of NG-monomethyl-L-arginine, bradykinin-induced vasodilatation is inhibited (p less than 0.01) and a bradykinin-induced vasoconstriction develops (p less than 0.001). NG-monomethyl-L-arginine does not significantly diminish acetylcholine-induced vasodilatation in the isolated lung. NG-monomethyl-L-arginine causes an endothelium-dependent vasoconstriction in pulmonary artery rings.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1984

Antagonism by ketanserin of 5-HT-induced vasoconstriction unmasks a 5-HT-induced vasodilation.

The effect of ketanserin on the action of 5-hydroxytryptamine (5-HT) and noradrenaline has been studied using the rat isolated perfused mesentery preparation. Both 5-HT and noradrenaline produced constriction in the mesenteric vessels. The responses to 5-HT and noradrenaline were greater in tissues from hypertensive animals. Responses to 5-HT were abolished by 1 nM ketanserin. Ketanserin was found to be a competitive antagonist of the noradrenaline-induced constrictions (pA2 = 7.5). In partially constricted tissues, 5-HT induced vasoconstriction and vasodilation. In the presence of ketanserin the vasoconstriction was reduced and the 5-HT-induced vasodilation was potentiated. The amount of potentiation of the 5-HT-induced vasodilation by ketanserin was similar in tissues from normotensive and hypertensive rats. It is suggested that the 5-HT-induced vasoconstriction is mediated by activation of 5-HT2 receptors. In the presence of ketanserin, the 5-HT2 receptor mediated vasoconstriction is antagonized, unmasking a 5-HT-induced vasodilation.

Amidines↗
PubMed1990

Non-adrenergic sympathetic vasoconstriction in the eye and some other facial tissues in the rabbit.

The effects of unilateral sympathetic nerve stimulation (SNS) on regional blood flow in the rabbit were studied with radioactive microspheres. SNS at 10 or 4 Hz caused an approximately 60% reduction in choroidal blood flow, which was partly resistant to alpha-adrenoceptor blockade with phenoxybenzamine. The vasoconstriction evoked by SNS at 2 Hz was completely abolished by alpha-adrenoceptor blockade. A similar response was seen in the iris, ciliary body, masseter muscle and lacrimal gland. In the harderian gland, however, SNS (2 Hz) after alpha-adrenoceptor blockade caused a significant reduction in blood flow. In the salivary glands, combined beta- and alpha-adrenoceptor blockade with propranolol and phenoxybenzamine revealed a slight non-adrenergic vasoconstriction during SNS at 10 Hz; however, the blood flow was significantly increased during SNS at 4 and 2 Hz following alpha-adrenoceptor blockade. These results indicate that there is a frequency-dependent, non-adrenergic component in the sympathetic vasoconstriction of the eye and several facial tissues. In the salivary glands, beta-adrenoceptor-mediated vasodilatation tends to mask a non-adrenergic vasoconstriction.

Adrenergic alpha-Antagonists↗
PubMed1995

Neuropeptide Y accounts for sympathetic vasoconstriction in guinea-pig vena cava: evidence using BIBP 3226 and 3435.

The ability of the novel, non-peptide, neuropeptide Y Y1 receptor antagonist, BIBP 3226 ((R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-argininami de), to antagonize neuropeptide Y- and sympathetic-mediated vasoconstriction was examined in isolated segments of the thoracic vena cava of guinea-pigs. Increasing concentrations (10(-9) - 10(-6) M) of BIBP 3226 caused a parallel and rightward shift in the neuropeptide Y dose-response curve but did not significantly change the effect of noradrenaline. The calculated pA2 value for BIBP 3226 was 8.0 +/- 0.08, a value fully compatible with the reported affinity at rodent and human neuronal Y1 receptors. BIBP 3226 (10(-6) M) also readily reversed the established vasocontraction induced by neuropeptide Y. BIBP 3226 (10(-6) M) markedly inhibited the slow long-lasting contraction evoked by high frequency electrical field stimulation, leaving a rapid component which was abolished by phentolamine. Its enantiomer, BIBP 3435 ((S)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-argininami de), which exerts a much weaker action on neuropeptide Y Y1 receptors, had no such inhibitory effect. In propranolol-pretreated vessels, the vasoconstriction evoked by nerve stimulation was enhanced; then BIBP 3226 inhibited the peak response by 44%, and the integrated contractile effect by 90%. We conclude that BIBP 3226 is a potent and competitive antagonist of neuropeptide Y Y1 receptor-mediated vasoconstriction in guinea-pig vena cava and that endogenous neuropeptide Y acting on the neuropeptide Y Y1 receptor is likely to account for the long-lasting component of the sympathetic vasoconstriction in response to high-frequency stimulation in this vessel.

Animals↗
PubMed1992

Mesenteric vasoconstriction in cardiogenic shock in pigs.

The quantitative impact of mesenteric vasoconstriction on the systemic hemodynamic response to cardiogenic shock induced by pericardial tamponade was evaluated. Graded increases in pericardial pressure produced corresponding decreases in cardiac output to 44% +/- 2% and arterial pressure to 64% +/- 3% of baseline and increases in total peripheral vascular resistance to 131% +/- 4% of baseline. Total mesenteric blood flow decreased disproportionately, to 28% +/- 3% of baseline, because of a disproportionate increase in mesenteric vascular resistance to 223% +/- 6% of baseline. Nonmesenteric vascular resistance increased only to 119% +/- 4% of baseline. Thus mesenteric vasoconstriction accounted for 42% of the increase in total peripheral resistance. Prior blockade of the renin-angiotensin axis ablated this response and eliminated the mesenteric contribution to systemic vascular resistance, while confirmed blockade of the alpha-adrenergic system or vasopressin system had no effect. Without shock, central intravenous infusions of angiotensin II (but not norepinephrine or vasopressin) closely mimicked this selective vasoconstriction. Angiotensin-mediated selective mesenteric vasoconstriction accounts for more than 40% of the overall increase in systemic vascular resistance in cardiogenic shock.

Animals↗
PubMed1982

Treating migraine by training in temporal artery vasoconstriction and/or cognitive behavioral coping: a one-year follow-up.

A one-year follow-up on 16 chronic migraine patients treated with vasoconstriction biofeedback of the temporal arteries (VT) or cognitive behavioral stress coping training (CT), or one of two serial variations of them, is reported: there were four experimental groups EG-1a: VT, 10 sessions; EG-1b: Vt, 5 sessions and CT, 5 sessions; EG-11a: CT, 10 sessions; EG-11b: CT, 5 sessions and VT, 5 sessions. Another group of 4 migraine patients was assigned to a waiting control. All treatment groups decreased the frequency, duration and intensity of headaches, as well as amount of medication from baseline to the one-year follow-up. However, there were no differences between the groups (the controls were not followed-up). During treatment, but not at follow-up 1 (two months after therapy), voluntary vasoconstriction was higher in EG-1a than in EG-11a, although all EGs vasoconstricted. Voluntary vasoconstriction was not tested at one-year follow-up. The cognitive training groups improved more in self-ratings of irritability, depression and positive self-evaluation than the biofeedback or control groups on follow-up 1, but this difference was not maintained at one year. All treatment groups showed deterioration in measure of excitement and depression, returning to pre-treatment levels. Improvements in irritability and positive-self-evaluation were however sustained at one year follow-up.

Adult↗
PubMed1984

Differential prejunctional effect of captopril and saralasin on neurogenic vasoconstriction in pithed normotensive rats.

The present study describes a differential inhibitory effect of captopril and [Sar1 Ala8]angiotensin II (saralasin) on the neurogenic vasoconstriction in pithed normotensive rats. In pithed normotensive rats with intact kidneys captopril more profoundly inhibited the vasopressor response to spinal stimulation than observed for saralasin. Bilateral nephrectomy also diminished the hypertensive response to spinal stimulation. After bilateral nephrectomy, 1 h previously, captopril but not saralasin diminished the hypertensive response to spinal stimulation. After bilateral nephrectomy, 18-24 h previously, captopril did not produce an additional reduction of the vasopressor response to spinal stimulation. In contrast, saralasin significantly potentiated the neurogenic vasoconstriction. The results suggest that both captopril and saralasin diminish the hypertensive response to spinal stimulation by producing dilatation of vascular smooth muscle in pithed normotensive rats. Apart from this common mechanism, a differential effect of captopril and saralasin on the neurogenic vasoconstriction can be observed. In contrast to saralasin, captopril may depress the neurogenic vasoconstriction in pithed normotensive rats by blocking the sympathofacilitatory action induced by subpressor levels of angiotensin II (AII). In pithed normotensive rats, saralasin may mimic the sympathofacilitatory action of subpressor AII.

Animals↗
PubMed1993

Effects of nordihydroguaiuretic acid on sulfidopeptide leukotriene activity and hypoxic pulmonary vasoconstriction in the isolated sheep lung.

Sulfidopeptide leukotrienes have been proposed as mediators of hypoxic pulmonary vasoconstriction. We studied the effects of nordihydroguaiuretic acid (NDGA), a lipoxygenase inhibitor, on hypoxic pulmonary vasoconstriction and on immunoreactive leukotriene C4 (i-LTC4) levels in lung lymph, perfusate and bronchoalveolar lavage (BAL) fluid in isolated, indomethacin treated, sheep lungs perfused with blood at a constant flow of 100 ml/kg/min. The protocol consisted of two randomized periods with inspired 02 concentration either 28.2 or 4.2%. Five groups of lungs were studied with calculated NDGA concentrations of 0 to 1300 microM. At the end of each period, i-LTC4 was measured in lung lymph, perfusate and BAL. NDGA levels were also measured. Consistent with our previous findings (10), hypoxia did not increase i-LTC4 levels in lymph, perfusate or BAL fluid. Although NDGA decreased i-LTC4 in perfusate in a dose-dependent manner, it did so at concentrations which were ten times lower than those causing inhibition of hypoxic vasoconstriction. These NDGA concentrations also inhibited vasomotor responses to KCl, serotonin and PGF2 alpha suggesting nonspecificity. These observations are not consistent with mediation of hypoxic vasoconstriction by i-LTC4.

Analysis of Variance↗
PubMed1990

Neural regulation of vascular tone and cold induced vasoconstriction in human finger skin.

Finger skin blood flow was measured by a laser Doppler during control conditions, after neural blockade at the finger base by prilocaine and after localized anaesthesia of the skin by lidocaine introduced iontophoretically into the finger skin. Vasoconstriction was achieved by local cooling of the finger and by iontophoretic administration of norepinephrine during the described three conditions. Compared to the control condition, blood flow increased after nerve block at the finger base but even more after local skin anaesthesia. This additional increase in blood flow after local application of lidocaine indicates that finger skin vascular tone is partly dependent on local reflexes. Vasoconstriction on local cooling was preserved after nerve blockade at the finger base but inhibited after local skin anaesthesia by iontophoresis of lidocaine. This inhibition was not due to paralysis of the vessel wall since vasoconstriction to norepinephrine was preserved. Thus, vasoconstriction in response to local cooling is mediated by local reflexes.

Blood Vessels↗
PubMed1990

Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of significant stenoses.

Cocaine increases myocardial oxygen demand and paradoxically decreases oxygen supply by reducing coronary blood flow. Such "inappropriate" vasoconstriction also occurs with exercise, which causes intense vasoconstriction of coronary artery segments narrowed by atherosclerosis. This study was done to assess the cocaine-induced change in vasomotor tone of diseased and nondiseased coronary artery segments. In 18 patients (15 men, 3 women, aged 35 to 67 years), coronary artery areas in diseased and nondiseased segments were quantitated before and 15 min after administration of intranasal saline solution (6 patients) or cocaine (2 mg/kg body weight) (12 patients). No variables changed after intake of the saline solution. In response to cocaine, the luminal areas of diseased and nondiseased segments decreased, but the magnitude of vasoconstriction was greater in the diseased segments (mean +/- SD 29 +/- 23% versus 13 +/- 8%, p less than 0.05). Thus, cocaine causes vasoconstriction of diseased and nondiseased coronary artery segments, but its effect is particularly marked in the former.

Adult↗
PubMed2006

Differential effects of phosphodiesterase-5 inhibitors on hypoxic pulmonary vasoconstriction and pulmonary artery cytokine expression.

BACKGROUND: Perioperative pulmonary hypertension is a challenging clinical problem with numerous etiologies including hypoxia, adrenergic stimulation, and local inflammation. New oral phosphodiesterase-5 (PDE-5) inhibitors used for the treatment of erectile dysfunction may have beneficial effects on the pulmonary vasculature owing to the abundance of PDE-5 receptors in the lung. The purpose of this study was to compare the efficacy of sildenafil, vardenafil, and tadalafil in preventing acute hypoxic pulmonary vasoconstriction and hypoxia-induced pulmonary artery tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1beta) expression. METHODS: Isolated rat pulmonary arteries suspended in physiologic organ baths for measurement of isometric force transduction were treated with vehicle (dimethyl sulfoxide), sildenafil, vardenafil, or tadalafil to assess (1) pulmonary artery relaxation; (2) inhibition of phenylephrine-induced pulmonary artery contraction; (3) inhibition of hypoxic pulmonary vasoconstriction (pO2 = 30-35 mm Hg); and (4) hypoxia-induced pulmonary artery TNF-alpha and IL-1beta expression (reverse transcriptase-polymerase chain reaction). RESULTS: Sildenafil, vardenafil, and tadalafil resulted in dose-dependent pulmonary artery relaxation and inhibited phenylephrine-induced pulmonary artery contraction, but only tadalafil significantly inhibited hypoxic pulmonary vasoconstriction (52.08% +/- 7.65% tadalafil versus 88.63% +/- 8.96% vehicle; 98.61% +/- 10.04% sildenafil; 68.46% +/- 15.84% vardenafil). Hypoxia-induced upregulation of TNF-alpha and IL-1beta mRNA in pulmonary artery was significantly decreased by tadalafil, but not sildenafil or vardenafil pretreatment. CONCLUSIONS: We conclude that sildenafil, vardenafil, and tadalafil were equally efficacious in causing pulmonary artery relaxation, but only tadalafil inhibited hypoxic pulmonary vasoconstriction and attenuated hypoxia-induced pulmonary artery TNF-alpha and IL-1beta expression.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2006

The angiotensin II receptor antagonist valsartan inhibits endothelin 1-induced vasoconstriction in the skin microcirculation in humans in vivo: influence of the G-protein beta3 subunit (GNB3) C825T polymorphism.

OBJECTIVE: We investigated the influence of angiotensin II receptor blockade on angiotensin II-induced, endothelin 1 (ET-1)-induced, and norepinephrine-induced vasoconstriction to further characterize interactions of the 3 major pressor systems. ET-1, angiotensin II, and norepinephrine act via G protein-coupled receptors with a possible involvement of the G-protein beta3 subunit (GNB3) C825T polymorphism. We studied the influence of this polymorphism on the responses to angiotensin II antagonism in the presence of ET-1, norepinephrine, and angiotensin II. METHODS: Twenty-five healthy men (mean age, 28.6 +/- 4 years; n = 14 CC, n = 9 CT, and n = 2 TT) were included in a double-blind, randomized, placebo-controlled crossover study. We used a laser Doppler imager to evaluate skin perfusion changes after injection of ET-1, angiotensin II, and norepinephrine (10(-18), 10(-16), and 10(-14) mol) after oral intake of the angiotensin II receptor antagonist valsartan (80 mg) or placebo. Data were analyzed with ANOVA or t test and are expressed as arbitrary perfusion units (PU) (mean +/- SEM). RESULTS: Valsartan abolished angiotensin II-induced vasoconstriction and, more importantly, also ET-1-induced vasoconstriction in the skin microcirculation (ET-1 placebo versus valsartan, - 33 +/- 10 PU versus +33 +/- 21 PU for CC [P = .02] and -71 +/- 25 PU versus +108 +/- 21 PU for CT/TT [P < .001]). For both ET-1 and angiotensin II, valsartan effects were greater in GNB3 835T-allele carriers (P = .007 and P = .03 for ET-1 and angiotensin II, respectively, for CC versus CT/TT). Norepinephrine-mediated constriction was not influenced by valsartan. These effects were independent of blood pressure. CONCLUSION: Our results indicate that the renin-angiotensin system may significantly contribute to ET-1-mediated microvascular responses. Valsartan inhibited local vasoconstriction to angiotensin II and ET-1 to a greater degree in carriers of the GNB3 825T allele, which adds to data from earlier studies implicating the C825T polymorphism as a pharmacogenetic marker for drug effects.

Adult↗
PubMed2004

Activation of histamine H3 receptors in human nasal mucosa inhibits sympathetic vasoconstriction.

The peripheral histamine H3 receptor is a presynaptic heterologous receptor located on postganglionic sympathetic nerve fibers innervating sympathetic effector systems such as blood vessels and the heart. An extensive body of evidence shows that activation of the histamine H3 receptor attenuates sympathetic tone by presynaptic inhibition of noradrenaline release. It is proposed that this sympathoinhibitory action, in vivo, leads to reduced vasoconstriction, thereby eliciting a vasodilatory effect. In humans, the peripheral histamine H3 receptor has also been shown to exert a sympathoinhibitory function on specific peripheral autonomic effector systems. For example, human saphenous vein and heart possess functional presynaptic histamine H3 receptors on the sympathetic nerve terminals that upon activation decrease the sympathetic tone to these respective organs. The present studies were conducted to define the role of histamine H3 receptors on neurogenic sympathetic vasoconstrictor responses in human nasal turbinate mucosa. Contractility studies were conducted to evaluate the effect of histamine H3 receptor activation on sympathetic vasoconstriction in surgically isolated human nasal turbinate mucosa. We found that the histamine H3 receptor agonist, (R)-alpha-methylhistamine (30 and 300 nM), inhibited electrical field stimulation-induced (neurogenic) sympathetic vasoconstriction in a concentration-dependent fashion. Pretreatment with the selective histamine H3 receptor antagonist, clobenpropit (100 nM), blocked the sympathoinhibitory effect of (R)-alpha-methylhistamine on the neurogenic sympathetic vasoconstriction. In addition, analysis of Taqman mRNA expression studies showed a specific, high level of distribution of the histamine H3 receptor localized in the human nasal mucosa. Taken together, these studies indicate that histamine H3 receptors modulate vascular contractile responses in human nasal mucosa most likely by inhibiting noradrenaline release from sympathetic nerve terminals in nasal mucosa. It is further suggested that histamine H3 receptors may play a role in the regulation of vascular tone and nasal patency in histamine-dependent allergic nasal congestive disease.

Adolescent↗
PubMed2005

Histamine-induced vasodilation and vasoconstriction in the mesenteric resistance artery of the rat.

The present study was designed to examine the vascular response to histamine in rat perfused mesenteric vascular beds with active tone. In preparations with intact endothelium, perfusion of histamine (1 nM-100 microM) produced a concentration-dependent vasodilation. Histamine-induced vasodilation was attenuated by L-NAME (nitric oxide (NO) synthase inhibitor, 100 microM) and olopatadine (histamine H(1) receptor antagonist, 1 microM) but not by lafutidine (histamine H(2) receptor antagonist, 1 microM). Cold-storage denervation (4 degrees C for 72 h) of the preparation with intact endothelium attenuated the histamine-induced vasodilation. In preparations without endothelium, histamine at low concentrations (1-100 nM) produced only a small and rapid vasodilation, whereas histamine at concentrations higher than 1 muM produced triphasic vascular responses: initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. Lafutidine abolished only the histamine-induced initial vasodilation. Olopatadine abolished the histamine-induced second vasoconstriction and third vasodilation. Cold-storage denervation of the denuded preparation abolished the histamine-induced second vasoconstriction and third vasodilation. These findings suggest that histamine induced endothelium-dependent vasodilation via endothelium histamine H(1) receptors and endothelium-independent vasodilation via smooth muscle histamine H(2) receptors. It is also suggested that the histamine-induced endothelium-independent vasoconstriction and vasodilation are mediated by histamine H(1) receptors and perivascular nerves.

Animals↗
PubMed2005

Effect of estrogen on coronary vasoconstriction in patients undergoing coronary angioplasty.

BACKGROUND: Estrogen has an antioxidant potential which may contribute to its cardioprotective effect. We sought to determine whether estrogen administration can affect coronary vasomotor tone in patients after angioplasty by reducing 8-iso-prostaglandin (PG) F(2alpha) concentrations, a bioactive product of lipid peroxidation. METHODS: The study was designed to prospectively investigate 30 consecutive patients scheduled for elective coronary angioplasty. Patients were randomized into two groups according to whether they did not (group 1, n = 15) or did have (group 2, n = 15) intracoronary (i.c.) treatment with estrogen prior to coronary angioplasty. RESULTS: There were no significant differences of collateral circulation assessed by intracoronary Doppler flow velocity during balloon inflations between the study groups. The diameters of the coronary artery at the dilated and distal segments were significantly reduced 15 min after dilation compared with those immediately after dilation in group 1 (both P < 0.0001). The vasoconstriction was significantly blunted in group 2. The 8-iso-PGF(2alpha) levels in plasma from the coronary sinus rose significantly from 194 +/- 45 to 390 +/- 97 pg/ml (P < 0.0001, 95% confidence intervals = 142-249 pg/ml) 15 min after angioplasty in group 1, which was attenuated after administering estrogen. Significant correlation was found between the changes of coronary vasomotion of the dilated segment and 8-iso-PGF(2alpha) levels in group 1 (r = 0.73, P = 0.002). CONCLUSIONS: 8-iso-PGF(2alpha) is released into the coronary circulation during angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction. Estrogen administration attenuated vasoconstriction by reducing the 8-iso-PGF(2alpha) levels. This finding may provide a new strategy to treat coronary vasoconstriction after angioplasty.

Angina Pectoris↗
PubMed2005

Large and small vessel vasoconstriction following coronary artery stenting. Effect of intra coronary nitroglycerine and relation to LDL cholesterol.

UNLABELLED: Percutaneous coronary intervention (PCI) with stent placement induces epicardial coronary vasoconstriction, which is resolved by intracoronary (IC) nitroglycerine (NTG). The effect of stenting on microvascular coronary circulation and coronary blood flow (CBF) is less well established, and the effect of NTG on CBF following stenting is unknown. We examined the time course, extent, and influence of NTG, on PCI induced coronary vasoconstriction. Secondarily we also did an explorative analysis to evaluate the effect of increased levels of low density lipoprotein cholesterol (LDL-Cholesterol) on CBF after stenting. METHODS: Single vessel PCI stent was performed in 19 patients (age 62+/-10 years). Immediately after PCI, a 0.014 Doppler flow-wire was positioned distal to the stent, and IC NTG 0.2 mg was given. Quantitative coronary angiography (QCA) and CBF measurements were taken at baseline, and at 10, 20 and 30 min following PCI. Further IC NTG 200 mug was given after the measurement at 30 min, and the measurements were repeated at 31 and 33 min. Coronary flow velocity reserve (CFVR) was measured with adenosine IC bolus. RESULTS: Compared to baseline, there were significant reductions in CBF (24.5+/-18.3%), (35+/-30 vs. 28+/-25 ml/min, p=0.001) and coronary arterial diameter (5.1+/-5.4%) (2.63+/-0.54 vs. 2.50 mm+/-0.53, p=0.008) within 30 min following PCI. Subsequent IC NTG reversed both small (28+/-25 vs. 44+/-30 ml/min, p<0.001) and large (2.50+/-0.53 vs. 2.80+/-0.59 mm, p=0.001) vessel PCI induced vasoconstriction. LDL-cholesterol was significantly correlated to the percent reduction of blood-flow within 30 min (r=0.515, p=0.024, n=19) and to the maximal CBF after NTG (r=0.520, p=0.022, n=19). CONCLUSION: Following PCI, both large and small vessel vasoconstriction are seen as manifest by a reduction in coronary conduit vessel diameter and in CBF. These effects are reversed by NTG. Serum levels of LDL are modestly related to the reduction of CBF and to the degree of NTG induced vasodilatation of coronary micro-vasculature.

Aged↗