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Journal of the American College of... Mar 1990This study was designed to test the efficacy of nitroglycerin and diltiazem in inhibiting in vivo platelet aggregation and reducing platelet-mediated vasoconstriction in...
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)
Topics: Animals; Blood Platelets; Coronary Disease; Coronary Vessels; Diltiazem; Dogs; Endothelium, Vascular; Hemodynamics; Nitroglycerin; Platelet Aggregation; Serotonin; Thromboxane A2; Vasoconstriction
PubMed: 2105989
DOI: 10.1016/0735-1097(90)90652-6 -
Japanese Journal of Pharmacology May 1993The mechanism of pindolol-induced vasoconstriction in isolated and perfused dog coronary arteries was studied. Single injections of pindolol (1-100 micrograms),... (Comparative Study)
Comparative Study
The mechanism of pindolol-induced vasoconstriction in isolated and perfused dog coronary arteries was studied. Single injections of pindolol (1-100 micrograms), propranolol (1-30 micrograms), and 5-hydroxytryptamine (5-HT, 0.001-1 microgram) produced a dose-related vasoconstriction in dog coronary arteries which were dilated by acetylcholine. l-Pindolol constricted coronary arteries, but d-pindolol did not. The responses to pindolol and propranolol were not affected by any of the following compounds (100 micrograms): bunazosin (a selective alpha 1-adrenergic antagonist), DG 5128 (a selective alpha 2-adrenergic antagonist), atropine (a muscarinic antagonist), chlorpheniramine (a selective H1-antagonist), cimetidine (a selective H2-antagonist), and ketanserin (a selective 5-HT2 antagonist). Methysergide (10 micrograms, a 5-HT1 and 5-HT2 antagonist) significantly reduced pindolol- and propranolol-induced vasoconstrictions, although it did not reduce norepinephrine-induced vasoconstriction in the presence of 5 microM propranolol. Methysergide (10 micrograms) and ketanserin (100 micrograms) significantly suppressed 5-HT-induced vasoconstriction. Diltiazem (100 micrograms, a calcium antagonist) and the incubation in Ca(2+)-free solution containing 1 mM EGTA for 1 hr significantly reduced the vasoconstrictions induced by pindolol and propranolol. The Ca(2+)-free solution containing 1 mM EGTA abolished the vasoconstriction induced by 5-HT in the presence of 1 microM ketanserine. In a solution containing 20 mM KCl, the vasoconstrictions caused by pindolol and propranolol were enhanced in dog coronary arteries. These results indicate that the direct contractile effects of pindolol on dog coronary arteries are mediated, at least partly, through 5-HT1-like receptors, but not through alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Acetylcholine; Adrenergic alpha-Antagonists; Animals; Coronary Vessels; Diltiazem; Dogs; Female; Femoral Artery; Histamine Antagonists; In Vitro Techniques; Isoproterenol; Male; Parasympatholytics; Perfusion; Pindolol; Potassium Chloride; Propranolol; Stereoisomerism; Vasoconstriction
PubMed: 8101886
DOI: 10.1254/jjp.62.67 -
Anesthesiology Apr 1995Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently... (Clinical Trial)
Clinical Trial Comparative Study
BACKGROUND
Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction.
METHODS
Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree C identified the vasoconstriction threshold.
RESULTS
In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degree C, 1.7 +/- 0.58 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degree C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01).
CONCLUSIONS
Vasoconstriction did not produce a full core temperature "plateau," because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximately 1-h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.
Topics: Adult; Body Temperature Regulation; Female; Humans; Hypothermia, Induced; Male; Middle Aged; Neurosurgery; Vasoconstriction
PubMed: 7717557
DOI: 10.1097/00000542-199504000-00008 -
Croatian Medical Journal Apr 2003To analyze published data related to modern insight in the etiology of preeclampsia. (Review)
Review
AIM
To analyze published data related to modern insight in the etiology of preeclampsia.
METHODS
We analyzed 38 published articles on the etiology of preeclampsia. The articles were identified by a combined search of PubMed database of the National Library of Medicine, USA, by using the key words "preeclampsia" and "cause/etiology". Full-text articles were retrieved from the library of Hamamatsu University School of Medicine and Japan's library network.
RESULTS
According to the reports, vasospasm and vascular endothelial injury were two major pathological conditions of preeclampsia. They could be classified into 4 types of uteroplacental circulation failure: 1) disturbance in the circulation from the aorta to the uterine artery, 2) disturbance in the circulation of the spiral artery, 3) disturbance in the circulation of the intervillous space, and 4) disturbance in the circulation of the uterine vein reflux disorder. Major vessel bed of the uteroplacental unit consists of trophoblast, not of endothelial cells. Moreover, the trophoblast has many cellular functions, such as endothelial, immune, neural, and hormonal, resulting in production of various vasoactive substances. Thus, trophoblastic injury induced by uteroplacental circulation failure could affect and deteriorate the systemic circulation of the mother, resulting in preeclamptic symptoms.
CONCLUSION
The development of preeclampsia could be envisioned as a series of events from uteroplacental circulation failure to trophoblastic injury to vascular endothelial injury or vasospasm. The concept of "trophoblastic injury attributable to the uteroplacental circulation failure" can be a signpost for further investigations into the etiology of preeclampsia and type-specific treatment of preeclampsia.
Topics: Endothelium, Vascular; Evidence-Based Medicine; Female; Humans; Placental Circulation; Pre-Eclampsia; Pregnancy; Trophoblasts; Vasoconstriction
PubMed: 12698504
DOI: No ID Found -
The Journal of Physiology Nov 2010
Comparative Study Review
Topics: Animals; Blood Pressure; Female; Humans; Male; Sex Characteristics; Sympathetic Nervous System; Vasoconstriction
PubMed: 21078602
DOI: 10.1113/jphysiol.2010.199935 -
Revista Brasileira de Anestesiologia 2010Peribulbar anesthesia can reduce ocular blood flow (OBF) by increasing intraocular pressure (IOP) or due to the action of drugs. Ropivacaine has low toxicity and... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND AND OBJECTIVES
Peribulbar anesthesia can reduce ocular blood flow (OBF) by increasing intraocular pressure (IOP) or due to the action of drugs. Ropivacaine has low toxicity and intrinsic vasoconstrictive properties, yet to be proven on the ocular vasculature. Measurements of ocular pulse amplitude (OPA) allow the indirect evaluation of the OBF. The objective of the present study was to evaluate through the OBF the vasoconstrictive properties of ropivacaine in peribulbar anesthesia.
METHODS
Forty eyes undergoing peribulbar anesthesia with 7 mL of anesthetic solution without vasoconstrictor were randomly divided into two groups: ropivacaine (n = 20) and bupivacaine (n = 20). The IOP, ocular perfusion pressure (OPP), OPA, hemodynamic parameters, and the degree of akinesia before and 5 and 10 minutes after the blockade were evaluated. A dynamic contour tonometer was used to evaluate ocular parameters. Sedation was similar in both groups.
RESULTS
A significant variation in hemodynamic parameters and intensity of the motor blockade was not observed between groups. Differences in IOP, OPP, and OPA (p < 0.05) were observed between both groups at 5 and 10 minutes. The variation of IOP at 5 and 10 minutes was -0.88% and -4.54%, respectively with ropivacaine, and 17.61% and 16.56% with bupivacaine. The change in OPP after 5 and 10 minutes was 1.5% and 4.2% with ropivacaine, and -7% and -6% with bupivacaine. Ocular pulse amplitude varied -55.59% and -59.67% with ropivacaine at 5 and 10 minutes, and -34.71% and -28.82% with bupivacaine.
CONCLUSIONS
Ropivacaine reduced more intensely the ocular pulse amplitude despite little changes in IOP and OPP. The reduction in ocular blood flow caused by ropivacaine can be attributed to its vasoconstrictive effect.
Topics: Adult; Amides; Anesthetics, Local; Bupivacaine; Conjunctiva; Double-Blind Method; Eye; Female; Humans; Male; Prospective Studies; Pterygium; Regional Blood Flow; Ropivacaine; Vasoconstriction
PubMed: 20863930
DOI: 10.1016/S0034-7094(10)70061-1 -
Journal of Pharmacological Sciences Sep 2021Given the interconnection between depressive and cardiovascular disorders, we investigated whether antidepressant treatment (fluoxetine) modifies the serotonergic...
Given the interconnection between depressive and cardiovascular disorders, we investigated whether antidepressant treatment (fluoxetine) modifies the serotonergic influence on rat vascular noradrenergic outflow. Twelve-week-old male Wistar rats received fluoxetine treatment (10 mg/kg/day; p.o.) for 14 days; then, they were pithed and prepared for sympathetic stimulation. Vasopressor responses were obtained by electrical stimulation of the sympathetic outflow (0.1, 0.5, 1, and 5 Hz) or i.v. noradrenaline (NA; 0.01, 0.05, 0.1, and 0.5 μg/kg). In fluoxetine-treated group, the electrical-induced vasoconstrictions were lower compared to non-treated rats. Intravenous infusion of 5-HT (10 μg/kg/min) inhibited the sympathetically-induced vasoconstrictions. Only 5-CT, 8-OH-DPAT and L-694,247 (5-HT, 5-HT and 5-HT agonists, respectively) mimicked 5-HT-induced inhibition, while α-methyl-5-HT (5-HT agonist) increased the vasopressor responses. The inhibitory effect of 5-HT was: a) no modified by SB269970 (5-HT antagonist); b) abolished by WAY-100,635 (5-HT antagonist) plus LY310762 (5-HT antagonist); and c) potentiated by ritanserin (5-HT receptor antagonist). The vasoconstrictions induced by exogenous NA were not modified by 5-CT but were increased by α-methyl-5-HT. Our results suggest that fluoxetine treatment decreases NA release at vascular level and changes 5-HT modulation on rat vascular noradrenergic neurotransmission, inducing sympatho-inhibition via prejunctional 5-HT receptors, and sympatho-potentiation via pre and/or postjunctional 5-HT receptors.
Topics: Animals; Antidepressive Agents; Blood Vessels; Electric Stimulation; Fluoxetine; Male; Norepinephrine; Rats, Wistar; Receptor, Serotonin, 5-HT2A; Serotonin; Sympathetic Nervous System; Synaptic Transmission; Vasoconstriction; Rats
PubMed: 34294372
DOI: 10.1016/j.jphs.2021.05.008 -
Experimental Physiology Sep 1995Although frequently unrecognized, hypoxic pulmonary vascular disease is an important cofactor in the morbidity and mortality of a wide spectrum of disease processes. The... (Review)
Review
Although frequently unrecognized, hypoxic pulmonary vascular disease is an important cofactor in the morbidity and mortality of a wide spectrum of disease processes. The hypoxic response incorporates two distinct phases, the acute hypoxic vasoconstrictor response and vascular remodelling associated with prolonged alveolar hypoxia. Understanding of the mechanisms causing both processes has increased rapidly and may result in the near future in specific treatment aimed at correcting underlying physiological abnormalities. However, currently available therapies remain limited to correction of the hypoxaemia and generalized non-specific pulmonary vasodilatation. The recent development of inhaled NO therapy represents a significant advance in the management of the acute hypoxic pulmonary vasoconstriction occurring during critical illness.
Topics: Animals; Humans; Hypertension, Pulmonary; Hypoxia; Pulmonary Circulation; Vasoconstriction
PubMed: 8546875
DOI: 10.1113/expphysiol.1995.sp003894 -
Circulation Research Jun 2011The coordination of vascular smooth muscle cell constriction plays an important role in vascular function, such as regulation of blood pressure; however, the mechanism...
RATIONALE
The coordination of vascular smooth muscle cell constriction plays an important role in vascular function, such as regulation of blood pressure; however, the mechanism responsible for vascular smooth muscle cell communication is not clear in the resistance vasculature. Pannexins (Panx) are purine-releasing channels permeable to the vasoconstrictor ATP and thus may play a role in the coordination of vascular smooth muscle cell constriction.
OBJECTIVE
We investigated the role of pannexins in phenylephrine- and KCl-mediated constriction of resistance arteries.
METHODS AND RESULTS
Western blot, immunohistochemistry, and immunogold labeling coupled to scanning and transmission electron microscopy revealed the presence of Panx1 but not Panx2 or Panx3 in thoracodorsal resistance arteries. Functionally, the contractile response of pressurized thoracodorsal resistance arteries to phenylephrine was decreased significantly by multiple Panx inhibitors (mefloquine, probenecid, and (10)Panx1), ectonucleotidase (apyrase), and purinergic receptor inhibitors (suramin and reactive blue-2). Electroporation of thoracodorsal resistance arteries with either Panx1-green fluorescent protein or Panx1 small interfering RNA showed enhanced and decreased constriction, respectively, in response to phenylephrine. Lastly, the Panx inhibitors did not alter constriction in response to KCl. This result is consistent with coimmunoprecipitation experiments from thoracodorsal resistance arteries, which suggested an association between Panx1 and α1D-adrenergic receptor.
CONCLUSIONS
Our data demonstrate for the first time a key role for Panx1 in resistance arteries by contributing to the coordination of vascular smooth muscle cell constriction and possibly to the regulation of blood pressure.
Topics: Animals; Connexins; Mice; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Nerve Tissue Proteins; Phenylephrine; Potassium Chloride; Receptors, Adrenergic, alpha-1; Vascular Resistance; Vasoconstriction
PubMed: 21546608
DOI: 10.1161/CIRCRESAHA.110.237594 -
Journal of the American College of... Jul 2013
Topics: Adipocytes; Arteries; Bariatric Surgery; Humans; Inflammation; Vasoconstriction
PubMed: 23665373
DOI: 10.1016/j.jacc.2013.04.028