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Annals of Medicine 1991Basal release of endothelium-derived relaxing factor (EDRF) and prostacyclin from intact vascular endothelium may inhibit continuously platelet aggregation. If local... (Review)
Review
Basal release of endothelium-derived relaxing factor (EDRF) and prostacyclin from intact vascular endothelium may inhibit continuously platelet aggregation. If local platelet aggregation occurs, platelet-derived adenine nucleotides stimulate the release of EDRF. Stimulated EDRF release may override the direct vasoconstrictor effects of other platelet products such as thromboxane and serotonin resulting in local vasodilatation. In addition, stimulation of EDRF release by adenine nucleotides may inhibit further platelet adhesion and aggregation by a feedback mechanism. Thus, intact vascular endothelium may play an important role in the defense against platelet deposition and vasospasm. In atherosclerosis, basal and stimulated release of EDRF is markedly reduced. Endothelial dysfunction will impair this protective mechanism and will favour vasoconstriction and further platelet disposition. Occurrence of occlusive thrombus formation in patients with coronary artery disease may be pathophysiologically related to this impairment of endothelial defense.
Topics: Animals; Arteriosclerosis; Endothelium, Vascular; Humans; Nitric Oxide; Platelet Aggregation; Vasoconstriction; Vasodilation
PubMed: 1756024
DOI: 10.3109/07853899109150516 -
AJNR. American Journal of Neuroradiology Oct 2020There is mounting evidence supporting the benefit of intra-arterial administration of vasodilators in diagnosing reversible cerebral vasoconstriction syndrome. We...
BACKGROUND AND PURPOSE
There is mounting evidence supporting the benefit of intra-arterial administration of vasodilators in diagnosing reversible cerebral vasoconstriction syndrome. We prospectively quantified the degree of luminal diameter dilation after intra-arterial administration of verapamil and its accuracy in diagnosing reversible cerebral vasoconstriction syndrome.
MATERIALS AND METHODS
Patients suspected of having intracranial arteriopathy on noninvasive imaging and referred for digital subtraction angiography were enrolled in a prospective registry. Intra-arterial verapamil was administered in vascular territories with segmental irregularities. The caliber difference (Caliber - Caliber) and the proportion of caliber change ([(Caliber - Caliber)/Caliber] × 100%) were used to determine the response to verapamil. The diagnosis of reversible cerebral vasoconstriction syndrome was made on the basis of clinical and imaging features at a follow-up appointment, independent of the reversibility of verapamil. Receiver operating characteristic curve analysis was performed to determine the best threshold.
RESULTS
Twenty-six patients were included, and 9 (34.6%) were diagnosed with reversible cerebral vasoconstriction syndrome. A total of 213 vascular segments were assessed on diagnostic angiography. Every patient with a final diagnosis of reversible cerebral vasoconstriction syndrome responded to intra-arterial verapamil. The maximal proportion of change (< .001), mean proportion of change (= .002), maximal caliber difference (= .004), and mean caliber difference (= .001) were statistically different between patients with reversible cerebral vasoconstriction syndrome and other vasculopathies. A maximal proportion of change ≥32% showed a sensitivity of 100% and a specificity of 88.2% to detect reversible cerebral vasoconstriction syndrome (area under the curve = 0.951). The Reversible Cerebral Vasoconstriction Syndrome-2 score of ≥5 points achieved a lower area under the curve (0.908), with a sensitivity of 77.8% and a specificity of 94.1%.
CONCLUSIONS
Objective measurement of the change in the arterial calibers after intra-arterial verapamil is accurate in distinguishing reversible cerebral vasoconstriction syndrome from other vasculopathies. A proportion of change ≥32% has the best diagnostic performance.
Topics: Adult; Angiography, Digital Subtraction; Female; Humans; Infusions, Intra-Arterial; Male; Middle Aged; Vasoconstriction; Vasodilator Agents; Vasospasm, Intracranial; Verapamil
PubMed: 32943423
DOI: 10.3174/ajnr.A6772 -
Journal of the American College of... Jan 2003
Topics: Coronary Artery Disease; Coronary Circulation; Coronary Stenosis; Humans; Myocardial Infarction; Polymorphism, Genetic; Receptors, Adrenergic, alpha; Risk Factors; Vasoconstriction
PubMed: 12535807
DOI: 10.1016/s0735-1097(02)02703-1 -
Pediatric Research Sep 2022Sodium bicarbonate (NaHCO) is no longer recommended by the Neonatal Resuscitation Program (NRP), but is still being used by some neonatologists. The effects of NaHCO on...
BACKGROUND
Sodium bicarbonate (NaHCO) is no longer recommended by the Neonatal Resuscitation Program (NRP), but is still being used by some neonatologists. The effects of NaHCO on cerebral hemodynamics are unclear. Therefore, we investigated the effects of NaHCO on cerebral blood flow (CBF) and cerebrovascular function using a newborn piglet model.
METHODS
Newborn pigs were anesthetized, intubated, and ventilated. Cranial windows were implanted to evaluate changes in pial arteriolar diameters (PADs) as a surrogate for CBF during a 4-h intravenous infusion of 3% NaHCO. Cerebrovascular reactivity to vasodilators and vasoconstrictors was investigated during vehicle control and during NaHCO infusion.
RESULTS
NaHCO infusion caused significant and progressive pial arteriolar vasoconstrictions. During NaHCO infusion, cerebrovascular reactivity was preserved. Adding vasodilators decreased cerebral vasoconstriction, while adding vasoconstrictors exaggerated cerebral vasoconstriction.
CONCLUSIONS
Intravenous infusion of NaHCO over 4 h caused progressive vasoconstriction of pial arterioles. Cerebrovascular function evaluated by the responses of pial arterioles to physiologically relevant vasoconstrictors and vasodilators was preserved during NaHCO infusion. A notable additional reduction of PADs was observed during NaHCO infusion in the presence of vasoconstrictors. Extrapolating our findings to human neonates should alarm the clinicians that using NaHCO in neonates may cause cerebral hypoperfusion.
IMPACT
Cerebral vasoconstriction occurs during slow infusion of 3% diluted NaHCO. Cerebral vasoconstriction is exaggerated when another vasoconstrictor is added during NaHCO infusion. Cerebrovascular function is preserved during NaHCO infusion. Clinicians should be aware of the risk of cerebral hypoperfusion with NaHCO infusion in vulnerable neonates.
Topics: Animals; Animals, Newborn; Cerebrovascular Circulation; Humans; Infant, Newborn; Resuscitation; Sodium Bicarbonate; Swine; Vasoconstriction; Vasoconstrictor Agents; Vasodilator Agents
PubMed: 34862458
DOI: 10.1038/s41390-021-01876-x -
British Journal of Pharmacology Jan 2020Endothelium-derived vasoconstriction is a hallmark of vascular dysfunction in hypertension. In some cases, an overproduction of endothelium-derived prostacyclin (PGI )...
BACKGROUND AND PURPOSE
Endothelium-derived vasoconstriction is a hallmark of vascular dysfunction in hypertension. In some cases, an overproduction of endothelium-derived prostacyclin (PGI ) can cause contraction rather than relaxation. Relaxin is well known for its vasoprotective actions, but the possibility that this peptide could also reverse endothelium-derived vasoconstriction has never been investigated. We tested the hypothesis that short-term relaxin treatment mitigates endothelium-derived vasoconstriction in spontaneously hypertensive rats (SHR).
EXPERIMENTAL APPROACH
Male Wistar Kyoto rats (WKY) and SHR were subcutaneously infused with either vehicle (20 mmol·L sodium acetate) or relaxin (13.3 μg·kg ·hr ) using osmotic minipumps for 3 days. Vascular reactivity to the endothelium-dependent agonist ACh was assessed in vitro by wire myography. Quantitative PCR and LC-MS were used to identify changes in gene expression of prostanoid pathways and PG production, respectively.
KEY RESULTS
Relaxin treatment ameliorated hypertension-induced endothelial dysfunction by increasing NO-dependent relaxation and reducing endothelium-dependent contraction. Notably, short-term relaxin treatment up-regulated mesenteric PGI receptor (IP) expression, permitting PGI -IP-mediated vasorelaxation. In the aorta, reversal of contraction was accompanied by suppression of the hypertension-induced increase in prostanoid-producing enzymes and reduction in PGI -evoked contractions.
CONCLUSIONS AND IMPLICATIONS
Relaxin has region-dependent vasoprotective actions in hypertension. Specifically, relaxin has distinct effects on endothelium-derived contracting factors and their associated vasoconstrictor pathways in mesenteric arteries and the aorta. Taken together, these observations reveal the potential of relaxin as a new therapeutic agent for vascular disorders that are associated with endothelium-derived vasoconstriction including hypertension.
Topics: Animals; Dose-Response Relationship, Drug; Endothelium, Vascular; Hypertension; Male; Mesenteric Arteries; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Relaxin; Vasoconstriction
PubMed: 31479151
DOI: 10.1111/bph.14858 -
Critical Care (London, England) 2001Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical... (Review)
Review
Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical mechanism and its exact physiological function. Recent work suggests an important role for pulmonary arteriolar smooth muscle cell oxygen-sensitive voltage-dependent potassium channels. Inhibition of these channels by decreased PO2 inhibits outward potassium current, causing membrane depolarization, and calcium entry through voltage-dependent calcium channels. Endothelium-derived vasoconstricting and vasodilating mediators modulate this intrinsic smooth muscle cell reactivity to hypoxia. However, refined modeling of hypoxic pulmonary vasoconstriction operating as a feedback mechanism in inhomogeneous lungs, using more realistic stimulus-response curves and confronted with direct measurements of regional blood flow distribution, shows a more effective than previously assessed ability of this remarkable intrapulmonary reflex to improve gas exchange and arterial oxygenation. Further studies could show clinical benefit of pharmacological manipulation of hypoxic pulmonary vasoconstriction, in circumstances of life-threatening hypoxemia.
Topics: Acute Disease; Anesthesia; Humans; Hypoxia; Oxygen; Pulmonary Artery; Pulmonary Veins; Respiratory Insufficiency; Vasoconstriction
PubMed: 11299064
DOI: 10.1186/cc989 -
American Journal of Physiology.... Sep 2007Sex differences exist in a variety of cardiovascular disorders. Sex hormones have been shown to mediate pulmonary artery (PA) vasodilation. However, the effects of...
Sex differences exist in a variety of cardiovascular disorders. Sex hormones have been shown to mediate pulmonary artery (PA) vasodilation. However, the effects of fluctuations in physiological sex hormone levels due to sex and menstrual cycle on PA vasoreactivity have not been clearly established yet. We hypothesized that sex and menstrual cycle affect PA vasoconstriction under both normoxic and hypoxic conditions. Isometric force displacement was measured in isolated PA rings from proestrus females (PF), estrus and diestrus females (E/DF), and male (M) Sprague-Dawley rats. The vasoconstrictor response under normoxic conditions (organ bath bubbled with 95% O(2)-5% CO(2)) was measured after stimulation with 80 mmol/l KCl and 1 mumol/l phenylephrine. Hypoxia was generated by changing the gas to 95% N(2)-5% CO(2). PA rings from PF demonstrated an attenuated vasoconstrictor response to KCl compared with rings from E/DF (75.58 +/- 3.2% vs. 92.43 +/- 4.24%, P < 0.01). Rings from M also exhibited attenuated KCl-induced vasoconstriction compared with E/DF (79.34 +/- 3.2% vs. 92.43 +/- 4.24%, P < 0.05). PA rings from PF exhibited an attenuated vasoconstrictor response to phenylephrine compared with E/DF (59.61 +/- 2.98% vs. 70.03 +/- 4.61%, P < 0.05). While the maximum PA vasodilation during hypoxia did not differ between PF, E/DF, and M, phase II of hypoxic pulmonary vasoconstriction was markedly diminished in the PA from PF (64.10 +/- 7.10% vs. 83.91 +/- 5.97% in M, P < 0.05). We conclude that sex and menstrual cycle affect PA vasoconstriction in isolated PA rings. Even physiological increases in circulating estrogen levels attenuate PA vasoconstriction under both normoxic and hypoxic conditions.
Topics: Animals; Estrogens; Female; Male; Menstrual Cycle; Pulmonary Artery; Rats; Rats, Sprague-Dawley; Sex Factors; Vasoconstriction
PubMed: 17595218
DOI: 10.1152/ajpendo.00201.2007 -
Annals of Medicine Apr 2000Several opposite effects of serotonin (5HT) on tumour growth have been reported. On one hand, 5HT is known as a growth factor for several types of nontumoural cells, and... (Review)
Review
Several opposite effects of serotonin (5HT) on tumour growth have been reported. On one hand, 5HT is known as a growth factor for several types of nontumoural cells, and it has been proposed to take part in the autocrine loops of growth factors contributing to cell proliferation in aggressive tumours such as small cell lung carcinoma. Depending on the tumour type either 5HT2 or 5HT1 receptor antagonist have been found to inhibit the 5HT-induced increase in tumour growth. In contrast, several authors have also reported that 5HT and 5HT2 agonist can inhibit tumour growth. Most often this effect has been considered to be related with the specific vasoconstrictive effect of 5HT or 5HT2 agonists on the vessels irrigating the tumour, which has been evidenced by intravital microscopy. Intravital microscopy studies have also shown that vessels perfusing the tumour exhibit a specific vasconstrictive response to 5HT1 agonists. In addition, 5HT has been shown to be involved in the effects of several anticancer treatments associated with the reduction of tumour flow. Finally, the specific vasoconstrictive effect of 5HT or 5HT receptor subtype agonists might also be useful in inducing hypoxia in tumours, which could be exploited in a strategy using hypoxia-selective cytotoxins or hypoxia-selective gene therapy.
Topics: Animals; Carcinoma, Small Cell; Endothelium, Vascular; Humans; Lung Neoplasms; Neoplasms; Neoplasms, Experimental; Serotonin; Serotonin Receptor Agonists; Vasoconstriction
PubMed: 10821326
DOI: 10.3109/07853890008998826 -
Biomedical Papers of the Medical... Dec 2007Humoral systems play an important role in the pathophysiology and development of chronic heart failure (CHF). (Review)
Review
BACKGROUND
Humoral systems play an important role in the pathophysiology and development of chronic heart failure (CHF).
METHODS
We conducted a search of neurohumoral activation in heart failure and its risk in the development of CHF.
RESULTS AND CONCLUSION
Neurohumoral factors may be divided into vasoconstrictive, vasodilative and cytokines. The main vasoconstrictive systems are the renin-angiotensin-aldosterone system (RAAS) and the sympathoadrenal system (SAS). Cytokines include tumour necrosis factor (TNF) alpha and interleukins. The systems of actions are interconnected and they mutually influence their secretion and activities. The possibilities of their detection and assessment for clinical purposes depend on their changes and kinetics in the organism and on the activity of individual metabolites. Apart from their vasoactive effects, the majority of humoral actions also interfere in the process of remodelling, function of the endothelium, blood elements, cardiomyocytes, cells of the smooth muscles, and in immunity as well as inflammatory processes. The rapid development of knowledge on the humoral actions in recent years has made possible their utilisation in diagnostics, treatment and prognosis.
Topics: Cytokines; Heart Failure; Humans; Neurosecretory Systems; Vasoconstriction; Vasodilation
PubMed: 18345252
DOI: 10.5507/bp.2007.035 -
Circulation Journal : Official Journal... Feb 2018The gastroepiploic artery (GEA) plays an important role in the era of multiple arterial revascularization, but spasm is a major matter of concern. The internal thoracic...
BACKGROUND
The gastroepiploic artery (GEA) plays an important role in the era of multiple arterial revascularization, but spasm is a major matter of concern. The internal thoracic artery has been shown to have a strong tendency to spasm in its distal bifurcating part, whereas the segmental difference in vasoreactivity of the GEA has never been performed.Methods and Results:The full length of the GEA obtained from 21 patients undergoing a total gastrectomy was divided into 3 sections: proximal (5 cm from the origin), middle, and distal (5 cm from the end). Concentration-response curves for vasoconstrictors (phenylephrine, prostaglandin F2α, and endothelin-1) and vasodilators (carperitide, nitroglycerin, and nifedipine) were then established using organ baths. All the vasoconstrictors and vasodilators produced concentration-dependent responses in each section. As the concentration of the vasoconstrictors increased, segments at the distal section showed a significantly greater contraction than those at the middle and proximal sections regardless of the type of vasoconstrictor. The effective concentration of drugs that caused 50% of the maximal response for endothelin-1 was significantly greater in the distal section than that in the proximal sections. No significant difference was found in vasodilators-induced relaxation.
CONCLUSIONS
The contractility increases toward to the end of the GEA. Clinically, the distal portion of the GEA should be trimmed off and not be used as an anastomotic site wherever possible.
Topics: Dinoprost; Dose-Response Relationship, Drug; Endothelin-1; Gastroepiploic Artery; Humans; Phenylephrine; Vasoconstriction; Vasoconstrictor Agents
PubMed: 29238009
DOI: 10.1253/circj.CJ-17-0943