Relevant bibliographies by topics / Vasodilators

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Vasodilators'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 June 2025

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Journal articles on the topic "Vasodilators"

1

Kitai, Takeshi, W. H. Wilson Tang, Andrew Xanthopoulos, et al. "Impact of early treatment with intravenous vasodilators and blood pressure reduction in acute heart failure." Open Heart 5, no. 2 (2018): e000845. http://dx.doi.org/10.1136/openhrt-2018-000845.

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ObjectiveAlthough vasodilators are used in acute heart failure (AHF) management, there have been no clear supportive evidence regarding their routine use. Recent European guidelines recommend systolic blood pressure (SBP) reduction in the range of 25% during the first few hours after diagnosis. This study aimed to examine clinical and prognostic significance of early treatment with intravenous vasodilators in relation to their subsequent SBP reduction in hospitalised AHF.MethodsWe performed post hoc analysis of 1670 consecutive patients enrolled in the Registry Focused on Very Early Presentation and Treatment in Emergency Department of Acute Heart Failure. Intravenous vasodilator use within 6 hours of hospital arrival and subsequent SBP changes were analysed. Outcomes were gauged by 1-year mortality and diuretic response (DR), defined as total urine output 6 hours posthospital arrival per 40 mg furosemide-equivalent diuretic use.ResultsOver half of the patients (56.0%) were treated with intravenous vasodilators within the first 6 hours. In this vasodilator-treated cohort, 554 (59.3%) experienced SBP reduction ≤25%, while 381 (40.7%) experienced SBP reduction >25%. In patients experiencing ≤25% drop in SBP, use of vasodilator was associated with greater DR compared with no vasodilators (p<0.001). Moreover, vasodilator treatment with ≤25% drop in SBP was independently associated with lower all-cause mortality compared with those treated without vasodilators (adjusted HR 0.74, 95% CI 0.57 to 0.96, p=0.028).ConclusionsIntravenous vasodilator therapy was associated with greater DR and lower mortality, provided SBP reduction was less than 25%. Our results highlight the importance in early administration of intravenous vasodilators without causing excess SBP reduction in AHF management.Clinical trial registrationURL: http://www.umin.ac.jp/ctr/ Unique identifier: UMIN000014105.
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Clifford, Philip S., and Ylva Hellsten. "Vasodilatory mechanisms in contracting skeletal muscle." Journal of Applied Physiology 97, no. 1 (2004): 393–403. http://dx.doi.org/10.1152/japplphysiol.00179.2004.

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Skeletal muscle blood flow is closely coupled to metabolic demand, and its regulation is believed to be mainly the result of the interplay of neural vasoconstrictor activity and locally derived vasoactive substances. Muscle blood flow is increased within the first second after a single contraction and stabilizes within ∼30 s during dynamic exercise under normal conditions. Vasodilator substances may be released from contracting skeletal muscle, vascular endothelium, or red blood cells. The importance of specific vasodilators is likely to vary over the time course of flow, from the initial rapid rise to the sustained elevation during steady-state exercise. Exercise hyperemia is therefore thought to be the result of an integrated response of more than one vasodilator mechanism. To date, the identity of vasoactive substances involved in the regulation of exercise hyperemia remains uncertain. Numerous vasodilators such as adenosine, ATP, potassium, hypoxia, hydrogen ion, nitric oxide, prostanoids, and endothelium-derived hyperpolarizing factor have been proposed to be of importance; however, there is little support for any single vasodilator being essential for exercise hyperemia. Because elevated blood flow cannot be explained by the failure of any single vasodilator, a consensus is beginning to emerge for redundancy among vasodilators, where one vasoactive compound may take over when the formation of another is compromised. Conducted vasodilation or flow-mediated vasodilation may explain dilation in vessels (i.e., feed arteries) not directly exposed to vasodilator substances in the interstitium. Future investigations should focus on identifying novel vasodilators and the interaction between vasodilators by simultaneous inhibition of multiple vasodilator pathways.
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Glenn, Thomas, Nicole Duster, Jerry Dwek, Jose Silva-Sepulveda, and Howaida G. El-Said. "Selective Use of Pulmonary Vasodilators in Patients with Fontan Physiology." Journal of Interventional Cardiology 2022 (November 10, 2022): 1–6. http://dx.doi.org/10.1155/2022/7602793.

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Background. Fontan-associated liver disease is a well-known sequela following the Fontan procedure for patients living with single-ventricle heart disease. Pulmonary vasodilators, such as phosphodiesterase type 5 inhibitors, have emerged as a potential therapeutic option for lowering central venous pressures by reducing pulmonary vascular resistance. Method. We performed a single-center retrospective review of Fontan patients who were placed on pulmonary vasodilator therapy with prehemodynamic and posthemodynamic, MR elastography, and histologic assessments. Results. A total of 125 patients with Fontan circulation underwent surveillance with cardiac catheterization during the review period. Fifty-three (42%) patients who did not have increased end-diastolic pressures at the time of cardiac catheterization were started on phosphodiesterase type 5 inhibitor therapy. Nine patients (17%) underwent posttherapy follow-up catheterization. The mean Fontan pressure decreased from 15.4 ± 3.3 mmHg to 13.3 ± 2.5 mmHg ( p = 0.026 ), after initiation of pulmonary vasodilatory therapy. There was no change in end-diastolic pressure, transpulmonary gradient, wedge pressure, pulmonary vascular resistance, cardiac index, or saturation. Eleven patients (21%) underwent pretherapy MR elastography testing with posttherapy follow-up MR elastography. We found no improvement in liver stiffness score following the application of pulmonary vasodilators. Three patients underwent pretherapy and posttherapy liver biopsies, with variable histological changes observed within the hepatic parenchyma. Conclusions. These data demonstrate indeterminate results for the selective use of pulmonary vasodilators but highlight the need for large prospective randomized control trials of pulmonary vasodilator therapies to fully assess the benefit of such therapies in Fontan-associated liver disease.
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Wunsch, Stacy A., Judy Muller-Delp, and Michael D. Delp. "Time course of vasodilatory responses in skeletal muscle arterioles: role in hyperemia at onset of exercise." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (2000): H1715—H1723. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1715.

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At the onset of dynamic exercise, muscle blood flow increases within 1–2 s. It has been postulated that local vasodilatory agents produced by the vascular endothelium or the muscle itself contribute to this response. We hypothesized that only vasodilators that act directly on the vascular smooth muscle could produce vasodilation of skeletal muscle arterioles in <2 s. To test this hypothesis, we determined the time course of the vasodilatory response of isolated skeletal muscle arterioles to direct application of potassium chloride, adenosine, acetylcholine, and sodium nitroprusside. Soleus and gastrocnemius muscles were dissected from the hindlimbs of male Sprague-Dawley rats. First-order arterioles (100–200 μm) were isolated, cannulated on micropipettes, and pressurized to 60 cmH2O in an organ bath. Vasodilatory agents were added directly to the bath, and diameter responses of the arterioles were recorded in real time on a videotape recorder. Frame-by-frame analysis of the diameter responses indicated that none of the vasodilator agents tested produced significant diameter increases in <4 s in either soleus or gastrocnemius muscle arterioles. These results indicate that, although these local vasodilators produce significant vasodilation of skeletal muscle resistance arterioles, these responses are not rapid enough (within 1–2 s) to contribute to the initiation of the exercise hyperemic response at the onset of dynamic exercise.
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Shiraishi, Yasuyuki, Shun Kohsaka, Toshiomi Katsuki, et al. "Benefit and harm of intravenous vasodilators across the clinical profile spectrum in acute cardiogenic pulmonary oedema patients." European Heart Journal: Acute Cardiovascular Care 9, no. 5 (2020): 448–58. http://dx.doi.org/10.1177/2048872619891075.

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Background: The absence of high quality, large-scale data that indicates definitive mortality benefits does not allow for firm conclusions on the role of intravenous vasodilators in acute heart failure. We aimed to investigate the associations between intravenous vasodilators and clinical outcomes in acute heart failure patients, with a specific focus on patient profiles and type of vasodilators. Methods: Data of 26,212 consecutive patients urgently hospitalised for a primary diagnosis of acute heart failure between 2009 and 2015 were extracted from a government-funded multicentre data registration system. Propensity scores were calculated with multiple imputations and 1:1 matching performed between patients with and without vasodilator use. The primary endpoint was inhospital mortality. Results: On direct comparison of the vasodilator and non-vasodilator groups after propensity score matching, there were no significant differences in the inhospital mortality rates (7.5% vs. 8.8%, respectively; P=0.098) or length of intensive/cardiovascular care unit stay and hospital stay between the two groups. However, there was a substantial difference in baseline systolic blood pressure by vasodilator type; favourable impacts of vasodilator use on inhospital mortality were observed among patients who had higher systolic blood pressures and those who had no atrial fibrillation on admission. Furthermore, when compared to nitrates, the use of carperitide (natriuretic peptide agent) was significantly associated with worse outcomes, especially in patients with intermediate systolic blood pressures. Conclusions: In acute heart failure patients, vasodilator use was not universally associated with improved inhospital outcomes; rather, its effect depended on individual clinical presentation: patients with higher systolic blood pressure and no atrial fibrillation seemed to benefit maximally from vasodilators. Trial registration: UMIN-CTR identifier, UMIN000013128
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Han, Ningxin, Hui Qi, Yujie Yin, et al. "The effectiveness of vasodilators on chronic obstructive pulmonary disease: A systematic review and meta-analysis." Medicine 103, no. 46 (2024): e39794. http://dx.doi.org/10.1097/md.0000000000039794.

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Background: Chronic obstructive pulmonary disease (COPD) is a complex progressive disease. Some vasodilators have been reported with therapeutic potential to protect vascular function therefore may delay the progression of COPD. Methods: We searched PubMed, Embase, Cochrane Library, Web of Science, OVID and Clinicaltrials.gov database for eligible randomized controlled trials (RCTs) published before January 1, 2024. RCTs which treatment with vasodilators to COPD patients were included. Gas-blood exchange indicators were the primary outcomes, and ventilation function and quality of life indicators were the secondary outcomes. Mean differences with 95% confidence intervals were extracted. Subgroup analysis of vasodilator category and COPD complicated with or without pulmonary hypertension (PH) were performed. The risk of bias was assessed using Cochrane risk of bias tool, and the meta-analysis was conducted. Results: Twenty studies with a total sample size of 986 were included. The results showed that the 2 types of drugs in vasodilators included PDE-5 inhibitors could improve DLCO (MD = 6.56 [95% CI (1.74, 11.39)], P = .008) and iNO could reduce PaCO2 (MD = −0.10 [95% CI (−0.17, −0.03)], P = .006). Vasodilators could reduce PaCO2 in COPD complicated with PH (COPD-PH) (MD = −0.10 [95% CI (−0.17, −0.03)], P = .006). There were no statistically significant differences in FEV1 (MD = 0.02 [95% CI (−0.11, 0.16)], P = .74), FEV1% predicted (MD = 0.07 [95% CI (−1.90, 2.05)], P = .94), FEV1/FVC (MD = 0.70 [95% CI (−4.02, 5.42)], P = .77) and V E /V CO2 (MD = −0.17 [95% CI (−2.39, 2.05)], P = .88) levels. The total SGRQ score was significantly lower in vasodilator groups (MD = −5.53 [95% CI (−9.81, −1.24)], P = .01). Conclusions: The therapeutic effects of vasodilators for COPD are controversial. In this meta-analysis, vasodilators have benefits in improving gas-blood exchange function and quality of life in COPD patients. However, vasodilators may have a limited capacity to improve pulmonary function.
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Morales-Cano, Daniel, Bianca Barreira, Beatriz De Olaiz Navarro, et al. "Oxygen-Sensitivity and Pulmonary Selectivity of Vasodilators as Potential Drugs for Pulmonary Hypertension." Antioxidants 10, no. 2 (2021): 155. http://dx.doi.org/10.3390/antiox10020155.

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Current approved therapies for pulmonary hypertension (PH) aim to restore the balance between endothelial mediators in the pulmonary circulation. These drugs may exert vasodilator effects on poorly oxygenated vessels. This may lead to the derivation of blood perfusion towards low ventilated alveoli, i.e., producing ventilation-perfusion mismatch, with detrimental effects on gas exchange. The aim of this study is to analyze the oxygen-sensitivity in vitro of 25 drugs currently used or potentially useful for PH. Additionally, the study analyses the effectiveness of these vasodilators in the pulmonary vs. the systemic vessels. Vasodilator responses were recorded in pulmonary arteries (PA) and mesenteric arteries (MA) from rats and in human PA in a wire myograph under different oxygen concentrations. None of the studied drugs showed oxygen selectivity, being equally or more effective as vasodilators under conditions of low oxygen as compared to high oxygen levels. The drugs studied showed low pulmonary selectivity, being equally or more effective as vasodilators in systemic than in PA. A similar behavior was observed for the members within each drug family. In conclusion, none of the drugs showed optimal vasodilator profile, which may limit their therapeutic efficacy in PH.
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Nawaytou, Hythem, Jeffrey R. Fineman, Shahin Moledina, Dunbar Ivy, Steven H. Abman, and Maria J. Del Cerro. "Practice patterns of pulmonary hypertension secondary to left heart disease among pediatric pulmonary hypertension providers." Pulmonary Circulation 11, no. 1 (2021): 204589402199144. http://dx.doi.org/10.1177/2045894021991446.

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Development of pulmonary hypertension (PH) in patients with left side heart disease (LHD) is a predictor of poor prognosis. The use of pulmonary vasodilators in PH associated with LHD (PH-LHD) is controversial. In this study, we describe the practice patterns regarding the use of pulmonary vasodilators in PH-LHD among a group of international pediatric PH specialists. A survey was distributed to the members of three pediatric PH networks: PPHNet, PVRI, and REHIPED. The survey queried participants on the rationale, indications, and contraindications of the use of pulmonary vasodilators in children with PH-LHD. Forty-seven PH specialists from 39 PH centers completed the survey. Participants included PH specialists from North America (57%), South America (15%), and Europe (19%). The majority of participants (74%) recommended the use of pulmonary vasodilators only in patients with combined pre-capillary and post-capillary pulmonary hypertension. Participants required the presence of clinical symptoms or signs of heart failure (68%) or right ventricular dysfunction by echocardiography (51%) in order to recommend pulmonary vasodilator therapy. There was no agreement regarding hemodynamic criteria used to recommend pulmonary vasodilators or the etiologies of LHD considered contraindications for using pulmonary vasodilators to manage PH-LHD. Of the available PH-targeted drugs, most participants preferred the use of phosphodiesterase-5-inhibitors for this indication. In conclusion, the practice of recommending pulmonary vasodilators in PH-LHD is highly variable among international pediatric PH specialists. Most specialists of those surveyed (57% in North America) would consider the use of pulmonary vasodilators in PH-LHD only if pre-capillary pulmonary hypertension and right ventricular dysfunction are present.
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Goyanes, Alice M., and Gustavo A. Heresi. "Medical Management of Chronic Thromboembolic Pulmonary Hypertension." Advances in Pulmonary Hypertension 21, no. 3 (2022): 88–92. http://dx.doi.org/10.21693/1933-088x-21.3.88.

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Medical therapy in chronic thromboembolic pulmonary hypertension (CTEPH) has two primary goals- to prevent recurrent thromboembolic events and to reduce right ventricular afterload with targeted medications (vasodilators) for pulmonary hypertension. These medical strategies are used in conjunction with mechanical treatments for CTEPH (pulmonary thromboendarterectomy (PTE) or balloon angioplasty). In the context of this review, we discuss anticoagulation strategies, patient selection for vasodilator therapy with particular focus on hemodynamic and clinically meaningful definitions of residual pulmonary hypertension after PTE and inoperable disease and then summarize the current randomized clinical trials (RCT) which have studied effectiveness of vasodilators in patients with CTEPH.
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Wallace, William D., Mehdi Nouraie, Stephen Y. Chan, and Michael G. Risbano. "Treatment of exercise pulmonary hypertension improves pulmonary vascular distensibility." Pulmonary Circulation 8, no. 3 (2018): 204589401878738. http://dx.doi.org/10.1177/2045894018787381.

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Exercise pulmonary hypertension (ePH) is an underappreciated form of exertional limitation. Despite normal resting pulmonary artery pressures, patients with ePH demonstrate early pulmonary vascular changes with reduced pulmonary arterial compliance (PAC) and vascular distensibility (α). Recent data suggest that targeted vasodilator therapy may improve hemodynamics in ePH, but it is not well-known whether such medications alter pulmonary vascular distensibility. Thus, we sought to evaluate if vasodilator therapy improved α a marker of early pulmonary vascular disease in ePH. Ten patients performed supine exercise right heart catheterization (exRHC) with bicycle ergometer to peak exercise. Patients diagnosed with ePH were treated with pulmonary vasodilators. A repeat symptom-limited exercise RHC was performed at least six months after therapy. Patients with ePH had evidence of early pulmonary vascular disease, as baseline PAC and α were reduced. After pulmonary vasodilator therapy, a number of peak exercise hemodynamics statistically improved, including a decrease of total pulmonary resistance and pulmonary vascular resistance, while cardiac output increased. Importantly, vasodilator therapy partially reversed the pathogenic decreases of α at the time of repeat exRHC. Pulmonary vascular distensibility, α, a marker of early pulmonary vascular disease, improves in ePH after therapy with pulmonary vasodilators.
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Dissertations / Theses on the topic "Vasodilators"

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D'Oyley, Heather M. "Vasodilators and venous tone." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27871.

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The objective of these experiments was to investigate the effects of various membrane receptor-mediated and receptor-independent vasodilators on the resistance and capacitance vessels of conscious, unrestrained rats by measuring mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of total body venous tone. ln the first set of experiments the dose-response effects of the directly-acting vasodilators nitroglycerin, sodium nitroprusside and hydralazine were determined in intact rats as well as in rats treated with the ganglionic blocker, hexamethonium. The effects of these drugs were compared with those of the vehicle, normal saline, in control rats. In intact rats, iv infusion of nitroglycerin did not alter MAP while iv infusions of nitroprusside and hydralazine caused dose-dependent decreases in MAP. In intact rats, nitroglycerin and sodium nitroprusside did. not affect MCFP while hydralazine increased MCFP. After treatment with hexamethonium all three drugs decreased MCFP, though the decreases in MCFP caused by hydralazine were not significantly different from the corresponding changes in saline-treated rats. Therefore, sodium nitroprusside and hydralazine but not nitroglycerin were effective arteriolar dilators in intact rats; all three drugs dilated arterioles in ganglionic-blocked rats, ln intact rats, the direct venodilator actions of nitroprusside and nitroglycerin were masked by endogenous sympathetic tone. When sympathetic nerve activity was attenuated, both drugs had venodilatory effects. Hydralazine, on the other hand, hao insignificant venodilatory effects both in the presence and absence of the sympathetic reflexes. In the second set of experiments we determined the dose-response effects of hexamethonium, phentolamine, prazosin and rauwolscine — the latter being non-selective ⍺, ⍺₁-selective, and ⍺₂-selective adrenoceptor antagonists, respectively — in intact rats. Prazosin and rauwolscine were also administered to rats with reflexly increased venous tone induced by the infusion of hydralazine. In intact rats iv infusions of prazosin, phentolamine and rauwolscine all caused dose-dependent decreases in MAP; only rauwolscine reduced MCFP to levels slightly below control. Hexamethonium caused a aecrease in MAP as well as a markea reduction in MCFP. After venous tone was raised by the infusion of hydralazine, both prazosin and rauwolscine dose-dependently decreased MCFP. Therefore, the resistance and capacitance vessels contain both ⍺₁- and ⍺₂-adrenoceptors. in the intact rat, however, the capacitance vessels are somewhat resistant to the effects of postjunctionally acting ⍺-antagonists in contrast to the effects of hexamethonium which acts at the level of the ganglion.<br>Medicine, Faculty of<br>Anesthesiology, Pharmacology and Therapeutics, Department of<br>Graduate
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Siddons, Thomas Edward. "The use of pulsed inhaled nitric oxide in the investigation and treatment of chronic disease affecting the pulmonary circulation." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274966.

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Talbot, Nicola Maria. "Metal nitrosyl and organic nitrates as novel vasodilators." Thesis, University of Exeter, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385724.

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Weldon, Hazel. "The synthesis of novel nitric oxide donors as potential vasodilators." Thesis, University of Exeter, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307295.

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Lo, Sze-man Irene. "A comparison of the vasoactive metabolites in the interstitial space of oxidative or glycolytic muscles in anaesthetised rats /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21790838.

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HYNES, MICHAEL RAY. "ENDOTHELIUM-DEPENDENT RELAXATION OF BLOOD VESSELS." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184134.

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Dilation of blood vessels in response to a large number of agents has been shown to be dependent on an intact vascular endothelium. The present studies examine some aspects of endothelium-dependent vasodilation in blood vessels of the rabbit and rat. Using the rabbit ear artery and the subtype-selective muscarinic antagonist pirenzepine, muscarinic receptors of the endothelium and smooth muscle cells were shown to be of the low affinity M₂ subtype. Inhibition of [³H](-)quinuclidinyl benzilate was used to determine affinity for the smooth muscle receptors while antagonism of methacholine induced vasodilation yielded the endothelial cell receptor affinity. The effect of increasing age (1-27 months) on endothelium-dependent relaxation was studied in aortic rings, perfused tail artery and perfused mesenteric bed of the Fisher 344 rat. Both aortic ring segments and perfused caudal arteries showed an age-related increase in sensitivity of endothelium-mediated relaxation to the cholinergic agonist methacholine. This increased sensitivity occurs between the ages of 6 and 12 months, with no further significant increase up to 27 months of age, suggesting this is a consequence of growth and development rather than old age. No difference with age in cholinergic relaxation was observed in the perfused mesenteric bed indicating either no change of sensitivity in smaller resistance vessels or an effect which is hidden in this more complex perfused system. In contrast to findings with cholinergic stimution, responses of the perfused caudal artery to the calcium ionophore A23187 were not altered with age. This suggests that the alteration with age in response to methacholine involves the muscarinic receptor or receptor coupling mechanism rather than the generation of, or response to, endothelium-derived relaxing factor (EDRF). The influence of endothelium on contractile responses was examined using the perfused caudal artery. Endothelium removal significantly increased contraction to the α-adrenergic agonists methoxamine and BH-T 920 as well as to transmural nerve stimulation. Inhibition of contraction to agents which must first cross the smooth muscle layer before reaching the endothelium suggests that a continuous or basal level of EDRF release is responsible for decreased contraction rather than an receptor stimulated release of EDRF.
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Reeves, Katherine Ann. "The cardiovascular actions of the isopropyl ester and other synthetic derivatives of palmitoyl carnitine." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260252.

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Joseph, Emlyn Clive. "Pathogenesis of arteriopathy induced by PDE III inhibitors in the rat and dog." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307684.

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Firkin, Catherine R. "A biomimetic approach to the synthesis of xestospongin A." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389208.

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羅詩敏 and Sze-man Irene Lo. "A comparison of the vasoactive metabolites in the interstitial space of oxidative or glycolytic muscles in anaesthetised rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223138.

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Books on the topic "Vasodilators"

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John, Gaddum. Vasodilator substances of the tissues. Cambridge University Press, 1986.

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Feletou, Michel. EDHF: The complete story. CRC/Taylor & Francis, 2006.

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1895-1967, Kilborn Leslie G., ed. Adrenalin vasodilator mechanisms in the cat at different ages. University Library, pub. by the Librarian, 1994.

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Pang, Catherine C. Y. The effects of drugs on the venous system. R.G. Landes, 1994.

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U, Abshagen, ed. Clinical pharmacology of antianginal drugs. Springer-Verlag, 1985.

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S, Manning Allan, and Szendey George L, eds. Prenylamine: A novel approach to myocardial protection. Raven Health Care Communications, 1988.

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Deutsche Gesellschaft für Neurochirurgie. Tagung. Stabilizing craniocervical operations: Calcium antagonists in SAH : current legal issues. Springer-Verlag, 1990.

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Brett, Stephen James. Inhaled vasodilator therapy, nitric oxide and pulmonary inflammation. University of Birmingham, 1998.

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M, Vanhoutte Paul, Shepherd John T. 1919-, International Union of Physiological Sciences. Congress, and International Symposium on Mechanisms of Vasodilatation (4th : 1986 : Rochester, Minn.), eds. Vasodilatation: Vascular smooth muscle, peptides, autonomic nerves, and endothelium. Raven Press, 1988.

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Frank, Cuttitta, and Martínez Alfredo, eds. Adrenomedulin. IOS Press, 1998.

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Book chapters on the topic "Vasodilators"

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Haas, Garrie J., and Carl V. Leier. "Vasodilators." In Congestive Heart Failure. Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8315-4_24.

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Roth, Stephen J., Ricardo Munoz, Carol G. Schmitt, Eduardo da Cruz, Jonathan Kaufman, and Cécile Tissot. "Vasodilators." In Handbook of Pediatric Cardiovascular Drugs. Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-953-8_4.

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Dowd, P. M. "Cutaneous Vasodilators." In Pharmacology of the Skin II. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74054-1_21.

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Opie, L. H., and U. Thadani. "Antianginal vasodilators." In Drugs for Heart Disease. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3294-5_4.

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Banik, Ratan K., and Jay S. Berger. "Peripheral Vasodilators." In Essentials of Pharmacology for Anesthesia, Pain Medicine, and Critical Care. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8948-1_16.

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Beghetti, Maurice, and Robin H. Steinhorn. "Selective Pulmonary Vasodilators." In Pediatric and Neonatal Mechanical Ventilation. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-01219-8_29.

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Booke, M., L. D. Traber, and D. L. Traber. "Vasodilators in Sepsis." In Shock, Sepsis, and Organ Failure — Nitric Oxide. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79343-1_13.

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Moncada, S., R. M. J. Palmer, and E. A. Higgs. "Endothelium-Derived Vasodilators." In Vascular Endothelium. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-8532-5_22.

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Butler, Anthony Robert, and Russell James Pearson. "Vasodilators for Biological Research." In Nitric Oxide Donors. Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603751.ch8.

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Rosenthal, Amnon. "Congestive Heart Failure: Vasodilators." In Pediatric Cardiology. Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4613-8598-1_323.

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Conference papers on the topic "Vasodilators"

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Dawes, Timothy, Konstantinos Dimopoulos, Colm Mccabe, et al. "Survival effects of pulmonary vasodilators in group 3 pulmonary hypertension." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa177.

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Lachant, D., A. Light, M. Lachant, and R. J. White. "Activity Does Not Increase After Adding Vasodilators in Pulmonary Arterial Hypertension." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3747.

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Hrustanovic-Kadic, M., J. S. S. Smith, and K. El-Kersh. "A 100-Year-Old CTEPH Patient Treated with Combined Pulmonary Artery Vasodilators." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7247.

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Chen, Cuiye, and Robert B. Roemer. "Modeling of Transient Tissue Temperatures and Biotransport of Vasodilators During Localized Heating." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASME, 2003. http://dx.doi.org/10.1115/imece2003-42044.

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Sanina, N. A. "NITROSYL FERREDOXINS MIMETICS AS PROMISING VASODILATORS IN REACTIONS WITH MODEL BIOLOGICAL SYSTEMS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. LLC Institute Information Technologies, 2024. http://dx.doi.org/10.47501/978-5-6044060-4-5.240-245.

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The paper presents data on the study of the interaction of original mimetics of nitrosyl [2Fe-2S] ferredoxins as donors of nitric oxide (NO) with model biological systems (serum albumin, mucin, hemoglobin, glutathione and cyclic nucleotides) using modern experimental and theo-retical methods.
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Williams, T. J., M. Rampart, S. Nourshargh, P. G. Hellewell, S. D. Brain, and P. J. Jose. "INTERACTION OF POLYMORPHONUCLEAR LEUKOCYTES AND ENDOTHELIAL CELLS : FUNCTIONAL CONSEQUENCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643985.

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The mechanisms involved in the accumulation of polymorphonuclear leukocytes (PMNs) in an inflammatory reaction are complex. A key phase in this process is the attachment of the PMN to the microvascular (venular in most tissues) endothelial cell, initiated by the extravascular generation of a chemical mediator. Experiments in vitro suggest that mediators, such as C5a, may act in vivo by stimulating the increased expression of the CD18 complex on the surface of the PMN within the venule lumen (1), whereas IL-1 may act by causing the expression of an adhesive molecule on the endothelial cell (2). In vitro the former process is rapid whereas the latter is slow in onset. We have measured the local accumulation of intravenously-injected Ulln-PMNs in response to intradermally-injected mediators in the rabbit, in order to investigate possible mechanisms in vivo. PMN accumulation was found to be rapid in onset in response to C5a, the rate of accumulation falling progressively to low levels by 4 hours. In contrast PMN accumulation in response to IL-1 was slow in onset, reaching a peak rate at 3-4 hours. Intradermal injection of the vasodilator prostaglandins PGI2; PGE2 and the neuropeptides VIP and CGRP caused a marked potentiation of the rate of leukocyte accumulation. PMN accumulation induced by C5a was associated with increased microvascular permeability, as indicated by the leakage of intravenously-injected 125I-albumin with a time-course in parallel with the rate of PMN accumulation enhanced by intradermally-injected vasodilators. Depletion of circulating PMNs abolishes these responses to C5a (3). In contrast, leukocyte accumulation induced by IL-1 was associated with little plasma protein leakage, even in the presence of intradermal vasodilators. This observation indicates that PMN emigration itself does not lead to increased microvascular permeability. C5a, but not IL-1, may stimulate emigrating PMNs to secrete an endogenous factor that increases permeability by an action on endothelial cells (3). This factor does not appear to be the phospholipid PAF (4). In contrast to the enhancing effects of local PGI2, intravenously-infused PGI2 inhibited PMN accumulation induced by C5a and IL-1, and plasma protein leakage induced by C5a (5). This effect is probably mediated by elevation of cyclic AMP in intravascular PMNs. We have shown that C5a stimulation of PMNs in contact with endothelial cells in vitro induces endothelial cell PGI2 secretion (6). Thus, PGI2 may be part of a negative feedback system in vivo to control interactions between PMNs and endothelial cells.These observations provide some clues to the intricacies of mechanisms of leukocyte accumulation in vivo.
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Vijayaraman, A., E. Homsy, N. Y. Bhatt, and N. Sood. "The Effects of Pulmonary Vasodilators on Concomitant Systemic Sclerosis Related Pulmonary Hypertension and Interstitial Lung Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3821.

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Urner, Tara, Eashani Sathialingam, Tisha Boodooram, et al. "Investigating pulsatile cerebral blood flow waveforms after subarachnoid hemorrhage with diffuse correlation spectroscopy." In Optics and the Brain. Optica Publishing Group, 2024. http://dx.doi.org/10.1364/brain.2024.btu3c.6.

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We quantify pulsatile microvascular cerebral blood flow waveforms at the cardiac frequency in subarachnoid hemorrhage (SAH) before and after treatment with a vasodilator to alleviate cerebral vasospasm. We observe a waveform response consistent with our previous observations in healthy adults undergoing hypercapnia, a known vasodilatory stimulus. These results extend the potential utility of BFI waveform quantification as a biomarker of vasomotor changes to a clinical case where such an indicator is much-needed.
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Fukihara, Jun, Reoto Takei, Hajime Sasano, et al. "Prediction of survival in patients with pulmonary hypertension associated with interstitial lung disease treated with pulmonary vasodilators." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa3499.

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Bollam, R. R., F. Mamauag, and S. A. A. Zaidi. "COVID-19 and Its Association with the Development of Pulmonary Hypertension: The Potential Role for Pulmonary Vasodilators." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5424.

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Reports on the topic "Vasodilators"

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Wu, Xiaoqi, Jisen Zhao, Maoxia Fan, and Dongo Guo. Quality of Evidence Supporting the Effects of Xinmailong injection in Heart Failure: An Overview of Systematic Reviews and Meta-Analyses. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.10.0023.

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Review question / Objective: 2.1.1 type of research SRs/MAs of RCT (randomized controlled trial) of Xinmailong injection for the treatment of heart failure. 2.1.2 Subject investigated All included patients met internationally recognized diagnostic criteria for heart failure.There are no limitations on age, gender, ethnicity, time of onset, source of cases and language of publication. 2.1.3 Type of Intervention The control group was treated with conventional basic Western medicine recommended by the guidelines related to heart failure[1, 11], including antiplatelet drugs, anticoagulants, vasodilators, beta-blockers,ACEI (angiotensin-converting enzyme inhibitors), lipid-lowering drugs, and diuretic agents. and other drug treatment. The intervention group was given Xinmailong injection on the basis of the control group.
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กาญจนทัต, อภิชาติ. โปรตีนไฮโดรไลเสตจากเมล็ดผลไม้ไทยเพื่อการบำบัดโรค : รายงานวิจัยฉบับสมบูรณ์ (ปีที่ 1). จุฬาลงกรณ์มหาวิทยาลัย, 2014. https://doi.org/10.58837/chula.res.2014.89.

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Blood pressure regulation is partially dependent on the renin-angiotensin system; renin acts on angiotensinogen to release angiotensin-I, which is further converted into the angiotensin II by the angiotensin I-converting enzyme (ACE). ACE plays a key physiological role in the regulation of blood pressure by virtue of two different reactions that it catalyzes: conversion of the inactive angiotensin I to the powerful vasoconstrictor angiotensin II, and inactivation of the vasodilator bradykinin. Crude extract and ammonium sulphate cut protein extracts, and their pepsin-pancreatin hydrolysates, from the seeds of 4 Thai fruits (i) Carica papaya L.; (papaya; unripen and ripen form), (ii) Nephelium lappaceum L. (rambutan) (iii) Dimocarpus longan Lour. subsp. (longan), and (iv) Litchi chinensis Sonn. (lychee) were screened for their in vitro angiotensin I- converting enzyme inhibitory (ACEI) activity. The protein hydrolysate of lychee seeds shows the highest potential of ACE inhibitory activity at IC50 value 0.22±0.010 mg protein/ml. The protein hydrolysate of unripen papaya seeds, longan seeds, and lychee seeds show uncompetitive and non-competitive inhibition with Ki values at 6.02, 2.82, and 5.62 mg protein/ml, with optimum pH in range of 6-8. After partial purification with ultrafiltration technique, UF-3 (below 5 kDa) of longan seeds show the highest inhibitory activity with IC50 values at 0.43±0.011 mg protein/ml. This fraction was subjected to RP-HPLC and five peaks were separated, and subjected to LC/MS/MS for amino acids sequences analysis. The P1-F1, P3-F1, and P3-F4 show the most inhibitory activity.
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Rumbaut Gil, Ana Laura. A Systemic Analysis of Vascular Dysfunction in Parkinson’s Disease: Reviewing the Roles of Astrocytes and COX-2. Florida International University, 2025. https://doi.org/10.25148/fiuurj.3.1.6.

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Although Parkinson’s Disease (PD) is the second most prevalent neurodegenerative disease in the U.S., the pathology remains an enigma. Many neuroinflammation hypotheses have been studied to explain its development. It’s shown that inflammatory markers such as COX-2 activity, which synthesizes the potent vasodilator PGE2, are overexpressed in PD. Additionally, astrocytes, regulators of inflammation in the brain and BBB, undergo important changes during PD. However, the vascular consequences that all this has for PD-led neurodegeneration are relatively unexplored. We conducted a systemic review of 793 articles of experimental studies that are publicly available across four online databases (PubMed, Florida International University Database, World of Science, and Scopus) related to the topic of vascularity and blood-brain barrier (BBB) in PD to summarize widely evidenced vascular changes in the disease. Present literature on astrocyte reactivity and COX-2 expression in PD was reviewed, to draw a parallel between these and the findings from our systemic analysis. Five important vascular changes were found in the systemic analysis drawn from the final 25 sources selected, with the most frequent change being an increase in BBB permeability. This observation was evidenced primarily in animal studies and was the only change noted through an in-vivo study. Other vascular changes found were a decrease in tight-junction proteins in the endothelium, the presence of angiogenesis markers, a change in vessel density, and a change in vessel width or thickness. Our literature review pointed to a connection between the function of astrocytes and the hyperactivity of COX-2 while our analysis observed changes in vascularity. The increase in BBB permeability and eventual disruption is an important hallmark of the vascular repercussions of PD. Due to astrocytes’ function in supporting the BBB and the vasodilating effect of COX-2 overexpression, we might consider this relationship a starting point for understanding neurodegeneration.
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