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1
Kitai, Takeshi, W. H. Wilson Tang, Andrew Xanthopoulos, Ryosuke Murai, Takafumi Yamane, Kitae Kim, Shogo Oishi, et al. "Impact of early treatment with intravenous vasodilators and blood pressure reduction in acute heart failure." Open Heart 5, no. 2 (July 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 (July 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 (October 1, 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, Kazumasa Harada, Tetsuro Miyazaki, Takamichi Miyamoto, Kenichi Matsushita, 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 (January 29, 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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Morales-Cano, Daniel, Bianca Barreira, Beatriz De Olaiz Navarro, María Callejo, Gema Mondejar-Parreño, Sergio Esquivel-Ruiz, Jose A. Lorente, et al. "Oxygen-Sensitivity and Pulmonary Selectivity of Vasodilators as Potential Drugs for Pulmonary Hypertension." Antioxidants 10, no. 2 (January 21, 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 (January 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 (July 1, 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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Stevenson, Lynne Warner, and Gregg Fonarow. "Vasodilators." Drugs 43, no. 1 (January 1992): 15–36. http://dx.doi.org/10.2165/00003495-199243010-00003.
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&NA;. "Vasodilators." Reactions Weekly &NA;, no. 1308 (July 2010): 33–34. http://dx.doi.org/10.2165/00128415-201013080-00099.
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Zimpfer, M., and Steltzer. "Vasodilators." Current Opinion in Anaesthesiology 3, no. 1 (February 1990): 107–9. http://dx.doi.org/10.1097/00001503-199002000-00024.
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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 (June 19, 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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Jones, D. "The Neglected saliva: medically important toxins in the saliva of human lice." Parasitology 116, S1 (1998): S73—S81. http://dx.doi.org/10.1017/s0031182000084961.
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SummaryAlthough there has been a great deal of research effort within the last two decades on identifying the active components of the saliva of blood-sucking ticks, mosquitoes, biting flies, fleas and bugs, essentially neglected have been the human lice. Despite initial reports in the early part of this century suggestive of vasodilatory, anticoagulant and immunosuppressive properties of the saliva, for the next 50 years there were no biochemical studies on the active principles. Very recently, anatomical and biochemical studies have begun to characterize the bioactive molecules in lice saliva. The louse stocks a salivary vasodilator in excess over what is needed for a single bite, and injects similar amounts at each successive bite. The vasodilator in lice saliva appears to have different pharmacological properties than peroxidative, oxidative and maxidilan types of vasodilators reported from other blood-sucking insects. Possible anticoagulant activities have also been characterized. This belated, but welcome, interest comes at a time of resurgence of lice-born disease in certain parts of Africa, and of resistance to chemical control in Europe and North America.
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Gillmeyer, Kari R., Donald R. Miller, Mark E. Glickman, Shirley X. Qian, Elizabeth S. Klings, Bradley A. Maron, Joseph T. Hanlon, Seppo T. Rinne, and Renda S. Wiener. "Outcomes of pulmonary vasodilator use in Veterans with pulmonary hypertension associated with left heart disease and lung disease." Pulmonary Circulation 11, no. 2 (April 2021): 204589402110017. http://dx.doi.org/10.1177/20458940211001714.
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Randomized trials of pulmonary vasodilators in pulmonary hypertension due to left heart disease (Group 2) and lung disease (Group 3) have demonstrated potential for harm. Yet these therapies are commonly used in practice. Little is known of the effects of treatment outside of clinical trials. We aimed to establish outcomes of vasodilator treatment for Groups 2/3 pulmonary hypertension in real-world practice. We conducted a retrospective cohort study of 132,552 Medicare-eligible Veterans with incident Groups 2/3 pulmonary hypertension between 2006 and 2016, and a secondary nested case–control study. Our primary outcome was a composite of death by any cause or selected acute organ failures. In our cohort analysis, we calculated adjusted risks of time to our outcome using Cox proportional hazards models with facility-specific random effects. In our case–control analysis, we used logistic mixed-effects models to estimate the effect of any past, recent, and cumulative exposure on our outcome. From our cohort study, 3249 (2.5%) Veterans were exposed to pulmonary vasodilators. Exposure to vasodilators was associated with increased risk of our primary outcome, in both Group 3 (HR: 1.58 (95% CI: 1.37–1.82)) and Group 2 (HR: 1.26 (95% CI: 1.12–1.41)) pulmonary hypertension patients. The case–control study determined odds of our outcome increased by 11% per year of exposure (OR: 1.11 (95% CI: 1.07–1.16)). Treating Groups 2/3 pulmonary hypertension with vasodilators in clinical practice is associated with increased risk of harm. This extension of trial findings to a real-world setting offers further evidence to limit use of vasodilators in Groups 2/3 pulmonary hypertension outside of clinical trials.
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Onoue, Hisashi, Nobuyoshi Kaito, Shogo Tokudome, Toshiaki Abe, Koichi Tashibu, Hiroyasu Nagashima, and Norio Nakamura. "Investigation of Postmortem Functional Changes in Human Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 13, no. 2 (March 1993): 346–49. http://dx.doi.org/10.1038/jcbfm.1993.44.
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This study demonstrated the time-dependent changes in postmortem responses of isolated human middle cerebral artery strips to vasodilators. The relaxation induced by prostaglandin (PG) I2 or nitroglycerin remained stable for 24 h postmortem. In arterial strips precontracted with PGF2α, substance P and bradykinin both elicited relaxation that was almost completely abolished by removal of the endothelium. The endothelium-dependent response to both peptides was significantly degraded in strips obtained >12 h postmortem. These results indicate a selective functional or anatomical vulnerability of the vascular endothelium compared with that of the vasodilator mechanisms of the smooth muscle in the postmortem period. However, cerebral arteries isolated from human cadavers within 12 h postmortem should be adequate for studies of both smooth muscle and endothelial reactivity to vasodilators.
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Altman, J., D. Dulas, T. Pavek, D. D. Laxson, D. C. Homans, and R. J. Bache. "Endothelial function in well-developed canine coronary collateral vessels." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 2 (February 1, 1993): H567—H572. http://dx.doi.org/10.1152/ajpheart.1993.264.2.h567.
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This study examined responses of coronary collateral blood flow to endothelial-dependent vasodilators. Studies were performed in 13 dogs 4-6 mo after embolic occlusion of the left anterior descending coronary artery (LAD). Collateral flow was determined as the sum of retrograde flow from the cannulated LAD, and continuing tissue flow was measured with microspheres administered during the retrograde flow collection. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left coronary arterial system. The endothelial-dependent vasodilators acetylcholine and bradykinin caused 21 +/- 7 and 25 +/- 8% increases of collateral flow, respectively (each P < 0.05). This was not different from the 28 +/- 8% increase in collateral flow produced by nitroglycerin. To determine whether vasodilator prostaglandins contributed to the increased collateral flow, studies were performed after cyclooxygenase blockade with indomethacin (5 mg/kg iv). Indomethacin caused a 30 +/- 9% decrease of retrograde flow during basal conditions but did not blunt the maximum collateral flow rates produced by acetylcholine, bradykinin, or nitroglycerin. These data demonstrate intact endothelial-dependent vasodilator mechanisms in the well-developed coronary collateral circulation.
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McAllister, Richard M., Michael D. Delp, and M. Harold Laughlin. "A Review of Effects of Hypothyroidism on Vascular Transport in Skeletal Muscle During Exercise." Canadian Journal of Applied Physiology 22, no. 1 (February 1, 1997): 1–10. http://dx.doi.org/10.1139/h97-001.
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Hypothyroidism is a common thyroid disease characterized by exercise intolerance. Both exercise capacity and endurance are compromised in the hypothyroid state. Studies involving rats performing treadmill running have shown that blood flows during exercise to high oxidative, extensor-type muscles are lower in hypothyroid rats compared with those in euthyroid rats. Abnormal cardiac and vascular function appear to contribute to this hxpoperfusion. Experiments involving isolated arterial vessel segments have demonstrated that potential for constriction is normal in vessels from hypothyroid animals; however, reduced vasodilator potential is associated with hypothyroidism. Dysfunction of both endothelium and vascular smooth muscle appear to contribute to blunted potential for vasodilation. Altered ability to generate vasodilatory substances and/or changes in responses to these vasodilators may account for vascular dysfunction. It appears that impaired vascular function interacts with other factors such as poor myocardial function and changes in energy metabolism to compromise exercise tolerance. Key words: blood flow, vasodilation, endothelium, smooth muscle, cGMP
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Tsoporis, J., B. X. Yuan, and F. H. Leenen. "Arterial vasodilators, cardiac volume load, and cardiac hypertrophy in normotensive rats." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 3 (March 1, 1989): H876—H880. http://dx.doi.org/10.1152/ajpheart.1989.256.3.h876.
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To assess a possible involvement of cardiac volume overload in the development of cardiac hypertrophy during chronic arterial vasodilator treatment, changes in indexes of cardiac volume load in relation to changes in cardiac anatomy were evaluated during treatment of normotensive rats with 120 mg/l hydralazine or 120 mg/l minoxidil, with drinking water. Long-term treatment with hydralazine, but not minoxidil, caused small decreases in systolic blood pressure; neither vasodilator affected heart rate with chronic treatment. Arterial vasodilator treatment for 2 wk or more resulted in increases in plasma and blood volumes by 10-20%. Both arterial vasodilators increased right atrial pressure and left ventricular end-diastolic pressure in the initial weeks of treatment. Only the minoxidil group showed a persistent increase in right atrial pressure throughout the treatment period. These hemodynamic changes were associated with increases in left ventricular (LV) internal diameter and right ventricular (RV) weight, and with minoxidil these changes were also associated with increased LV weight. LV wall thickness did not increase. Cardiac volume overload therefore indeed occurs during treatment with arterial vasodilators and may contribute to their effects on cardiac anatomy (i.e., development of RV hypertrophy and, in the case of minoxidil, also, eccentric LV hypertrophy), which are consistent with cardiac volume overload.
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Wang, Wuwan, Xiankang Hu, Weitin Liao, W. H. Rutahoile, David J. Malenka, Xiaofang Zeng, Yunjing Yang, Panpan Feng, Li Wen, and Wei Huang. "The efficacy and safety of pulmonary vasodilators in patients with Fontan circulation: a meta-analysis of randomized controlled trials." Pulmonary Circulation 9, no. 1 (July 4, 2018): 204589401879045. http://dx.doi.org/10.1177/2045894018790450.
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No previous meta-analysis has evaluated the efficacy and safety of pulmonary vasodilators in Fontan physiology. Recent relative trials have obtained conflicting results regarding improvements in peak oxygen consumption; the relatively small number of patients in each study may be a limiting factor. We aimed to evaluate the efficacy and safety of pulmonary vasodilators in Fontan patients. Relevant studies were identified by searching the PubMed, Embase, and Cochrane Library databases. Pooled outcomes were determined to assess the efficacy and safety of pulmonary vasodilators in Fontan patients. Nine randomized controlled studies involving 381 patients with Fontan circulation were included. Pulmonary vasodilator therapy led to significant improvement (mean difference = −0.39, 95% CI: [−0.72, −0.05]) in the New York Heart Association (NYHA) functional class. The 6-minute walking distance (6MWD) was significantly increased by 134 m (95% CI: [86.07, 181.94]), and the peak VO2 was also significantly improved (mean difference = 1.42 ml·(kg·min)-1, 95% CI: [0.21, 2.63]). Additionally, the mean pulmonary artery pressure (mPAP) was significantly reduced (mean difference = −2.25 mmHg, 95% CI: [−3.00, −1.50]). No significant change was found in mortality or in brain natriuretic peptide (BNP) or N-terminal pronatriuretic peptide (NT-proBNP). Four studies reported no side effects and good drug tolerance, and two studies reported mild adverse effects. The present meta-analysis indicated that pulmonary vasodilators (primarily the PDE-5 inhibitor and endothelin-1 receptor antagonist) significantly improved the hemodynamics of Fontan patients, reduced the NYHA functional class and increased the 6MWD. The peak oxygen consumption was also improved. No significant change was observed in mortality or in the BNP or NT-proBNP level. Overall, the pulmonary vasodilators were well tolerated. This finding needs to be confirmed in future studies.
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Toda, Noboru, and Tomio Okamura. "Cerebral Vasodilators." Japanese Journal of Pharmacology 76, no. 4 (1998): 349–67. http://dx.doi.org/10.1254/jjp.76.349.
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Jeremiasen, Ida, Karin Tran-Lundmark, Nikmah Idris, Phan-Kiet Tran, and Shahin Moledina. "Pulmonary Vasodilator Therapy in Children with Single Ventricle Physiology: Effects on Saturation and Pulmonary Arterial Pressure." Pediatric Cardiology 41, no. 8 (July 30, 2020): 1651–59. http://dx.doi.org/10.1007/s00246-020-02424-w.
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AbstractIn children with single ventricle physiology, increased pulmonary vascular resistance may impede surgical progression or result in failing single ventricle physiology. The use of pulmonary vasodilators has been suggested as a potential therapy. However, knowledge on indication, dosage, and effect is limited. A retrospective case notes review of all (n = 36) children with single ventricle physiology, treated with pulmonary vasodilators by the UK Pulmonary Hypertension Service for Children 2004–2017. Therapy was initiated in Stage 1 (n = 12), Glenn (n = 8), or TCPC (n = 16). Treatment indications were high mean pulmonary arterial pressure, cyanosis, reduced exercise tolerance, protein-losing enteropathy, ascites, or plastic bronchitis. Average dose of sildenafil was 2.0 mg/kg/day and bosentan was 3.3 mg/kg/day. 56% had combination therapy. Therapy was associated with a reduction of the mean pulmonary arterial pressure from 19 to 14 mmHg (n = 17, p < 0.01). Initial therapy with one or two vasodilators was associated with an increase in the mean saturation from 80 to 85%, (n = 16, p < 0.01). Adding a second vasodilator did not give significant additional effect. 5 of 12 patients progressed from Stage 1 to Glenn, Kawashima, or TCPC, and 2 of 8 from Glenn to TCPC during a mean follow-up time of 4.7 years (0–12.8). Bosentan was discontinued in 57% and sildenafil in 14% of treated patients and saturations remained stable. Pulmonary vasodilator therapy was well tolerated and associated with improvements in saturation and mean pulmonary arterial pressure in children with single ventricle physiology. It appears safe to discontinue when no clear benefit is observed.
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Fineman, J. R., M. R. Crowley, M. A. Heymann, and S. J. Soifer. "In vivo attenuation of endothelium-dependent pulmonary vasodilation by methylene blue." Journal of Applied Physiology 71, no. 2 (August 1, 1991): 735–41. http://dx.doi.org/10.1152/jappl.1991.71.2.735.
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In vitro evidence suggests that resting pulmonary vascular tone and endothelium-dependent pulmonary vasodilation are mediated by changes in vascular smooth muscle concentrations of guanosine 3′,5′-cyclic monophosphate (cGMP). We investigated this hypothesis in vivo in 19 mechanically ventilated intact lambs by determining the hemodynamic effects of methylene blue (a guanylate cyclase inhibitor) and then by comparing the hemodynamic response to five vasodilators during pulmonary hypertension induced by the infusion of U-46619 (a thromboxane A2 mimic) or methylene blue. Methylene blue caused a significant time-dependent increase in pulmonary arterial pressure. During U-46619 infusions, acetylcholine, ATP-MgCl2, sodium nitroprusside, isoproterenol, and 8-bromo-cGMP decreased pulmonary arterial pressure. During methylene blue infusions, the decreases in pulmonary arterial pressure caused by acetylcholine and ATP-MgCl2 (endothelium-dependent vasodilators) and sodium nitroprusside (an endothelium-independent guanylate cyclase-dependent vasodilator) were attenuated by greater than 50%. The decreases in pulmonary arterial pressure caused by isoproterenol and 8-bromo-cGMP (endothelium-independent vasodilators) were unchanged. This study in intact lambs supports the in vitro evidence that changes in vascular smooth muscle cell concentrations of cGMP in part mediate resting pulmonary vascular tone and endothelium-dependent pulmonary vasodilation.
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Kaul, Dhananjay K., Xiaoqin Zhang, Trisha Dasgupta, and Mary E. Fabry. "Arginine therapy of transgenic-knockout sickle mice improves microvascular function by reducing non-nitric oxide vasodilators, hemolysis, and oxidative stress." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 1 (July 2008): H39—H47. http://dx.doi.org/10.1152/ajpheart.00162.2008.
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In sickle cell disease, nitric oxide (NO) depletion by cell-free plasma hemoglobin and/or oxygen radicals is associated with arginine deficiency, impaired NO bioavailability, and chronic oxidative stress. In transgenic-knockout sickle (BERK) mice that express exclusively human α- and βS-globins, reduced NO bioavailability is associated with induction of non-NO vasodilator enzyme, cyclooxygenase (COX)-2, and impaired NO-mediated vascular reactivity. We hypothesized that enhanced NO bioavailability in sickle mice will abate activity of non-NO vasodilators, improve vascular reactivity, decrease hemolysis, and reduce oxidative stress. Arginine treatment of BERK mice (5% arginine in mouse chow for 15 days) significantly reduced expression of non-NO vasodilators COX-2 and heme oxygenase-1. The decreased COX-2 expression resulted in reduced prostaglandin E2(PGE2) levels. The reduced expression of non-NO vasodilators was associated with significantly decreased arteriolar dilation and markedly improved NO-mediated vascular reactivity. Arginine markedly decreased hemolysis and oxidative stress and enhanced NO bioavailability. Importantly, arteriolar diameter response to a NO donor (sodium nitroprusside) was strongly correlated with hemolytic rate (and nitrotyrosine formation), suggesting that the improved microvascular function was a response to reduced hemolysis. These results provide a strong rationale for therapeutic use of arginine in sickle cell disease and other hemolytic diseases.
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Lermioglu, F., J. Goyal, and A. Hassid. "Cell density modulates the decrease of cytosolic free Ca2+ induced by atrial natriuretic hormone, S-nitroso-N-acetylpenicillamine and 8-bromo cyclic GMP in cultured rat mesangial cells." Biochemical Journal 274, no. 2 (March 1, 1991): 323–28. http://dx.doi.org/10.1042/bj2740323.
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Cyclic GMP-elevating agents, including atrial natriuretic hormone and NO-generating vasodilators, decrease cytosolic free Ca2+ levels in mesangial cells. We have investigated the role of cell density as a modulator of the decrease in cytosolic free Ca2+ induced by the cyclic GMP (cGMP)-elevating vasodilators atrial natriuretic peptide (99-126) [ANP (99-126); ‘atriopeptin 28′] and the NO-generating vasodilator S-nitroso-N-acetylpenicillamine (SNAP), in cultured rat mesangial cells. Increasing cell density was significantly correlated with the decrease in cytosolic free Ca2+ induced by ANP (99-126) or SNAP. Moreover, this effect was independent of the cells' proliferative status. ANP (99-126) and SNAP induced greater fold stimulation of cGMP accumulation in high-density cells, but the levels of cGMP elicited by high concentrations of ANP (99-126) or SNAP were similar in high- and low-density cells. 8-Bromo cGMP was more effective in decreasing cytosolic free Ca2+ in high- than in low-density cells, suggesting that the greater effectiveness of ANP (99-126) and SNAP was, in part, due to greater effectiveness of endogenous cGMP in high-density cells. The results document that cell density, but not proliferative status, plays an important role in the modulation of intracellular Ca2+ dynamics in rat mesangial cells by atriopeptins, NO-generating vasodilators and cGMP.
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Russ, R. D., and B. R. Walker. "Maintained endothelium-dependent pulmonary vasodilation following chronic hypoxia in the rat." Journal of Applied Physiology 74, no. 1 (January 1, 1993): 339–44. http://dx.doi.org/10.1152/jappl.1993.74.1.339.
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We have previously demonstrated that arginine vasopressin (AVP) dilates the preconstricted pulmonary vasculature via the release of nitric oxide (NO). However, recent evidence suggests that NO release in response to other agents may be suppressed in lungs from animals that have been chronically exposed to hypoxia. The purpose of the present experiment was to determine whether vasopressinergic pulmonary vasodilation is similarly affected by chronic exposure to hypoxia (barometric pressure = 380 Torr for 4 wk). Inhibition of NO synthesis with N omega-nitro-L-arginine (L-NNA) had no effect on baseline perfusion pressure in isolated salt-perfused lungs from either control or chronically hypoxic rats. Similarly, pulmonary vasodilatory responses to AVP and the calcium ionophore A23187 were unaffected by chronic hypoxic exposure. Pretreatment with the cyclooxygenase inhibitor meclofenamate did not alter vasopressinergic pulmonary vasodilation in lungs from either control or chronically hypoxic animals, ruling out involvement of vasodilator prostaglandins in the response to AVP. In contrast, vasodilatory responses to both AVP and A23187 were inhibited by L-NNA pretreatment not only in lungs from control animals but also in lungs from chronically hypoxic rats, suggesting the involvement of NO in the vasodilatory response. The inhibition by L-NNA was reversible by prior addition of excess L-arginine but not by D-arginine. In addition, vasodilatory responses to the endothelium-independent vasodilators sodium nitroprusside and isoproterenol were unaffected by chronic hypoxic exposure. We conclude that endothelium-dependent vasodilation remains intact in male Sprague-Dawley rats after chronic hypoxic exposure.
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Ogawa, Haruo, Junya Kusumoto, Tadashi Nomura, Kazunobu Hashikawa, Hiroto Terashi, and Shunsuke Sakakibara. "Wire Myography for Continuous Estimation of the Optimal Concentration of Topical Lidocaine as a Vasodilator in Microsurgery." Journal of Reconstructive Microsurgery 37, no. 06 (January 31, 2021): 541–50. http://dx.doi.org/10.1055/s-0040-1722759.
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Abstract Background Intraoperative vasospasm during reconstructive microvascular surgery is often unpredictable and may lead to devastating flap loss. Therefore, various vasodilators are used in reconstructive microsurgery to prevent and relieve vasospasm. Lidocaine is a vasodilator commonly used in microvascular surgery. Although many reports have described its in vitro and in vivo concentration-dependent vasodilatory effects, limited studies have examined the pharmacological effects of lidocaine on blood vessels in terms of persistence and titer. Methods In this study, the vasodilatory effect of lidocaine was examined by using the wire myograph system. Abdominal aortas were harvested from female rats, sliced into rings of 1-mm thickness, and mounted in the wire myograph system. Next, 10, 5, 2, and 1% lidocaine solutions were applied to the artery, and the change in vasodilation force, persistence of the force, and time required to reach equilibrium were measured. Results The vasodilatory effect was confirmed in all groups following lidocaine treatment. Although strong vasodilation was observed in the 10% lidocaine group, it was accompanied by irreversible degeneration of the artery. Vasodilation in the 1% lidocaine group was weaker than that in the other groups 500 seconds after lidocaine addition (p < 0.05). Between the 5 and 2% lidocaine groups, 5% lidocaine showed a stronger vasodilatory effect 400 to 600 seconds after lidocaine addition (p < 0.01); however, there was no significant difference in these groups after 700 seconds. Additionally, there was no difference in the time required for the relaxation force to reach equilibrium among the 5, 2, and 1% lidocaine groups. Conclusion Although our study confirmed the dose-dependent vasodilatory effect of lidocaine, 5% lidocaine showed the best vasodilatory effect and continuity with minimal irreversible changes in the arterial tissue.
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Ueda, Misato, Yasuki Hirayama, Haruo Ogawa, Tadashi Nomura, Hiroto Terashi, and Shunsuke Sakakibara. "Vasodilating Effects of Antispasmodic Agents and Their Cytotoxicity in Vascular Smooth Muscle Cells and Endothelial Cells—Potential Application in Microsurgery." International Journal of Molecular Sciences 24, no. 13 (June 29, 2023): 10850. http://dx.doi.org/10.3390/ijms241310850.
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This study aimed to elucidate the vasodilatory effects and cytotoxicity of various vasodilators used as antispasmodic agents during microsurgical anastomosis. Rat smooth muscle cells (RSMCs) and human coronary artery endothelial cells (HCAECs) were used to investigate the physiological concentrations and cytotoxicity of various vasodilators (lidocaine, papaverine, nitroglycerin, phentolamine, and orciprenaline). Using a wire myograph system, we determined the vasodilatory effects of each drug in rat abdominal aortic sections at the concentration resulting in maximal vasodilation as well as at the surrounding concentrations 10 min after administration. Maximal vasodilation effect 10 min after administration was achieved at the following concentrations: lidocaine, 35 mM; papaverine, 0.18 mM; nitroglycerin, 0.022 mM; phentolamine, 0.11 mM; olprinone, 0.004 mM. The IC50 for lidocaine, papaverine, and nitroglycerin was measured in rat abdominal aortic sections, as well as in RSMCs after 30 min and in HCAECs after 10 min. Phentolamine and olprinone showed no cytotoxicity towards RSMCs or HCAECs. The concentrations of the various drugs required to achieve vasodilation were lower than the reported clinical concentrations. Lidocaine, papaverine, and nitroglycerin showed cytotoxicity, even at lower concentrations than those reported clinically. Phentolamine and olprinone show antispasmodic effects without cytotoxicity, making them useful candidates for local administration as antispasmodics.
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Yuchi, Yunosuke, Ryohei Suzuki, Narumi Ishida, Shuji Satomi, Takahiro Saito, Takahiro Teshima, and Hirotaka Matsumoto. "Comparative Study of Cardiovascular Effects of Selected Pulmonary Vasodilators in Canine Models of Mitral Valve Disease." Biology 13, no. 5 (April 30, 2024): 311. http://dx.doi.org/10.3390/biology13050311.
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Previous reports have shown that various oral pulmonary vasodilators are effective against canine pulmonary hypertension (PH). However, no studies have compared their hemodynamic effects. We aimed to compare the hemodynamic effects of 15 µg/kg beraprost sodium, 1.0 mg/kg sildenafil, and their combination, in dogs with experimentally induced mitral regurgitation. This experimental crossover study evaluated the hemodynamic and functional effects of oral pulmonary vasodilators by application of right-sided heart catheterization and echocardiography. Beraprost significantly decreased pulmonary and systemic vascular resistance. Additionally, beraprost increased right-ventricular stroke volume and left-ventricular cardiac output without worsening left-heart size and left-atrial pressure. The pulmonary vasodilatory effects of sildenafil were stronger, and its systemic vasodilatory effects were weaker than those of beraprost. However, sildenafil significantly increased the left-ventricular volume, left-atrial pressure indicator, and right-ventricular cardiac output. Combination therapy resulted in the strongest pulmonary and systemic vasodilating effects without worsening the left-heart size and left-atrial pressure indicators. Both beraprost and sildenafil were effective against canine PH; however, sildenafil was associated with the risk of worsening left-heart loading. Combination therapy with beraprost and sildenafil synergistically dilated pulmonary and systemic vessels, indicating a more potent treatment option for severe PH cases.
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Merkus, Daphne, David B. Haitsma, Tse-Yeung Fung, Yvette J. Assen, Pieter D. Verdouw, and Dirk J. Duncker. "Coronary blood flow regulation in exercising swine involves parallel rather than redundant vasodilator pathways." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 1 (July 2003): H424—H433. http://dx.doi.org/10.1152/ajpheart.00916.2002.
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In dogs, only combined blockade of vasodilator pathways [via adenosine receptors, nitric oxide synthase (NOS) and ATP-sensitive K+ (KATP) channels] results in impairment of metabolic vasodilation, which suggests a redundancy design of coronary flow regulation. Conversely, in swine and humans, blocking KATP channels, adenosine receptors, or NOS each impairs coronary blood flow (CBF) at rest and during exercise. Consequently, we hypothesized that these vasodilators act in parallel rather than in redundancy to regulate CBF in swine. Swine exercised on a treadmill (0–5 km/h), during control and after blockade of KATP channels (with glibenclamide), adenosine receptors [with 8-phenyltheophylline (8-PT)], and/or NOS [with Nω-nitro-l-arginine (l-NNA)]. l-NNA, 8-PT, and glibenclamide each reduced myocardial O2 delivery and coronary venous O2 tension. These effects of l-NNA, 8-PT, and glibenclamide were not modified by simultaneous blockade of the other vasodilators. Combined blockade of KATP channels and adenosine receptors with or without NOS inhibition was associated with increased H+ production and impaired myocardial function. However, despite an increase in O2 extraction to >90% during administration of l-NNA + 8-PT + glibenclamide, vasodilator reserve could still be recruited during exercise. Thus in awake swine, loss of KATP channels, adenosine, or NO is not compensated for by increased participation of the other two vasodilator mechanisms. These findings suggest a parallel rather than a redundancy design of CBF regulation in the porcine circulation.
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McQuillan, L. P., G. K. Leung, P. A. Marsden, S. K. Kostyk, and S. Kourembanas. "Hypoxia inhibits expression of eNOS via transcriptional and posttranscriptional mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 5 (November 1, 1994): H1921—H1927. http://dx.doi.org/10.1152/ajpheart.1994.267.5.h1921.
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Normal blood vessel tone is maintained by a balance of vasoconstrictors and vasodilators produced by endothelial cells in the vasculature. Nitric oxide (NO) is a potent vasodilator that causes vascular smooth muscle cell relaxation by elevating intracellular guanosine 3',5'-cyclic monophosphate (cGMP) levels. The physiological mechanisms regulating NO production in the vasculature are not completely understood. We report here that production of this vasodilator by vascular endothelial cells can be significantly suppressed by hypoxia. Exposing human endothelial cells to low PO2 results in 40–60% reduction in the steady-state mRNA levels of endothelial constitutive NO synthase (eNOS), the major enzyme responsible for NO production in these cells. The lower levels of eNOS mRNA result from decreased transcription of the gene as well as reduced message stability. In endothelial-smooth muscle cell co-culture experiments, hypoxic endothelial cells stimulated significantly less cGMP production by smooth muscle cells than the corresponding normoxic controls. This inhibitory effect of hypoxia on NOS production by endothelial cells occurs after 24 h of hypoxia and persists for at least 48 h. These new findings suggest that hypoxia might cause changes in blood vessel tone through compound mechanisms: by increasing the production of endothelium-derived vasoconstrictors and, as shown here, by suppressing the production of vasodilators like NO.
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Huraux, Catherine, Tetsuji Makita, Felix Montes, Fania Szlam, and Jerrold H. Levy. "A Comparative Evaluation of the Effects of Multiple Vasodilators on Human Internal Mammary Artery." Anesthesiology 88, no. 6 (June 1, 1998): 1654–59. http://dx.doi.org/10.1097/00000542-199806000-00030.
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Background Vasospasm of arterial grafts represents an unpredictable complication of coronary artery surgery and may compromise myocardial revascularization, and treatment is based on empirical therapy with nitroglycerin. Because of the potential for tolerance to nitroglycerin to occur, the authors studied different vasodilators acting through separate pathways on segments of human internal mammary artery. Methods Isolated vascular rings were precontracted with norepinephrine (1 microM), KCl, or the thromboxane A2 analogue (U46619, 10 nm). Nitroglycerin (a nitrovasodilator), milrinone (a type III phosphodiesterase inhibitor), papaverine (a phosphodiesterase inhibitor), prostaglandin E1, and isradipine (a dihydropyridine calcium channel blocker) were added in a cumulative fashion. Results The analysis of the concentration-response curves showed that vasodilators induced 90-100% relaxation of the constricted segments with norepinephrine or the thromboxane A2 analogue, except prostaglandin E1, which produced 73% relaxation at maximal concentrations. The effective concentrations of vasodilator agent that caused 50% relaxation for nitroglycerin and milrinone were within the range of the reported therapeutic concentrations in plasma. Isradipine was also effective at reversing receptor-mediated contraction (maximal relaxation=100% in internal mammary artery contracted with norepinephrine; maximal relaxation=0% in internal mammary artery contracted with the thromboxane A2 analogue). Conclusions Vasodilator drugs acting through multiple pathways are effective at reversing in vitro vasoconstriction.
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Reddy, V. M., J. Wong, J. R. Liddicoat, M. Johengen, R. Chang, and J. R. Fineman. "Altered endothelium-dependent responses in lambs with pulmonary hypertension and increased pulmonary blood flow." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 2 (August 1, 1996): H562—H570. http://dx.doi.org/10.1152/ajpheart.1996.271.2.h562.
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To investigate early endothelial function associated with increased pulmonary blood flow, vascular shunts were placed between the ascending aorta and main pulmonary artery in 18 late-gestation fetal sheep. Four weeks after delivery, the lambs were instrumented to measure vascular pressures and blood flows, and blood was collected to measure plasma concentrations of guanosine 3',5'-cyclic monophosphate [cGMP, the second messenger to nitric oxide (NO)-mediated vasodilation] and L-arginine (the precursor for NO synthesis). The responses to the endothelium-dependent vasodilators acetylcholine (ACh, 1.0 microgram/kg) and ATP (0.1 mg.kg-1.min-1), the endothelium-independent vasodilators M & B-22948 (a cGMP-specific phosphodiesterase inhibitor, 2.5 mg/kg) and inhaled NO (40 ppm), and N omega-nitro-L-arginine (an inhibitor of NO synthase, 5 mg/kg) were then compared with responses in 12 age-matched controls. Vasodilator responses in control lambs were determined during pulmonary hypertension induced by U-46619 (a thromboxane A2 mimic). Shunted lambs displayed a selective impairment of endothelium-dependent pulmonary vasodilation, an augmented pulmonary vasoconstricting response to NO synthase inhibition, increased plasma cGMP concentrations, and decreased L-arginine concentrations. Taken together, these data suggest that lambs with pulmonary hypertension and increased pulmonary blood flow have early aberrations in endothelial function, as manifested by increased basal NO activity, that cannot be further increased by agonist-induced endothelium-dependent vasodilators.
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Kvietys, P. R., C. A. Navia, A. J. Premen, and D. N. Granger. "Quantitative assessment of the two-component model of intestinal circulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 4 (October 1, 1986): G446—G452. http://dx.doi.org/10.1152/ajpgi.1986.251.4.g446.
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Recently a two-component model of the intestinal circulation was proposed to explain the effects of vasodilators on intestinal oxygenation. This model assumes that the intestine is composed of two regions: one region in which oxygen uptake is blood flow independent (well perfused and normoxic) and a second region in which oxygen uptake is blood flow dependent (under-perfused and hypoxic). The model predicts that total intestinal oxygen uptake is increased by a vasodilator only if the blood flow-dependent region is affected. We used a systems analysis approach to predict the various boundary conditions that must be imposed on the two-component model for it to simulate experimental observations. The mathematical model was based on current concepts and available data regarding intestinal hemodynamics and oxygen exchange. The model simulations predict that 30-70% of the intestine must be hypoxic (regions where oxygen uptake is blood flow dependent) for the two-component hypothesis to adequately explain published observations. Since the existence of such an extensive hypoxic region seems unlikely for the normal intestine, the predictive value of the two-component hypothesis may be of limited value for describing the effects of vasodilators on oxygen uptake in the normal intestine. However, the two-component model may be useful in predicting the effects of vasodilators on intestinal oxygen uptake in the ischemic intestine.
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Cohn, Jay N., Gordon T. McInnes, and Alexander M. Shepherd. "Direct-Acting Vasodilators." Journal of Clinical Hypertension 13, no. 9 (July 18, 2011): 690–92. http://dx.doi.org/10.1111/j.1751-7176.2011.00507.x.
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Vogel, Robert A. "Vintners and vasodilators." Journal of the American College of Cardiology 41, no. 3 (February 2003): 479–81. http://dx.doi.org/10.1016/s0735-1097(02)02825-5.
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Fayyaz, Mohammed, Muzamil Rana, Suresh Kacham, Clay Padginton, Bong Hee Sung, Michael F. Wilson, and Paresh Dandona. "Antioxidants are vasodilators." Journal of the American College of Cardiology 27, no. 2 (February 1996): 130. http://dx.doi.org/10.1016/s0735-1097(96)80744-3.
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Boley, Scott J., and Lawrence J. Brandt. "Selective mesenteric vasodilators." Gastroenterology 91, no. 1 (July 1986): 247–49. http://dx.doi.org/10.1016/0016-5085(86)90466-x.
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Kahale, Pravin, Pijush Kanti Biswas, Sunil George, Sree Ranga P. C., Pankaj Singh, Sanjoy K. Nag, and Soumen Roy. "Preference and practice of Indian physicians towards the use of vasodilator di-hydralazine in the management of resistant hypertension." International Journal of Advances in Medicine 7, no. 12 (November 23, 2020): 1781. http://dx.doi.org/10.18203/2349-3933.ijam20204986.
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Background: The treatment modalities of resistant hypertension (RH) remain a clinical challenge, often requiring secondary/add-on drugs with first-line therapy to control blood pressure (BP). This study was conducted to explore and understand the preferences and practices of Indian physicians towards the use of vasodilator (especially di-hydralazine) in the management of RH.Methods: This was a cross-sectional, observational, web-based physician survey. The study included cardiologist, nephrologist and consultant physicians from different geographical regions of India. A web-based physician survey questionnaire (PSQ) was created in google forms and the link was circulated to the physicians. Responses obtained were analysed.Results: A total of 457 physicians participated in this survey. In majority of the physicians, vasodilators were the treatment choice as secondary or add-on drugs with first line therapy to control BP in RH; especially hydralazine/di-hydralazine preferred the most. Majority of the physicians preferred to combine vasodilator with beta blocker and diuretic in patients with uncontrolled and RH. Cardiac failure, followed by chronic kidney disease (CKD), diabetes, dyslipidaemia, hypertensive emergency and angina were the common patient profile in RH in which majority physicians prescribed vasodilator (di-hydralazine). Majority of the physicians rated vasodilator di-hydralazine as “good-very good” in terms of efficacy, safety, tolerability, patient compliance and patient satisfaction in RH.Conclusions: Overall, vasodilators (hydrazinophthalazine derivatives) are preferred as add-on drugs along with first-line drugs in RH. Physician’s opinion towards the use of di-hydralazine was positive. Di-hydralazine may be preferred as an add-on therapeutic option to control BP in RH, however randomized clinical trials are needed for recommendation in cardio-renal medicine.
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Enomoto, Masahiro, Amish Jain, Jingyi Pan, Yulia Shifrin, Todd Van Vliet, Patrick J. McNamara, Robert P. Jankov, and Jaques Belik. "Newborn rat response to single vs. combined cGMP-dependent pulmonary vasodilators." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 2 (January 15, 2014): L207—L215. http://dx.doi.org/10.1152/ajplung.00164.2013.
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Inhaled nitric oxide (NO) and other cGMP- or cAMP-dependent pulmonary vasodilators are often used in combination for the treatment of the persistent pulmonary hypertension of the newborn syndrome. There is in vitro evidence to indicate that NO downregulate the pulmonary vascular response to cGMP-dependent agonists raising concern as to whether a synergistic effect is observed when employing a combined strategy in newborns. Hypothesizing that a synergistic effect is absent, we evaluated newborn and juvenile rat pulmonary arteries to determine the individual and combined vasodilatory effect of cGMP- and cAMP-dependent agonists. In precontracted near-resistance pulmonary arteries, the addition of sildenafil reduced vasorelaxation response to NO donor S-nitroso- N-acetyl penicillamine (SNAP). A similar decrease in SNAP-induced vasodilation was observed in arteries pretreated with BAY 41–2272 (10−9 M), a soluble guanylate cyclase stimulator cGMP, and its downstream protein kinase activator. cGMP also reduced the vasorelaxant response to the cAMP-dependent forskolin. Inhibition of endogenous vascular NO generation enhanced SNAP-induced relaxation. The present data suggest that the mechanism involved in the cGMP desensitization to other relaxant agonists involves downregulation of the small heat shock protein HSP20 and is evident in rat pulmonary and systemic vascular smooth muscle cells. In newborn rats with chronic hypoxia-induced pulmonary hypertension, the combination of sildenafil and inhaled NO resulted in a lesser reduction in pulmonary vascular resistance compared with their individual effect. These data suggest that clinical exposure to one cGMP-dependent pulmonary vasodilator may affect the response to other cGMP- or cAMP-mediated agonists.
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Hyman, A. L., P. J. Kadowitz, and H. L. Lippton. "Methylene blue selectively inhibits pulmonary vasodilator responses in cats." Journal of Applied Physiology 66, no. 3 (March 1, 1989): 1513–17. http://dx.doi.org/10.1152/jappl.1989.66.3.1513.
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The effects of methylene blue on vascular tone and the responses to pressor and depressor substances were investigated in the constricted feline pulmonary vascular bed under conditions of controlled blood flow and constant left atrial pressure. When tone was elevated with U46619, intralobar injections of acetylcholine, bradykinin, nitroglycerin, isoproterenol, epinephrine, and 8-bromoguanosine-3′,5′-cyclic monophosphate (8-bromo-cGMP) dilated the pulmonary vascular bed. Intralobar infusions of methylene blue elevated lobar arterial pressure without altering base-line left atrial or aortic pressure, heart rate, or cardiac output. When methylene blue was infused in concentrations that raised lobar arterial pressure to values similar to those attained during U46619 infusion, the pulmonary vasodilator responses to acetylcholine, bradykinin, and nitroglycerin were reduced significantly, whereas vasodilator responses to isoproterenol, epinephrine, and 8-bromo-cGMP were not altered. Moreover, the pressor responses to angiotensin II and BAY K 8644 during U46619 infusion and during methylene blue infusion were similar. The enhancing effects of methylene blue on vascular tone and inhibiting effects of this agent on responses to acetylcholine, bradykinin, and nitroglycerin were reversible. These responses returned to control value when tone was again increased with U46619, 30–45 min after the methylene blue infusion was terminated. The present data are consistent with the hypothesis that cGMP may play a role in the regulation of tone in the feline pulmonary vascular bed and in the mediation of vasodilator responses to the endothelium-dependent vasodilators, acetylcholine and bradykinin, and to nitrogen oxide-containing vasodilators such as nitroglycerin.
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Oltman, C. L., J. L. Parker, and M. H. Laughlin. "Endothelium-dependent vasodilation of proximal coronary arteries from exercise-trained pigs." Journal of Applied Physiology 79, no. 1 (July 1, 1995): 33–40. http://dx.doi.org/10.1152/jappl.1995.79.1.33.
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We recently reported that alpha-adrenergic vasoconstriction is blunted and adenosine-induced vasodilation is enhanced in proximal coronary arteries of exercise-trained miniature swine [C. L. Oltman, J. L. Parker, H. R. Adams, and M. H. Laughlin. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H372-H382, 1992]. The purpose of the present study was to determine whether this model of exercise training also alters endothelium-dependent vasodilator responses of proximal coronary arteries. Female Yucatan miniature swine were exercise trained (ET) on a motor-driven treadmill or were cage confined (Sed) for 13–20 wk. Exercise tolerance, heart weight-to-body weight ratios, and skeletal muscle oxidative capacity were all significantly greater in ET than in Sed animals. Vasodilator responses were evaluated in vitro by determining concentration-response curves by using vascular rings (3.5–4 mm in axial length) isolated from right and left coronary arteries. Vasorelaxation responses were determined, after tone had been produced with either 30 microM prostaglandin F2 alpha, 30 mM KCl, or 30 nM endothelin. Concentration-response curves were obtained to endothelium-dependent vasodilators including bradykinin (10(-9)-10(-6) M), substance P (10(-12)-10(-6) M), clonidine (10(-9)-10(-6) M), serotonin (10(-10)-10(-5) M), and the Ca2+ ionophore A-23187 (10(-10)-10(-6) M). Endothelium-independent vasodilator responses to sodium nitroprusside (10(-9)-10(-4) M) were not different between arteries from Sed and ET. Bradykinin, substance P, and A-23187 were potent vasodilators in arteries from both groups, whereas serotonin and clonidine did not consistently produce vasodilation.
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Kondo, Uruo, Si-Oh Kim, and Paul A. Murray. "Propofol Selectively Attenuates Endothelium-dependent Pulmonary Vasodilation in Chronically Instrumented Dogs." Anesthesiology 93, no. 2 (August 1, 2000): 437–46. http://dx.doi.org/10.1097/00000542-200008000-00023.
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Background The objective was to investigate the effects of propofol anesthesia on the pulmonary vascular response to endothelium-dependent and -independent vasodilators, compared with the responses measured in the conscious state. Methods Twenty-six conditioned, male, mongrel dogs were instrumented long-term to measure the left pulmonary vascular pressure-flow relation. Pressure-flow plots were measured on separate days in conscious and propofol-anesthetized (5.0 mg/kg plus 0.5 mg. kg-1. min-1 intravenously) dogs at baseline, after preconstriction with the thromboxane mimetic U46619, and during the cumulative intravenous administration of endothelium-dependent (acetylcholine and bradykinin) and -independent (proline-nitric oxide) vasodilators. Results Propofol had no effect on the baseline pressure-flow relation compared with the conscious state. A lower (P < 0.05) dose of U46619 was necessary to achieve the same degree of preconstriction during propofol anesthesia. The pulmonary vasodilator responses to bradykinin and proline-nitric oxide were similar in the conscious and propofol-anesthetized states. In contrast, the pulmonary vasodilator response to acetylcholine was markedly attenuated (P < 0.01) during propofol anesthesia. The intralipid vehicle for propofol had no effect on the acetylcholine dose-response relation. Conclusion These results suggest that propofol causes a specific defect in the signal transduction pathway for acetylcholine-induced pulmonary vasodilation. This defect involves the endothelial and not the vascular smooth muscle component of the response.
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Hintze, T. H., M. G. Currie, and P. Needleman. "Atriopeptins: renal-specific vasodilators in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (April 1, 1985): H587—H591. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h587.
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Conscious dogs were instrumented to study the effects of atriopeptins (I, II, III) on renal, iliac, mesenteric, and coronary blood flow. Intravenous injection of atriopeptins II and III caused a dose-related increase in renal blood flow, whereas atriopeptin I had no effect. Atriopeptins II and III at 5 micrograms/kg increased renal blood flow 27 +/- 5.0% from 252 +/- 29 ml/min and 18 +/- 2.9% from 238 +/- 32 ml/min and reduced renal vascular resistance 24 +/- 3.2% from 0.431 +/- 0.048 mmHg X ml-1 X min and 15.1 +/- 1.2% from 0.443 +/- 0.023 mmHg X ml-1 X min, respectively. Atriopeptin I, II, or III exerted no significant effect on systemic arterial pressure, heart rate, coronary, mesenteric, or iliac blood flows. Doses of nitroglycerin (25 micrograms/kg) that increased renal blood flow (28 +/- 5.0%) to a degree comparable to atriopeptins II and III also caused increases in coronary, iliac, and mesenteric blood flows and produced falls in systemic blood pressure and a reflex tachycardia. Thus in the conscious dog, atriopeptins II and III are potent selective renal vasodilators that do not exhibit systemic hemodynamic effects in contrast to nitroglycerin, a nonselective vasodilator. Cleavage at the carboxy terminal end of these peptides to yield atriopeptin I abolishes the renal vasodilator action entirely.
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Habila, Tahir, Mebrouk Belghobsi, Mohamed-Zakaria Stiti, Eric Goffin, Pascal de Tullio, Gilles Faury, Bernard Pirotte, and Smail Khelili. "Synthesis and vasodilator activity of 3,4-dihydropyrimidin-2(1H)-ones bearing urea, thiourea, and sulfonylurea moieties." Canadian Journal of Chemistry 97, no. 1 (January 2019): 20–28. http://dx.doi.org/10.1139/cjc-2018-0239.
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A series of novel 3,4-dihydropyrimidin-2(1H)-ones bearing urea, thiourea, and sulfonylurea moieties were synthesized and pharmacologically evaluated as vasodilator agents. The most interesting vasodilators were the thiourea derivatives 6a and 6b and the urea derivatives 6f–6i and 7f–7h, although the ureas were relatively more active than thioureas. Twenty-fold more active than diazoxide, the urea 6g was the most potent vasodilator (EC50 = 0.983 ± 0.061 μmol/L) and proved to act as a voltage-gated calcium channel blocker. The lack of activity of sulfonylureas, 6k and 7j, could be attributed to their partial ionization at the physiological pH because of their acidic character. It should be interesting to investigate a larger number of compounds, including N-methylated sulfonylureas, to increase the vasodilator activity and to explore other biological models.
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Jackson, W. F. "Arteriolar tone is determined by activity of ATP-sensitive potassium channels." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (November 1, 1993): H1797—H1803. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1797.
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The role of ATP-sensitive potassium channels (KATP) in determining resting arteriolar tone and vasodilator reactivity was assessed in superfused, hamster microcirculatory beds studied via intravital microscopy. Under resting conditions, the selective KATP blocker, glibenclamide, produced concentration-dependent vasoconstriction in both the cheek pouch and the cremaster muscle. Concentration-related constriction of cheek pouch arterioles was also observed with tetrapentylammonium, although this agent appeared to have toxic effects on the microcirculation. Glibenclamide (2 microM) abolished arteriolar vasodilation to cromakalim and pinacidil over a concentration range (10 nM-1 microM) in which these agents are selective KATP agonists and also significantly inhibited adenosine-, carbacyclin-, and isoproterenol-induced vasodilation. In contrast, responses to other vasodilators were not significantly affected [methacholine, forskolin, and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP)] or only slightly depressed (sodium nitroprusside). Thus the activity of KATP determines, in part, resting arteriolar tone in the hamster. Furthermore, vasodilators like adenosine, beta-adrenergic agonists, and prostacyclin appear to act through these ion channels by a mechanism that may not involve cAMP.
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Kalábová, Silvie, Klára Marešová, and Marta Karhanová. "Non-Arteritic Anterior Ischaemic Optic Neuropathy: Treatment and Risk Factors." Czech and Slovak Ophthalmology 76, no. 2 (October 1, 2020): 78–87. http://dx.doi.org/10.31348/2020/15.
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Aim: To ascertain whether various therapeutic procedures in non-arteritic anterior ischaemic optic neuropathy (NAION) have an impact on the resulting visual acuity of the affected eye. To assess the prevalence of risk factors that accompany this disease according to the literature. Methods: The retrospective study enrolled 55 eyes of 53 patients (41 men, 12 women) with an age range of 46 to 85 years (mean 64.9; median 64.0) who were hospitalized at the Department of Ophthalmology of the Faculty of Medicine and Dentistry and the University Hospital in Olomouc with the diagnosis of NAION between 2005 and 2016, and who received systemic treatment with intravenous vasodilators, either alone or in combination with intravenous corticosteroids. Central visual acuity (CVA) prior to treatment and immediately after its termination was evaluated. CVA was measured using the Snellen chart and is presented in decimal values. Using medical history data and medical records, the presence of systemic disease, namely hypertension, type 2 diabetes mellitus, and hypercholesterolaemia, was studied in these patients and evaluated for a possible association with NAION. Results: In the group of patients who were treated with intravenous vasodilators, the resulting CVA improved by 0.083 on average. In the group of patients who, in addition to vasodilator therapy, also received treatment with corticosteroids, the resulting CVA improved by only 0.03 on average. Although there was a more prominent improvement in CVA in the group treated with intravenous vasodilators alone, this difference was not statistically significant. At least one risk factor was found in the vast majority of the patients (96%). Eighty percent of the patients had hypertension, 43.6% of them were treated for diabetes mellitus, and 72.7% of the patients took drugs for hypercholesterolaemia. A combination of all these conditions was found in 36.4% of the patients. The proportion of smokers and past smokers did not exceed that of non-smokers. Conclusion: The mean improvement in the resulting CVA in patients after systemic therapy with vasodilators alone was greater than in those treated with a combination of vasodilators and corticosteroids; however, this difference was not statistically significant. In most patients in the group, at least one systemic risk factor was noted, most frequently hypertension. The prevalence rate of systemic risk factors was comparable to that reported in the literature.
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Sheikh, Naveen. "Pulmonary Arterial Hypertension Associated With Congenital Heart Disease." University Heart Journal 12, no. 1 (September 17, 2017): 31–33. http://dx.doi.org/10.3329/uhj.v12i1.34022.
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The management of patients with congenital heart disease (CHD) and pulmonary arterial hypertension (PAH) has changed dramatically with the development of targeted therapy with selective pulmonary vasodilators. It is important to develop evidence-based guidelines for the management of these patients, and to achieve this, a register of adult Bangladeshi patients with PAH associated with CHD should be established. At the World Symposium in Nice, France, in 2013, the consensus was reached that patients with a pulmonary resistance of < 4 Wood Units (WU)û0m2 have operable disease, and patients with a pulmonary resistanceof > 8 WUû0m2 have inoperable disease. However, these criteria are conservative. Some patients with a pulmonary resistance of > 8 WUû0m2 and a good response to a pulmonary vasodilator test have operable disease and a favorable clinical course long after repair of CHD. The criteria determining operability in patients with PAH associated with CHD in the era of pulmonary vasodilators should be established using data obtained from patient registers and/or multicenter studies. The optimal management of Eisenmenger syndrome should also be established using data obtained from patient registers. Prospective studies should be conducted to determine the life expectancy of patients with Eisenmenger syndrome in the era of targeted therapy. A relatively mild increase in pulmonary resistance may result in failure of a Fontan circulation. The effects of pulmonary vasodilators on the long-term prognosis of patients who have undergone the Fontan operation are still unclear. (Int Heart J 2015; 56: S1-S3).University Heart Journal Vol. 12, No. 1, January 2016; 31-33
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Jones, N. S., and L. D. Lewis. "Ergotamine-induced Peripheral Ischaemia Reversed by Oral Thymoxamine Hydrochloride." Human Toxicology 5, no. 1 (January 1986): 61–62. http://dx.doi.org/10.1177/096032718600500114.
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Although there is no generally accepted therapy for ergotamine-induced vasoconstriction, infusion of directly acting vasodilators is regarded presently as the treatment of choice. We present a case of peripheral arterial ischaemia secondary to excessive use of ergotamine suppositories, which was reversed with oral thymoxamine hydrochloride (an α 1-adrenoceptor antagonist) and ergotamine withdrawal. We suggest that in patients with ergotamine-induced peripheral arterial vasoconstriction with no evidence of gangrene, oral thymoxamine may be considered as a useful adjunct or possible alternative to infused vasodilator treatment.
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Day, Ronald W. "Acute vasodilator testing following Fontan palliation: an opportunity to guide precision care?" Cardiology in the Young 30, no. 6 (May 22, 2020): 829–33. http://dx.doi.org/10.1017/s1047951120001110.
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AbstractBackground:Pulmonary vasodilators improve the functional capacity of some patients with pulmonary arterial hypertension. However, pulmonary vasodilators frequently fail to improve unequivocal endpoints of efficacy in patients with lower pulmonary arterial pressures who have been palliated with a Fontan procedure.Objective:Haemodynamic measurements and the results of acute vasodilator testing in a subset of patients were reviewed to determine whether some patients acutely respond more favourably to sildenafil and might be candidates for precision care with a phosphodiesterase V inhibitor long term.Materials and Methods:Heart catheterisation was performed in 11 patients with a Fontan procedure. Haemodynamic measurements were performed before and after treatment with intravenous sildenafil (mean 0.14, range 0.05–0.20 mg/kg). Results (mean ± standard deviation) were compared by paired and unpaired t-tests to identify statistically significant changes.Results:Sildenafil was acutely associated with changes in mean pulmonary arterial pressure, transpulmonary gradient, indexed blood flow, and indexed vascular resistance. Changes in mean pulmonary arterial pressure were greater for patients with a mean pulmonary arterial pressure greater than 14 mmHg compared to patients with a lower mean pulmonary arterial pressure. Changes in transpulmonary gradient were greater for patients with a transpulmonary gradient greater than 5 mmHg compared to patients with a lower transpulmonary gradient.Conclusion:Sildenafil acutely decreases mean pulmonary arterial pressure and transpulmonary gradient and causes greater acute changes in patients with higher mean pulmonary arterial pressures and transpulmonary gradients. Haemodynamic measurements and vasodilator testing might help to guide precision care following Fontan palliation.
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Cogswell, Andria M., Philip J. Johnson, and H. Richard Adams. "Evidence for endothelium-derived relaxing factor/nitric oxide in equine digital arteries." American Journal of Veterinary Research 56, no. 12 (December 1, 1995): 1637–41. http://dx.doi.org/10.2460/ajvr.1995.56.12.1637.
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Abstract Objective To test the hypothesis that endothelium-derived nitric oxide modulates vasomotor reactivity in equine digital arteries. Design Digital arteries were isolated from adult horses, and their vasodilator properties were examined in an in vitro controlled environment. Animals Five adult horses (1 gelding, 4 mares) without evidence of hoof or vascular disease were studied. Procedure Arterial rings with or without endothelium were exposed to endothelium-dependent vasodilator drugs in the presence or absence of a pharmacologic inhibitor of the enzyme nitric oxide synthase. Results Vasodilator effects of 3 endothelium-dependent vasorelaxant agents were significantly greater in endothelium-intact vessels than in endothelium-denuded vessels. Moreover, a nitric oxide synthase inhibitor reduced vasodilator responses to endothelium-dependent vasodilators in endothelium-intact arteries, but had no discernable effects in endothelium-denuded arteries. Conclusions These findings indicate the presence of endothelium-derived relaxing factor/nitric oxide in blood vessels of horses, and identify vascular endothelium as an endogenous modulator of vasomotor tone in the digital arteries of this species.