Abnormal vascular responses in human chronic cardiac failure are both endothelium dependent and endothelium independent

Maguire, S.; Nugent, Ailish G.; McGurk, C.; Johnston, G D; Nicholls, D. P.

doi:10.1136/hrt.80.2.141

Cited by 50 publications

(45 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…27,43 The present and previous 10,44 findings show that local heatinginduced cutaneous vasodilation is attenuated in patients with CHF. These observations are consent with those of others showing that patients with CHF exhibit attenuated endothelium-dependent vasodilation of the peripheral circulation, 38,45,46 including skin. 47 However, it is recognized that the present results do not permit the discrimination between altered responsiveness to vasodilator agents, such as nitric oxide, from possible structural changes in the cutaneous vasculature with CHF, previously shown in these patients.…”

Section: Cui Et Al Thermal Regulatory Responses In Chf 2289supporting

confidence: 91%

Effects of Heat Stress on Thermoregulatory Responses in Congestive Heart Failure Patients

et al. 2005

View full text Add to dashboard Cite

Background-Clinical observations suggest that tolerance to heat stress may be impaired in patients with cardiovascular diseases, particularly those associated with impaired ventricular function and congestive heart failure (CHF). However, thermoregulatory function during a controlled heat stress challenge in patients with CHF has not been studied. Methods and Results-To test the hypothesis that thermoregulatory responses are attenuated in such patients, we assessed cutaneous vasodilation and sweat rate in patients with stable class II-III CHF and in matched healthy subjects during passive whole-body heating. Whole-body heating induced a similar increase in internal temperature (Ϸ0.85°C) in both groups. The sweating responses in patients with CHF were not significantly different from that in control subjects. In contrast, the elevation in forearm cutaneous vascular conductance in patients with CHF was reduced by nearly 50% relative to the control subjects (3.8Ϯ0.8 versus 6.9Ϯ1.0 mL/100 mL tissue per minute per 100 mm Hg, Pϭ0.04). Moreover, maximal cutaneous vasodilator capacity to direct local heating in patients with CHF was also significantly lower than in control subjects, suggesting that vascular remodeling may be limiting cutaneous vasodilation during hyperthermia. Conclusions-These observations suggest that patients with CHF exhibit attenuated cutaneous vasodilator responses to both whole-body and local heating, whereas sweating responses are preserved. Attenuated cutaneous vasodilation may be a potential mechanism for heat intolerance in patients with CHF.

show abstract

Section: Cui Et Al Thermal Regulatory Responses In Chf 2289supporting

confidence: 91%

Effects of Heat Stress on Thermoregulatory Responses in Congestive Heart Failure Patients

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Studies to establish whether basal nitric oxide (NO) production is altered in HF patients have yielded conflicting results. [28][29][30][31][32] One study by Maguire et al 33 supports previous observations that NO does not contribute to basal vascular tone in patients with HF. It has been suggested that endothelial damage could result in a reduction in the availability of endothelium-derived NO from either decreased production or increased breakdown.…”

Section: Endothelial Dysfunctionsupporting

confidence: 68%

“…33,50 Some evidence suggests that over time arterial compliance decreases. 51,52 Abnormal smooth muscle function may result from altered responsiveness or impaired diffusion of NO through the arterial wall.…”

Section: Vascular Smooth Muscle Abnormalitiesmentioning

confidence: 99%

Why do patients with heart failure suffer from erectile dysfunction? A critical review and suggestions on how to approach this problem

et al. 2005

View full text Add to dashboard Cite

Chronic heart failure (HF) is an increasingly common cardiovascular disorder. The goal of healthcare providers is to optimize quality of life in this population, including sexual health. Up to 75% of patients with HF report erectile dysfunction (ED). As HF is a condition with distinct physiologic sequelae, some unique organic and psychological factors contributing to ED in this patient population have been identified, along with risk factors common to the development of coronary artery disease, HF and ED. This review describes contributing factors to ED in the setting of HF and highlights treatment considerations for this distinct patient population.

show abstract

“…There is evidence that vascular smooth muscle sensitivity to NO is reduced in diabetes (Maguire et al, 1998). Therefore, we evaluated endothelial-independent relaxation in rat coronary arteries by analyzing concentration responses to the NO donor SNP.…”

Section: Simvastatin Improves Coronary Endothelial Dysfunction 389mentioning

confidence: 99%

Simvastatin Improves Diabetes-Induced Coronary Endothelial Dysfunction

Tawfik

El-Remessy

Matragoon

et al. 2006

J Pharmacol Exp Ther

View full text Add to dashboard Cite

3-Hydroxy-3-methylglutaryl CoA reductase inhibitors decrease cardiovascular morbidity in diabetic patients, but the mechanism is unclear. We studied the actions of simvastatin (SIM) in enhancing NO bioavailability and reducing oxidative stress in coronary vessels from diabetic rats and in rat coronary artery endothelial cells (RCAEC) exposed to high glucose. Coronary arteries isolated from diabetic rats showed decreases in acetylcholine (ACh)-mediated maximal relaxation from 81.0 Ϯ 4.5% in controls to 43.5 Ϯ 7.6% at 4 weeks and 22.3 Ϯ 0.6% at 10 weeks of diabetes. This effect was associated with oxidative stress in coronary vessels as shown by dichlorofluorescein (DCF) imaging and nitrotyrosine labeling. Diabetes also reduced trans-coronary uptake of [ 3 H]L-arginine. Supplemental L-arginine (50 mg/kg/day p.o.) did not improve coronary vasorelaxation to ACh. However, SIM treatment (5 mg/kg/day subcutaneously) improved maximal ACh relaxation to 65.8 Ϯ 5.1% at 4 weeks and 47.1 Ϯ 3.9% at 10 weeks. Coronary arteries from rats treated with both SIM and L-arginine demonstrated the same maximal relaxation to ACh (66.1 Ϯ 3%) as SIM alone. Mevalonate and L-NAME (N -nitro-L-arginine methyl ester hydrochloride) inhibited the response to ACh in SIM-treated diabetic rats. Coronary arteries from all groups relaxed similarly to sodium nitroprusside. SIM increased endothelial NO synthase protein levels and blocked diabetes-induced increases in DCF and nitrotyrosine labeling in diabetic coronary vessels. SIM treatment restored normal NO levels in media from high-glucosetreated RCAEC and plasma of diabetic rat. Treatment with SIM or the NADPH oxidase inhibitor apocynin also blocked high-glucoseinduced increases in reactive oxygen species and superoxide formation in RCAEC. Taken together, these data suggest that SIM improves diabetes-induced coronary dysfunction by reducing oxidative stress and increasing NO bioavailability.

show abstract

Abnormal vascular responses in human chronic cardiac failure are both endothelium dependent and endothelium independent

Cited by 50 publications

References 40 publications

Effects of Heat Stress on Thermoregulatory Responses in Congestive Heart Failure Patients

Effects of Heat Stress on Thermoregulatory Responses in Congestive Heart Failure Patients

Why do patients with heart failure suffer from erectile dysfunction? A critical review and suggestions on how to approach this problem

Simvastatin Improves Diabetes-Induced Coronary Endothelial Dysfunction

Contact Info

Product

Resources

About