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Chronic heart failure does not attenuate the total activity of sympathetic outflow to skin during whole-body heating.

ABSTRACT: Previous studies show that the rise in skin blood flow and cutaneous vascular conductance during heat stress is substantially attenuated in chronic heart failure (CHF) patients. The mechanisms responsible for this finding are not clear. In particular, little is known regarding the responses of skin sympathetic nerve activity (SSNA) that control the skin blood flow during heat stress in CHF patients. We examined the effects of a modest heat stress to test the hypothesis that SSNA responses could be attenuated in CHF.We assessed SSNA (microneurography) from the peroneal nerve and skin blood flow (forearm laser Doppler) in 9 patients with stable class II-III CHF and in matched healthy subjects during passive whole-body heating with a water-perfused suit. Whole-body heating induced similar increases in internal temperature (?0.6 °C) in both groups. Whole-body heat stress evoked similar SSNA activation in CHF patients (?891±110 U/min) and the control subjects (?787±84 U/min; P=0.66), whereas the elevation in forearm cutaneous vascular conductance in patients with CHF was significantly lower than that in healthy control subjects (?131±29% vs. ?623±131%; P=0.001).The present data show that SSNA activation during a modest whole-body heat stress is not attenuated in CHF. Thus, the attenuated skin vasodilator response in CHF patients is not attributable to a reduction in total activity of sympathetic outflow to skin.

SUBMITTER: Cui J

PROVIDER: S-EPMC3738175 | biostudies-literature | 2013 Mar

REPOSITORIES: biostudies-literature

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Chronic heart failure does not attenuate the total activity of sympathetic outflow to skin during whole-body heating.

Cui Jian J Boehmer John P JP Blaha Cheryl C Lucking Robert R Kunselman Allen R AR Sinoway Lawrence I LI

Circulation. Heart failure 20130208 2

<h4>Background</h4>Previous studies show that the rise in skin blood flow and cutaneous vascular conductance during heat stress is substantially attenuated in chronic heart failure (CHF) patients. The mechanisms responsible for this finding are not clear. In particular, little is known regarding the responses of skin sympathetic nerve activity (SSNA) that control the skin blood flow during heat stress in CHF patients. We examined the effects of a modest heat stress to test the hypothesis that SS ...[more]

PMID: 23395933

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Project description:The aim of the present study was to determine if renal sympathetic denervation (RSD) may alleviate isoproterenol-induced left ventricle remodeling, and to identify the underlying mechanism. A total of 70 rats were randomly divided into control (n=15), sham operation (n=15), heart failure (HF) with sham operation (HF + sham; n=20) and HF with treatment (HF + RSD; n=20) groups. The HF model was established by subcutaneous injection of isoproterenol; six weeks later, 1eft ventricular internal diameter at end?systole (LVIDs), left ventricular systolic posterior wall thickness (LVPWs), 1eft ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured. Plasma norepinephrine (NE), angiotensin II (Ang II) and aldosterone (ALD) levels were measured by ELISA. Myocardial collagen volume fraction (CVF) was determined by Masson's staining. Reverse transcription?quantitative polymerase chain reaction was used to determine the mRNA expression levels of ventricular transforming growth factor?? (TGF??), connective tissue growth factor (CTGF) and microRNAs (miRs), including miR?29b, miR?30c and miR?133a. The results demonstrated that LVIDs and LVPWs in the HF + RSD group were significantly decreased compared with the HF + sham group. By contrast, LVFS and LVEF in the HF + RSD group were significantly increased compared with the HF + sham group. RSD significantly reduced the levels of plasma NE, Ang II and ALD. CVF in the HF + RSD group was reduced by 38.1% compared with the HF + sham group. Expression levels of TGF?? and CTGF were decreased, whereas those of miR?29b, miR?30c and miR?133a were increased, in the HF + RSD group compared with the HF + sham group. These results indicated that RSD alleviates isoproterenol?induced left ventricle remodeling potentially via downregulation of TGF??/CTGF and upregulation of miR?29b, miR?30c and miR?133a. RSD may therefore be an effective non?drug therapy for the treatment of heart failure.

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Chronic heart failure does not attenuate the total activity of sympathetic outflow to skin during whole-body heating.

Publications

Chronic heart failure does not attenuate the total activity of sympathetic outflow to skin during whole-body heating.

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