Abstract-The forearm vasodilator response to mental stress is multifactorial and widely variable among individuals. We evaluated the association between the heart rate and forearm vascular conductance (FVC) responses to a color word test in 101 healthy adults. We found a striking correlation between heart rate and FVC (r = 0.66, p < 0.001), which remained significant when controlling for subject characteristics, blood pressure, and catecholamines. This suggests that the mechanical stimulation is one of the key factors that contribute to the increase in FVC during mental stress.Synopsis-Our major new finding is that there is a strong correlation between the increase in heart rate and the increase in forearm vascular conductance during mental stress.
Variation in the beta-1 and beta-2 adrenergic receptor genes (ADRB1 and ADRB2, resp.) may influence cardiovascular reactivity including orthostatic stress. We tested this hypothesis in a head-up tilt (HUT) screening protocol in healthy young adults without history of syncope. Following brachial arterial catheter insertion, 120 subjects (age 18–40, 72 females, Caucasian) underwent 5 min 60° HUT. Polymorphisms tested were: Ser49/Gly and Arg389/Gly in ADRB1; Arg16/Gly, Gln27/Glu, and Thr164/Ile in ADRB2. Three statistical models (recessive, dominant, additive) were evaluated using general linear models with analysis for each physiologic variable. A recessive model demonstrated a significant association between Arg16/Gly and: absolute supine and upright HR; HUT-induced change in cardiac index (CI), stroke index (SI) and systemic vascular resistance (SVR); and supine and upright norepinephrine values. Blood pressure was not influenced by genotype. Fewer associations were present for other polymorphisms: Ser49/Gly and the change in SI (dominant model), and Arg389/Gly and supine and HUT norepinephrine (additive model). We conclude that in this population, there is a robust association between Arg16/Gly and HUT responses, such that 2 copies of Arg16 increases supine and upright HR, and greater HUT-induced decreases in CI and SI, with greater increases in SVR and norepinephrine. ADRB1 gene variation appears to impact SI and plasma NE levels but not HR. Whether ADRB2 gene variation is ultimately disease-causing or disease-modifying, this study suggests an association between Arg16/Gly and postural hemodynamics, with sympathetic noradrenergic activity affected in a similar direction. This may have implications in the development of orthostatic disorders.
Phosphodiesterase (PDE) III is an enzyme in vascular smooth muscle that metabolizes cyclic adenosine monophosphate (cAMP). Milrinone inhibits PDE III, increasing the availability of cAMP. Cyclic guanosine monophosphate (cGMP), which is regulated by nitric oxide (NO), also inhibits PDE III. The endothelial NO component of prostacyclin (PGI2)‐mediated vasodilation is reduced in aging. This study investigated if PGI2‐mediated vasodilation during concomitant inhibition of endothelial NO and smooth muscle PDE III is affected by healthy aging. PDE III was inhibited with milrinone in 10 older subjects and 10 young matched controls while simultaneously infusing NG‐monomethyl‐l‐arginine acetate (l‐NMMA) to remove the confounding inhibitory effects of cGMP on PDE III. Incremental doses of PGI2 and sodium nitroprusside (SNP) were administered to the brachial artery during separate trials. l‐NMMA decreased baseline blood flow similarly, and the addition of milrinone increased baseline blood flow similarly in both groups. The forearm blood flow responses to PGI2 were similar between groups (younger: 7.62 ± 0.72; older: 6.88 ± 0.81 mL•dL−1 FAV•min−1 at the highest dose of PGI2). SNP responses were also similar. This study suggests that the vasodilator pathway associated with PDE III function, the bioavailability of cAMP, and the interaction with cGMP may be preserved in healthy aging. Clin Trans Sci 2010; Volume 3: 239–242.
Purpose We studied patients with palmar hyperhidrosis before and after endoscopic thoracic sympathotomy (ETS) to determine the effect of chronic sympathetic denervation on 1) forearm blood flow (FBF) response to mental stress and 2) exercise tolerance. Methods and Results 22 healthy patients were evaluated before ETS, and 17 returned after surgery (11 F; 19–32 yr). We measured heart rate (HR; 12-lead), blood pressure, and FBF (plethysmography, ml/100ml forearm volume/min). Supine HR tended to decrease after ETS (69 ± 10 vs 66 ± 6, p=0.2). Mental stress FBF was recorded during baseline, 3 min Stroop Color Word test, and 2 min recovery. Mental stress responses were unaffected by ETS. However during post-mental stress recovery period, ETS resulted in a significant elevation in FBF (2 ± 1 vs 3 ± 1), FVC (3 ± 1 vs 4 ± 2), and a decrease in FVR (52 ± 22 vs 32 ± 16, p < 0.01 for all). ETS resulted in a reduction in pre-exercise seated baseline HR (94 ± 2.5 beats/min preoperatively vs 84 ± 4.3 beats/min post-operatively, p<0.05), maximal HR response to cycle exercise, and exercise systolic blood pressure (172 ± 5.2 mmHg pre-op vs 158 ± 5.9 mmHg postop, p<0.05) but not mean or diastolic pressure. VO2 max and exercise duration determined by cycle ergometry was unchanged. Conclusions Functional evidence of upper limb denervation is observed during the FBF recovery period from mental stress and hemodynamic alterations associated with upright cycle exercise. However, the sustained exercise capacity suggests modest clinical consequences.
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