Skin-surface cooling elicits a pronounced systemic pressor response, which has previously been reported to be associated with peripheral vasoconstriction and may not fully account for the decrease in systemic vascular conductance. To test the hypothesis that whole body skin-surface cooling would also induce renal and splanchnic vasoconstriction, 14 supine subjects performed 26 skin-surface cooling trials (15-18 degrees C water perfused through a tube-lined suit for 20 min). Oral and mean skin temperature, heart rate, stroke volume (Doppler ultrasound), mean arterial blood pressure (MAP), cutaneous blood velocity (laser-Doppler), and mean blood velocity of the brachial, celiac, renal, and superior mesenteric arteries (Doppler ultrasound) were measured during normothermia and skin-surface cooling. Cardiac output (heart rate x stroke volume) and indexes of vascular conductance (flux or blood velocity/MAP) were calculated. Skin-surface cooling increased MAP (n = 26; 78 +/- 5 to 88 +/- 5 mmHg; mean +/- SD) and decreased mean skin temperature (n = 26; 33.7 +/- 0.7 to 27.5 +/- 1.2 degrees C) and cutaneous (n = 12; 0.93 +/- 0.68 to 0.36 +/- 0.20 flux/mmHg), brachial (n = 10; 32 +/- 15 to 20 +/- 12), celiac (n = 8; 85 +/- 22 to 73 +/- 22 cm.s(-1).mmHg(-1)), superior mesenteric (n = 8; 55 +/- 16 to 48 +/- 10 cm.s(-1).mmHg(-1)), and renal (n = 8; 74 +/- 26 to 64 +/- 20 cm.s(-1).mmHg(-1); all P < 0.05) vascular conductance, without altering oral temperature, cardiac output, heart rate, or stroke volume. These data identify decreases in vascular conductance of skin and of brachial, celiac, superior mesenteric, and renal arteries. Thus it appears that vasoconstriction in both peripheral and visceral arteries contributes importantly to the pressor response produced during skin-surface cooling in humans.
Cardiovascular-related mortality peaks during cold winter months, particularly in older adults. Acute physiological responses, such as increases in blood pressure, in response to cold exposure may contribute to these associations. To determine whether the blood pressure-raising effect (pressor response) of non-internal body temperature-reducing cold stress is greater with age, we measured physiological responses to 20 min of superficial skin cooling, via water-perfused suit, in 12 younger [25 +/- 1 (SE) yr old] and 12 older (65 +/- 2 yr old) adults. We found that superficial skin cooling elicited an increase in blood pressure from resting levels (pressor response; P < 0.05) in younger and older adults. However, the magnitude of this pressor response (systolic and mean blood pressure) was more than twofold higher in older adults (P < 0.05 vs. younger adults). The magnitude of the pressor response was similar at peripheral (brachial) and central (estimated in the aorta) measurement sites. Regression analysis revealed that aortic pulse wave velocity, a measure of central arterial stiffness obtained before cooling, was the best predictor of the increased pressor response to superficial skin cooling in older adults, explaining approximately 63% of its variability. These results indicate that there is a greater pressor response to non-internal body temperature-reducing cold stress with age in humans that may be mediated by increased levels of central arterial stiffness.
Newcomer SC, Sauder CL, Kuipers NT, Laughlin MH, Ray CA. Effects of posture on shear rates in human brachial and superficial femoral arteries. Am J Physiol Heart Circ Physiol 294: H1833-H1839, 2008. First published February 1, 2008 doi:10.1152/ajpheart.01108.2007.-Shear rate is significantly lower in the superficial femoral compared with the brachial artery in the supine posture. The relative shear rates in these arteries of subjects in the upright posture (seated and/or standing) are unknown. The purpose of this investigation was to test the hypothesis that upright posture (seated and/or standing) would produce greater shear rates in the superficial femoral compared with the brachial artery. To test this hypothesis, Doppler ultrasound was used to measure mean blood velocity (MBV) and diameter in the brachial and superficial femoral arteries of 21 healthy subjects after being in the supine, seated, and standing postures for 10 min. MBV was significantly higher in the brachial compared with the superficial femoral artery during upright postures. Superficial femoral artery diameter was significantly larger than brachial artery diameter. However, posture had no significant effect on either brachial or superficial femoral artery diameter. The calculated shear rate was significantly greater in the brachial (73 Ϯ 5, 91 Ϯ 11, and 97 Ϯ 13 s Ϫ1 ) compared with the superficial femoral (53 Ϯ 4, 39 Ϯ 77, and 44 Ϯ 5 s Ϫ1 ) artery in the supine, seated, and standing postures, respectively. Contrary to our hypothesis, our current findings indicate that mean shear rate is lower in the superficial femoral compared with the brachial artery in the supine, seated, and standing postures. These findings of lower shear rates in the superficial femoral artery may be one mechanism for the higher propensity for atherosclerosis in the arteries of the leg than of the arm. atherosclerosis; conduit artery diameter; leg and arm vasculature; lesion formation
The purpose of this study was to determine neurovascular responses to mental stress (MS) in the supine and upright postures. MS was elicited in 23 subjects (26 +/- 1 yr) by 5 min of mental arithmetic. In study 1 (n = 9), Doppler ultrasound was used to measure mean blood flow velocity in the renal (RBFV) and superior mesenteric arteries (SMBFV), and venous occlusion plethysmography was used to measure forearm blood flow (FBF). In study 2 (n = 14), leg blood flow (LBF; n = 9) was measured by Doppler ultrasound, and muscle sympathetic nerve activity (MSNA; n = 5) was measured by microneurography. At rest, upright posture increased heart rate and MSNA and decreased LBF, FBF, RBFV, and SMBFV and their respective conductances. MS elicited similar increases in mean arterial blood pressure ( approximately 12 mmHg) and heart rate ( approximately 17 beats/min), regardless of posture. MS in both postures elicited a decrease in RBFV, SMBFV, and their conductances and an increase in LBF, FBF, and their conductances. Changes in blood flow were blunted in the upright posture in all vascular beds examined, but the pattern of the vascular response was the same as the supine posture. MS did not change MSNA in either posture (change: approximately 1 +/- 3 and approximately 3 +/- 3 bursts/min, respectively). In conclusion, the augmented sympathetic activity of the upright posture does not alter heart rate, mean arterial blood pressure, or MSNA responses to MS. MS elicits divergent vascular responses in the visceral and peripheral vasculature. These results indicate that, although the upright posture attenuates vascular responses to MS, the pattern of neurovascular responses does not differ between postures.
Mental stress (MS) is a known trigger of myocardial infarction and sudden death. By activating the sympathetic nervous system, MS may have deleterious effect on the cardiovascular system but this process is not completely understood. The primary aim of this study was to quantify the effect of MS on skin sympathetic nerve activity (SSNA). The secondary aim was to determine the reproducibility of SSNA to MS within a given day and ~1 week later. Ten subjects (26±1 yr.) performed two bouts of mental arithmetic lasting 3 min. The bouts were separated by 45 min. One week later the subjects returned to repeat MS. All experiments were conducted in the supine posture during the morning hours. To maintain neutral skin temperature, each subject wore a custom suit (34-35°C). Skin blood flow and sweat rate were measured on the dorsal foot. MS elicited a marked increase in SSNA within the first 10 s (184±42%; P<0.01) in all subjects, which was less during the remaining period of MS but remained elevated (87±20; P<0.01). The pattern of responses to MS was unchanged during the second bout (10 s, 247±55%; 3 min avg., 133±29%) and during the retest 1 week later (10 s, 196±55%; 3 min avg., 117±36%). MS did not significantly affect cutaneous vascular conductance or sweat rate during any trial. In summary, MS elicits robust and reproducible increases in SSNA in humans which may be followed over time to observe alterations in the regulation of the autonomic nervous system.
Background and objectiveIncreasing mortality and decreasing life expectancy in the USA are largely attributable to accidental overdose, alcohol-related disease and suicide. These ‘deaths of despair’ often follow years of morbidity, yet little is known about trends in the clinical recognition of ‘diseases of despair’. The objective of this study is to characterise rates of clinically documented diseases of despair over the last decade and identify sociodemographic risk factors.DesignRetrospective study using a healthcare claims database with 10 years of follow-up.SettingParticipants resided nationwide but were concentrated in US states disproportionately affected by deaths of despair, including Pennsylvania, West Virginia and Delaware.ParticipantsCohort included 12 144 252 participants, with no restriction by age or gender.Outcome measuresDiseases of despair were defined as diagnoses related to alcohol misuse, substance misuse and suicide ideation/behaviours. A lookback period was used to identify incident diagnoses. Annual and all-time incidence/prevalence estimates were computed, along with risk for current diagnosis and patterns of comorbidity.Results515 830 participants received a disease of despair diagnosis (58.5% male, median 36 years). From 2009 to 2018, the prevalence of alcohol-related, substance-related and suicide-related diagnoses respectively increased by 37%, 94%, and 170%. Ages 55–74 had the largest increase in alcohol/substance-related diagnoses (59% and 172%). Ages <18 had the largest increase in suicide-related diagnoses (287%). Overall, odds for current-year diagnosis were higher among men (adjusted OR (AOR) 1.49, 95% CI 1.47 to 1.51), and among those with Affordable Care Act or Medicare coverage relative to commercial coverage (AOR 1.30, 1.24 to 1.37; AOR 1.51, 1.46 to 1.55).ConclusionsIncreasing clinical rates of disease of despair diagnoses largely mirror broader societal trends in mortality. While the opioid crisis remains a top public health priority, parallel rises in alcohol-related diagnoses and suicidality must be concurrently addressed. Findings suggest opportunities for healthcare systems and providers to deploy targeted prevention to mitigate the progression of morbidities towards mortality.
Melatonin is synthesized and released into the circulation by the pineal gland in a circadian rhythm. Melatonin has been demonstrated to differentially alter blood flow to assorted vascular beds by the activation of different melatonin receptors in animal models. The purpose of the present study was to determine the effect of melatonin on blood flow to various vascular beds in humans. Renal (Doppler ultrasound), forearm (venous occlusion plethysmography), and cerebral blood flow (transcranial Doppler), arterial blood pressure, and heart rate were measured in 10 healthy subjects (29±1 yr; 5 men and 5 women) in the supine position for 3 min. The protocol began 45 min after the ingestion of either melatonin (3 mg) or placebo (sucrose). Subjects returned at least 2 days later at the same time of day to repeat the trial after ingesting the other substance. Melatonin did not alter heart rate and mean arterial pressure. Renal blood flow velocity (RBFV) and renal vascular conductance (RVC) were lower during the melatonin trial compared with placebo (RBFV, 40.5±2.9 vs. 45.4±1.5 cm/s; and RVC, 0.47±0.02 vs. 0.54±0.01 cm·s(-1)·mmHg(-1), respectively). In contrast, forearm blood flow (FBF) and forearm vascular conductance (FVC) were greater with melatonin compared with placebo (FBF, 2.4±0.2 vs. 1.9±0.1 ml·100 ml(-1)·min(-1); and FVC, 0.029±0.003 vs. 0.023±0.002 arbitrary units, respectively). Melatonin did not alter cerebral blood flow measurements compared with placebo. Additionally, phentolamine (5-mg bolus) after melatonin reversed the decrease in RVC, suggesting that melatonin increases sympathetic outflow to the kidney to mediate renal vasoconstriction. In summary, exogenous melatonin differentially alters vascular blood flow in humans. These data suggest the complex nature of melatonin on the vasculature in humans.
Muller MD, Sauder CL, Ray CA. Melatonin attenuates the skin sympathetic nerve response to mental stress. Am J Physiol Heart Circ Physiol 305: H1382-H1386, 2013. First published August 30, 2013 doi:10.1152/ajpheart.00470.2013.-Melatonin attenuates muscle sympathetic nerve responses to sympathoexcitatory stimuli, but it is unknown whether melatonin similarly attenuates reflex changes in skin sympathetic nerve activity (SSNA). In this double-blind, placebo-controlled, crossover study, we tested the hypothesis that melatonin (3 mg) would attenuate the SSNA response to mental stress (mental arithmetic). Twelve healthy subjects underwent experimental testing on two separate days. Three minutes of mental stress occurred before and 45 min after ingestion of melatonin (3 mg) or placebo. Skin temperature was maintained at 34°C. Reflex increases in SSNA (peroneal nerve), mean arterial pressure, and heart rate (HR) to mental stress before and after melatonin were determined. Melatonin lowered HR (pre, 66 Ϯ 3 beats/min; and post, 62 Ϯ 3 beats/min, P ϭ 0.046) and SSNA (pre, 14,282 Ϯ 3,706 arbitrary units; and post, 9,571 Ϯ 2,609 arbitrary units, P ϭ 0.034) at rest. In response to mental stress, SSNA increases were significantly attenuated following melatonin ingestion (second minute, 114 Ϯ 30 vs. 74 Ϯ 14%; and third minute, 111 Ϯ 29 vs. 54 Ϯ 12%, both P Ͻ 0.05). The mean arterial pressure increase to mental stress was blunted in the third minute (20 Ϯ 2 vs. 17 Ϯ 2 mmHg, P ϭ 0.032), and the HR increase was blunted in the first minute (33 Ϯ 3 vs. 29 Ϯ 3 beats/min, P ϭ 0.034) after melatonin. In summary, exogenous melatonin attenuates the SSNA response to mental stress. autonomic nervous system; blood pressure; heart rate MELATONIN IS AN ENDOGENOUS hormone secreted by the pineal gland in a circadian rhythm. This hormone is mechanistically linked to the sleep-wake cycle, and peak plasma levels are evident in the early morning (1:00 to 5:00 AM) (19,27). For this reason, melatonin is commonly ingested in high doses to improve sleep (i.e., 3 to 5 mg, which leads to Ͼ50 times above physiological levels). In addition to its effectiveness as a sleep aid, mounting evidence suggests that exogenous melatonin has widespread effects on immune response, aging, and cancer (c.f., 7, 37). Furthermore, melatonin supplementation has been reported to reduce blood pressure in patients with metabolic syndrome (20) and essential hypertension (30). One mechanism by which melatonin decreases blood pressure could be its effect on cardiovascular reflexes.In previous studies, our laboratory demonstrated that melatonin attenuated increases in muscle sympathetic nerve activity (MSNA) to both lower body negative pressure (24) and headdown rotation (14). These findings suggest that melatonin attenuates reflex changes in sympathetic outflow during postural change. However, the effect of melatonin on reflex changes in skin sympathetic nerve activity (SSNA) is unknown. The interaction of melatonin on SSNA is important to understand because both participate in t...
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