Black esophagus or AEN syndrome is an important cause of upper gastrointestinal hemorrhage with striking endoscopic presentation in a clinically compromised individual with multiple co-morbidities. Structured conservative management with correction of underlying etiology and acid suppression is essential to improved prognosis. Associated duodenal pathology on endoscopy is a reflection of the degree of initial insult and a clinical predictor for potential stricture development. Proximal extension of the black esophagus may be related to the degree of hyperglycemia. Increased awareness of AEN syndrome will lead to early recognition and proper treatment.
Patel HM, Mast JL, Sinoway LI, Muller MD. Effect of healthy aging on renal vascular responses to local cooling and apnea. J Appl Physiol 115: 90 -96, 2013. First published May 2, 2013 doi:10.1152/japplphysiol.00089.2013.-Sympathetically mediated renal vasoconstriction may contribute to the pathogenesis of hypertension in older adults, but empirical data in support of this concept are lacking. In 10 young (26 Ϯ 1 yr) and 11 older (67 Ϯ 2 yr) subjects, we quantified acute hemodynamic responses to three sympathoexcitatory stimuli: local cooling of the forehead, cold pressor test (CPT), and voluntary apnea. We hypothesized that all stimuli would increase mean arterial blood pressure (MAP) and renal vascular resistance index (RVRI) and that aging would augment these effects. Beat-bybeat MAP, heart rate (HR), and renal blood flow velocity (from Doppler) were measured in the supine posture, and changes from baseline were compared between groups. In response to 1°C forehead cooling, aging was associated with an augmented MAP (20 Ϯ 3 vs. 6 Ϯ 2 mmHg) and RVRI (35 Ϯ 6 vs. 16 Ϯ 9%) but not HR. In older adults, there was a positive correlation between the cold-induced pressor response and forehead pain (R ϭ 0.726), but this effect was not observed in young subjects. The CPT raised RVRI in both young (56 Ϯ 13%) and older (45 Ϯ 8%) subjects, but this was not different between groups. Relative to baseline, end-expiratory apnea increased RVRI to a similar extent in both young (46 Ϯ 14%) and older (41 Ϯ 9%) subjects. During sympathetic activation, renal vasoconstriction occurred in both groups. Forehead cooling caused an augmented pressor response in older adults that was related to pain perception. cold face test; renal blood flow; vasoconstriction; peripheral chemoreflex; noxious cooling THE KIDNEY IS A VITAL ORGAN for salt and water homeostasis and receives ϳ20% of cardiac output in resting humans (60). Furthermore, the renal vasculature is innervated by sympathetic nerves that allow for alpha adrenergic-mediated vasoconstriction during times of stress (i.e., exercise and orthostasis) (6, 43). As such, acute adjustments in renal blood flow importantly contribute to whole-body fluid balance and blood pressure control. It follows that chronic impairments in this process (e.g., enhanced water reabsorption and/or enhanced vasoconstriction) predispose an individual to hypertension. Considering that aging itself is a risk factor for hypertension (44,67), and glomerular filtration rate declines with age (12,14), baseline impairments in renal function combined with sympathetic activation may negatively affect the elderly. Therefore, a better understanding of the renal circulation in older adults may have clinical relevance. However, there is currently little experimental data (42, 61) regarding the effect of healthy aging on renal vasoconstriction during sympathoexcitatory stress.Cold temperatures are seasonally experienced in most regions of the world. The compensatory physiological responses to cold involve the sympathetic nervous ...
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Clinical evidence indicates that obstructive sleep apnea is more common and more severe in men compared with women. Sex differences in the vasoconstrictor response to hypoxemia-induced sympathetic activation might contribute to this clinical observation. In the current laboratory study, we determined sex differences in the acute physiological responses to maximal voluntary end-expiratory apnea (MVEEA) during wakefulness in healthy young men and women (26 ± 1 yr) as well as healthy older men and women (64 ± 2 yr). Mean arterial pressure (MAP), heart rate (HR), brachial artery blood flow velocity (BBFV, Doppler ultrasound), and cutaneous vascular conductance (CVC, laser Doppler flowmetry) were measured, and changes in physiological parameters from baseline were compared between groups. The breath-hold duration and oxygen-saturation nadir were similar between groups. In response to MVEEA, young women had significantly less forearm vasoconstriction compared with young men (ΔBBFV: 2 ± 7 vs. -25 ± 6% and ΔCVC: -5 ± 4 vs. -31 ± 4%), whereas ΔMAP (12 ± 2 vs. 16 ± 3 mmHg) and ΔHR (4 ± 2 vs. 6 ± 3 bpm) were comparable between groups. The attenuated forearm vasoconstriction in young women was not observed in postmenopausal women (ΔBBFV -21 ± 5%). We concluded that young women have blunted forearm vasoconstriction in response to MVEEA compared with young men, and this effect is not evident in older postmenopausal women. These data suggest that female sex hormones dampen neurogenic vasoconstriction in response to apnea-induced hypoxemia.
Forehead cooling activates the sympathetic nervous system and can trigger angina pectoris in susceptible individuals. However, the effect of forehead cooling on coronary blood flow velocity (CBV) is not well understood. In this human experiment, we tested the hypotheses that forehead cooling reduces CBV (i.e., coronary vasoconstriction) and that this vasoconstrictor effect would be enhanced under systemic β-adrenergic blockade. A total of 30 healthy subjects (age range, 23-79 years) underwent Doppler echocardiography evaluation of CBV in response to 60 s of forehead cooling (1°C ice bag on forehead). A subset of subjects (n = 10) also underwent the procedures after an intravenous infusion of propranolol. Rate pressure product (RPP) was used as an index of myocardial oxygen demand. Consistent with our first hypothesis, forehead cooling reduced CBV from 19.5 ± 0.7 to 17.5 ± 0.8 cm/s (P < 0.001), whereas mean arterial pressure increased by 11 ± 2 mmHg (P < 0.001). Consistent with our second hypothesis, forehead cooling reduced CBV under propranolol despite a significant rise in RPP. The current studies indicate that forehead cooling elicits a sympathetically mediated pressor response and a reduction in CBV, and this effect is augmented under β-blockade. The results are consistent with sympathetic activation of β-receptor coronary vasodilation in humans, as has been demonstrated in animals.
We sought to determine how the aging left ventricle (LV) responds to sympathetic nervous system (SNS) activation. Three separate echocardiographic experiments were conducted in 11 healthy young (26 ± 1 yr) and 11 healthy older (64 ± 1 yr) adults. Tissue Doppler imaging was used to measure systolic myocardial velocity (S(m)), early diastolic myocardial velocity (E(m)), and late diastolic myocardial velocity (A(m)) during isometric fatiguing handgrip (IFHG), a 2-min cold pressor test (CPT), and 5 min of normobaric hypoxia. Heart rate (HR) and mean arterial pressure (MAP) were also monitored on a beat-by-beat basis; rate pressure product (RPP) was used as an index of myocardial oxygen demand. At peak IFHG, the groups had similar increases in RPP, but the ΔS(m) was significantly greater (i.e., larger impairment) in the older subjects (-0.82 ± 0.13 cm/s) compared with the young subjects (0.37 ± 0.30 cm/s). At peak IFHG, the ΔE(m) was similar between older (-1.59 ± 0.68 cm/s) and young subjects (-1.06 ± 0.76 cm/s). In response to the CPT, both S(m) and E(m) were reduced in the older adults but did not change relative to baseline in the young subjects. Normobaric hypoxia elevated HR and RPP in both groups but did not alter Tissue Doppler parameters. These data indicate that S(m) and E(m) are reduced in healthy older adults during IFHG and CPT. We speculate that suboptimal LV adaptations to SNS stress may partly explain why acute heavy exertion can trigger myocardial ischemia.
In response to hypoxia, a net vasodilation occurs in the limb vasculature in young healthy humans and this is referred to as “hypoxia‐induced vasodilation”. We performed two separate experiments to determine (1) if hypoxia‐induced forearm vasodilation is impaired in older men (n = 8) compared to young men (n = 7) and (2) if acute systemic infusion of ascorbic acid would enhance hypoxia‐induced vasodilation in older men (n = 8). Heart rate, mean arterial pressure, oxygen saturation, minute ventilation, forearm vascular conductance (FVC, Doppler ultrasound), and cutaneous vascular conductance (CVC, laser Doppler flowmetry) were recorded continuously while subjects breathed 10% oxygen for 5 min. Changes from baseline were compared between groups and between treatments. The older adults had a significantly attenuated increase in FBF (13 ± 4 vs. 30 ± 7%) and FVC (16 ± 4 vs. 30 ± 7%) in response to 5 min of hypoxia. However, skin blood flow responses were comparable between groups (young: 35 ± 9, older: 30 ± 6%). In Experiment 2, FVC responses to 5 min of breathing 10% oxygen were not significantly different following saline (3 ± 10%) and ascorbic acid (8 ± 10%) in the older men. Ascorbic acid also had no physiological effects in the young men. These findings advance our basic understanding of how aging influences vascular responses to hypoxia and suggest that, in healthy humans, hypoxia‐induced vasodilation is not restrained by reactive oxygen species.
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