Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether the voluntary contractions of exercise interfere with involuntary shivering contractions, four male subjects were each exposed to a 10 degrees C environment for 60 min of rest followed by either another rest period or 30 min of cycleergometer exercise. On different days exercise was performed at zero load, light load, and moderate load. Each experiment was performed twice, resulting in a minimum of eight experiments for each subject. Esophageal temperature (Tes), eight skin temperatures (Tsk), oxygen uptake (VO2), and the integrated electrical activity from a neck muscle (EMG) were continuously monitored. Pedaling flushed cold blood into the body core, causing Tes to fall. The rate and absolute magnitude of the decrease in Tes was proportional to the intensity of exercise. Thermoregulatory VO2 (attributable to shivering) and EMG were inversely related both to Tsk during rest, prior to any changes in Tes, and to Tes during exercise, when Tsk was constant, once shivering thresholds were surpassed. The slope of the thermoregulatory VO2-to-Tes relation was significantly suppressed by increasing exercise intensity. The slope of the EMG-to-Tes relation was similarly suppressed; since the neck muscles are not involved in the additional acitivity of exercise, we concluded that the graded inhibition of shivering during exercise was of central origin rather than from the rhythmic contractions required to sustain exercise.
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PMID:Thermogenic control during exercise in a cold environment. 51 10

Four healthy males exercised in two experiments at ambient temperatures of 22, 29, and 36 degrees C with the relative humidity at 30% in all environments (Tdp = 3.9, 9.9, and 15.8 degrees C). One experiment in each environment was done 150 min after 30 mg oral pyridostigmine bromide (PYR) administration, and the second experiment was done on a separate day with no medication (CON). Red blood cell cholinesterase was 39 +/- 7% lower after PYR (11.8 vs 7.2 micromol.ml-1.min-1). Esophageal (Tes) and mean skin temperature (Tsk), forearm blood flow (FBF), forearm sweating, and skin blood flow (SkBF) were measured twice each minute during a 15-min rest period and during 30-min of seated cycle exercise at approximately 58% Vo2peak. Whole body sweating was determined from weight changes before and after exercise. PYR decreased heart rate at rest and during exercise at 29 degrees C and 36 degrees C (8bpm, p less than 0.05). Resting SkBF was 40% lower at 29 degrees C and 30% lower at 36 degrees C after PYR compared to CON (p less than 0.05). There was no effect of PYR on heat production at rest or during exercise. Tsk was different in the three conditions by design, but was unchanged by PYR. Tes was not different at rest in any condition, but was elevated during exercise at 36 degrees C (0.1 degree C, p less than 0.05) in PYR compared to CON. These data suggest that pyridostigmine ingestion decreased skin blood flow, which may limit exercise thermoregulation in more severe environments.
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PMID:Human temperature regulation during exercise after oral pyridostigmine administration. 231 75

Four healthy adult males volunteered for this study, which followed informed-consent procedures administered by our local Human Use Committee. Esophageal (Tes) and mean skin (Tsk, eight site) temperatures, forearm sweating rate (ms), metabolism (M), heart rate (HR), and forearm blood flow (FBF) were measured at rest and during forearm blood flow (FBF) were measured at rest and during exercise [55% oxygen consumption (Vo2) peak] during control experiments and after 2 mg im atropine (ATR). Experiments were randomized and separated by at least 72 h. ATR increased heart rate at rest by 15 beats/min and during exercise by 24 beats/min. ATR decreased whole body sweating by 57%. All eight local skin temperatures were higher in ATR than in control. Tsk was 32.6 degrees C in ATR and 31.0 degrees C in control (P less than 0.01). During exercise, ATR increased vasodilation of the forearm compared with control. The slope of FBF to Tes increased over 300% in ATR experiments compared with control (P less than 0.05). The higher sensible heat flux from this vasodilation decreased Tes during exercise, which further decreased sweating. Skin blood flow remained elevated as Tes decreased, suggesting that local vasodilatory factors promoted atropine-induced cutaneous vasodilation.
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PMID:Atropine-induced cutaneous vasodilation decreases esophageal temperature during exercise. 258 34

This report summarizes a tightly controlled laboratory study in which the thermoregulatory effects of an intramuscular injection of atropine sulfate (2 mg) were compared with a placebo injection of sterile saline during exposure to a cool environment. Four subjects were tested during seated cycle exercise at a moderate exercise intensity (55% Vo2 peak) at an ambient temperature of 22 degrees C (37% relative humidity; ambient water vapor pressure 1.0 kPa). Esophageal temperature (Tes), mean weighted skin temperature (Tsk), and forearm sweating rate (ms) were continuously measured during 30 min of rest and 35 min of exercise. Skin blood flow (FBF) from the forearm was measured twice each minute by venous occlusion plethysmography. Whole-body sweating was calculated from weight changes pre- and post-exercise. The expected decrease in whole-body and local sweating rate (-57% and -68%, respectively) occurred in the atropine-treated subjects. By 10-15 min of exercise, dry heat loss (R + C, radiative and convective heat exchange) was significantly elevated from the head, chest, back, arm, forearm, and thigh in the atropine experiments. Core temperature actually decreased 0.2 degrees C (p less than 0.05) in the atropine-treated subjects during exercise as a result of enhanced dry heat exchange. By 25 min of exercise. FBF was 98% (p less than 0.05) greater after atropine treatment. These results show that the peripheral modification of cutaneous blood flow which occurs in atropine-treated subjects is sufficient to markedly alter heat exchange in a cool environment.
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PMID:Heat exchange through cutaneous vasodilation after atropine treatment in a cool environment. 292 91

Localized cutaneous vasodilation (flush) is seen following systemic atropine administration. To verify calculated enhanced dry heat loss with actual changes in cutaneous blood flow, four men were studied in both control and atropine (0.025 mg.kg-1; im) experiments (Ta = 30 degrees C, Tdp = 7 degrees C) during moderate exercise (55% VO2 peak). Esophageal temperature (Tes) and arm sweating (ms) by local dewpoint were measured continously. Skin (forearm) blood flow (FBF) was measured twice each minute by venous occlusion plethysmography. Injection of atropine (2 mg) caused an increased sensitivity (+85%, p less than 0.01) in FBF to Tes with no change in the vasodilator threshold. An elevated Tes onset (0.3 degrees C, p less than 0.05) for sweating occurred with no change in the sensitivity of ms to Tes (-27%, p less than 0.20). No elevation in either forearm or Tsk occurred before the onset of vasodilation, however, both mean skin (Tsk) and local arm temperatures were higher in the atropine experiments after 15 min of exercise. Systemic atropine resulted in higher cutaneous vasodilation at the same core temperature with the local skin temperature following passively. The effect of systemic atropine in stimulation of increased cutaneous vasodilation is suggested to result by a combination of central and local responses which may be mediated through the release of vasoactive sustances.
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PMID:Cutaneous blood flow and local sweating after systemic atropine administration. 343 54

The effects of intramuscular saline (control), atropine (2 mg), and/or pralidoxime (600 mg) on heat exchange was evaluated in four healthy males during seated, cycle exercise (55% Vo2 peak) in a temperate environment (Ta = 30.3 degrees C, Pw = 1.0 kPa). Esophageal (Tes), rectal (Tre), and mean skin temperatures (Tsk), and chest and forearm sweating (ms) were continuously measured. Skin blood flow (FBF) from the forearm was measured twice each minute by venous occlusion plethysmography. Whole body sweating was calculated from weight changes. The expected result of atropine injection, decreased eccrine sweating (-60%, p less than 0.05) and elevated esophageal (+0.4 degree C, p less than 0.05) and skin temperatures (+2.1 degrees C, p less than 0.05) was observed relative to control. Heart rate (+28 b X min-1) and FBF (+9 ml X 100 ml-1 X min-1) were higher after atropine. Pralidoxime, in general, did not affect the core and skin temperature responses to the exercise differently from control; however, a slightly elevated FBF (+3 ml X 100 cc-1 X min-1, 33%) compensated for the reduction in whole body sweating (-45%, p less than 0.05] that we observed. The combination of the drugs resulted in significantly higher esophageal (0.4 degree C) and skin (0.9 degree C) temperatures than atropine alone, as has been previously shown. The thermoregulatory disadvantage of inhibited sweating by atropine was partially compensated for by enhanced skin blood flow in this environment where Ta less than Tsk. Pralidoxime was shown to decrease whole body sweating, by a mechanism as yet unexplained.
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PMID:Human thermoregulation after atropine and/or pralidoxime administration. 360 15

The changes in the central control of sweating were investigated in five sleeping subjects under neutral and warm conditions [operative temperature (To) = 30, 33, and 34 degrees C; dew-point temperature = 10 degrees C]. Esophageal (Tes) and mean skin (Tsk) temperatures, chest sweat rate (msw,1), and concomitant electroencephalographic data were recorded. Throughout the night, msw,1 was measured under a local thermal clamp of 38 degrees C. Results showed that the thermal environment exerted a strong influence on both the levels and the time patterns of body temperatures. Moreover, local sweating rate correlated positively with Tes, and this relationship varied according to sleep stages. For a given Tes level, there was a sleep stage-related gradation in msw,1 that was higher in slow-wave sleep (SWS) than in stage 1-2 and the lowest in rapid-eye-movement (REM) sleep. This is explained by a change in the excitability or the sensitivity of the thermoregulatory system. The msw,1 differences between stage 1-2 and SWS are accounted for by a decrease in the Tes threshold (Tset) for sweating while the slope of the msw,1-Tes relation remains unchanged. The lower msw,1 in REM sleep is explained by a lesser slope for the msw,1-Tes relation without any Tset change from stage 1-2.
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PMID:Sweating responses and body temperatures during nocturnal sleep in humans. 382 11

Five males [age 28 +/- 8 yr; maximum O2 uptake (VO2max) 50 +/- 6 ml O2 . kg-1 . min-1; body wt 70 +/- 3 kg; DuBois surface area 1.85 +/- 0.02 m2] exercised on a cycle ergometer, placed on a Potter scale, at 31% VO2max for up to 2 h at an ambient temperature (Ta) of 25 degrees C and a dew-point temperature of 15 degrees C. Air movement was varied from still air to 0.4 and 2 m/s. Each subject, in separate runs, wore a track suit (TS ensemble) of 60% polyester-40% cotton (effective clo = 0.5); a Gortex parka (GOR ensemble), covering a sweat shirt and bottom of TS (effective clo = 1.4); or the TS ensemble covered by polyethylene overgarment (POG ensemble). Esophageal, skin temperature (Tsk) at eight sites, and heart rate were continuously recorded. Dew-point sensors recorded temperatures under the garments at ambient and chest (windward site) and midscapular sites. Local skin wettedness (loc w) and ratio of evaporative heat loss (Esk) to maximum evaporative capacity were determined. An observed average effective permeation (Pe, W . m-2 . Torr-1) was calculated as Esk/loc w (Ps,sk - Pw), where w is the average of chest and back loc w and (Ps,sk - Pw) is the gradient of skin saturation vapor pressure at Tsk and Ta. Additionally, the local effective evaporative coefficient was determined for chest and back sites by Esk/(Ps,dpl - Pw). The GOR ensemble produced an almost as high a Pe as the TS ensemble (82-86% of Pe with TS in still air and 0.4- and 2-m/s conditions). Direct dew-point recording offers an easy practical dimension to the study of efficacy of latent heat loss and skin wettedness properties through garments.
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PMID:Evaluation of vapor permeation through garments during exercise. 398 Mar 94

Nonevaporative heat loss [ radiation (R) and convection (C) ] and evaporative heat loss [ evaporation (E) ] from the hand (Rh + Ch) and (Eh) were measured in four healthy men exercised on a bicycle ergometer at 20, 35, and 45% of VO2max at an ambient temperature (Ta) of 20 degrees C with a gradient layer type direct hand calorimeter. Esophageal (Tes) and mean skin temperatures (Tsk) were continuously measured. Leg exercise at these intensities produced initially a fall followed by an increase in (Rh + Ch). Tes was positively correlated to % VO2max during exercise. Thermal conductance in the hand (k) was computed by dividing the total heat loss from the hand (Rh + Ch + Eh) by the difference between Tes and mean hand temperature. All subjects had significantly lower (Rh + Ch) and k at a given Tes during exercise with a higher intensity. The slope indicating the relation between (Rh + Ch) and Tes was 9.18, 6.25, and 5.04 W per degree C at 20, 35, and 45% VO2max, respectively. The slope of k vs. Tes was 28.64, 20.82, and 16.61 W/m2 X degree C degree C at 20, 35, and 45% VO2max, respectively. These results indicated that thermoregulatory vasodilation was reduced by the increasing reflex vasoconstrictor tone caused by increasing intensity of exercise as a non-thermal factor.
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PMID:Peripheral vascular tone during heat load is modified by exercise intensity. 668 35

The Esophageal Obturator Airway (EOA) has been considered an effective ventilatory technique for cardiopulmonary resuscitation; however, few studies of its field effectiveness have been performed. We evaluated the EOA in 158 cases of prehospital cardiac arrest resuscitated by EMT II personnel utilizing the EOA for airway maintenance. The time of insertion from arrival of the unit and the number of unsuccessful attempts were recorded. The EOA took longer than 4 minutes to insert in 47% of cases. It was incapable of being placed in 18.3% of cases, and required two or more attempts at insertion in 30%. There were six survivors in this series (3.7%). Subsequently, we measured arterial blood gas levels during ventilation with the EOA and after endotracheal intubation in 13 patients. Arterial oxygen tension greater than 60 mm Hg was achieved in only four of 13 patients with the EOA. All patients were hypercarbic and acidotic using the EOA. There was marked improvement in all parameters following ET intubation. The EOA presents technical problems which make it inferior to ET tubes in resuscitation of individuals in the field with cardiac arrest. Close monitoring of its use should be undertaken in areas where it is the primary method for airway maintenance.
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PMID:A field evaluation of the Esophageal Obturator Airway. 684 35


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