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Biomedical subjects

L A Stephenson

Publications and source records attributed to L A Stephenson.

17 recordsLinked to original sources
PubMed1990

Acetylcholinesterase inhibitor, pyridostigmine bromide, reduces skin blood flow in humans.

Five subjects exercised on a cycle ergometer for 30 min at 55% peak oxygen consumption on two occasions in an environmental test chamber (ambient temperature = 29 degrees C; dew point temperature = 10 degrees C). Pyridostigmine bromide (PYR), an acetylcholinesterase (AChE) inhibitor, was ingested (30 mg) approximately 150 min before one experiment, and no drug was administered during the other experiment (control). Red blood cell AChE inhibition averaged 40 (+/- 7)% during PYR treatment. Esophageal temperature (Tes), an eight site-derived mean skin temperature, forearm blood flow (FBF; venous occlusion plethysmography), skin blood flow (SkBF; laser-Doppler velocimetry), and metabolic rate (indirect calorimetry) were measured. SkBF decreased 37% after PYR treatment compared with control (P less than or equal to 0.05). The Tes threshold for initiation of cutaneous vasodilation was 36.8 (+/- 0.3) degrees C for the control treatment and 37.0 (+/- 0.3) degrees C for the PYR treatment (P less than or equal to 0.01). FBF was not significantly different between treatments, whereas heart rate was reduced by 7 and 9 beats/min during rest and exercise, respectively (P less than or equal to 0.01). The increased threshold for initiation of cutaneous vasodilation with AChE inhibition by PYR is compatible with nonthermal modulation of the control of thermoregulation through increased acetylcholine (ACh) accumulation. This could potentiate preganglionic transmission to enhance adrenergic vasoconstrictor tone. One suggested mechanism possible at the neuroeffector junction of the sweat gland may be that accumulated ACh diffusion across the adventitia of adjacent arterioles to muscarinic receptors initiates contraction of the smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Human temperature regulation during exercise after oral pyridostigmine administration.

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.

Administration, Oral↗
PubMed1989

Circadian variations in plasma renin activity, catecholamines and aldosterone during exercise in women.

Four women were studied at 0400 h and 1600 h to determine if their hormonal and hemodynamic responses to exercise varied with the circadian cycle. Esophageal temperature was measured during rest and exercise (60% peak VO2; 30 min) in a warm room (Ta = 35 degrees C; PH2O = 1.7 kPa). Venous blood samples were drawn during rest and exercise and hemoglobin concentration (Hb), hematocrit (Hct), plasma osmolality (Posm), plasma protein concentration (Pp), colloid osmotic pressure (COP), plasma renin activity (PRA), cortisol, aldosterone, norepinephrine (NE) and epinephrine (E) were determined. Changes in plasma volume (PV) were estimated from changes in Hb and Hct. The relative hemoconcentration (-11.2%) was similar at 0400 h and 1600 h, but the absolute PV was smaller at 1600 h than at 0400 h (p = 0.03). The responses of Posm, Pp and COP to exercise were unaffected by time of day. Although PRA was not different at the two times of day, PRA was 244% greater during exercise at 1600 h, but only 103% greater during exercise at 0400 h. The normal circadian rhythms in plasma aldosterone (p = 0.043) and plasma cortisol (p = 0.004) were observed. Plasma aldosterone was 57% greater during exercise, while plasma cortisol did not change. The change in E and NE was greater at 0400 h, but this was due to the lower resting values of the catecholamines at 0400 h. These data indicate that time of day generally did not affect the hormonal or hemodynamic responses to exercise, with the exception that PRA was markedly higher during exercise at 1600 h compared to 0400 h.

Adult↗
PubMed1989

Control of sweating during the human menstrual cycle.

Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4-7) phase and during the luteal (L, days 19-22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (Tes), mean skin temperature (Tsk), oxygen uptake and forearm sweating (ms) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at approximately 80% VO2 peak during which the environmental chamber was controlled at Ta = 50.0 degrees C, rh = 14% (Pw = 1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at approximately 85% VO2 peak at Ta = 35 degrees C and rh = 25% (Pw = 1.4 kPa). The normal L increase in resting Tes (approximately 0.3 degrees C) occurred in all seven subjects. Tsk was higher during L than F in all experiments conducted at 50 degrees C. During exercise and passive heat exposure, the Tes threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of ms to Tes between menstrual cycle phases. This rightward or upward shift in Tes threshold for initiation of sweating averaged 0.5 degrees C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.

Adult↗
PubMed1989

Atropine-induced cutaneous vasodilation decreases esophageal temperature during exercise.

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.

Adult↗
PubMed1989

Heat exchange through cutaneous vasodilation after atropine treatment in a cool environment.

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.

Adolescent↗
PubMed1988

Plasma volume during heat stress and exercise in women.

Five women were studied during exercise and passive heating to determine whether PV dynamics were affected by the menstrual cycle. The exercise bout (80% VO2 peak) on a modified cycle ergometer and the passive heat stress were done in a hot environment (Ta = 50 degrees C, Pw = 1.61 kPa) during the follicular and luteal phase. Esophageal temperature (Tes) was measured continuously. Blood samples were drawn after each 0.2 degree C increase in Tes and VO2 was measured at that time. Initial PV was estimated at rest during the follicular phase. PV changes from rest were calculated at each Tes from Hb and Hct. During passive heating, PV decreased by a mean volume of 156 (+/- 80) ml to 2.83 (+/- 0.09) l in the follicular phase. During the luteal phase, there was a larger volume reduction (300 +/- 100 ml) during passive heating, and the final PV was lower than in the follicular phase and averaged 2.47 +/- 0.18 l. During exercise, PV decreased 463 (+/- 90) ml to 2.50 (+/- 0.11) l in the follicular and 381 (+/- 70) ml to 2.50 (+/- 0.23) l in the luteal phase. These data indicate that there is a menstrual cycle effect on PV dynamics during passive heating such that more fluid is shifted out of the vasculature during the luteal phase. During severe exercise there is a greater fluid loss during the follicular phase, yet the final PV is not different between phases.

Adult↗
PubMed1988

Exercise thermoregulation after prolonged wakefulness.

The effect of 33 h of wakefulness on the control of forearm cutaneous blood flow and forearm sweating during exercise was studied in three men and three women. Subjects exercised for 30 min at 60% peak O2 consumption while seated behind a cycle ergometer (Ta = 35 degrees C, Pw = 1.0 kPa). We measured esophageal temperature (Tes), mean skin temperature, and arm sweating continuously and forearm blood flow (FBF) as an index of skin blood flow, twice each minute by venous occlusion plethysmography. During steady-state exercise, Tes was unchanged by sleep loss. The sensitivity of FBF to Tes was depressed an average of 30% (P less than 0.05) after 33 h of wakefulness with a slight decrease (-0.15 degrees C, P less than 0.05) in the core temperature threshold for vasodilatory onset. Sleep loss did not alter the Tes at which the onset of sweating occurred; however, sensitivity of arm sweating to Tes tended to be lower but was not significant. Arm skin temperature was not different between control and sleep loss experiments. Reflex cutaneous vasodilation during exercise appeared to be reduced by both central and local factors after 33 h of wakefulness.

Adult↗
PubMed1988

Heat exchange during encapsulation in a chemical warfare agent protective patient wrap in four hot environments.

Tolerable encapsulation time in a Chemical Warfare Agent Protective Patient Wrap (dry insulative value = 1.44 clo; permeability index = 0.25) was determined in four hot environments including a simulated solar heat load (1152 W.m-2) for eight males. Mean body temperature (Tb), evaporative heat loss (EHL), dry heat gain (R + C), metabolic rate (M), and net heat flow (Msk) were measured or calculated from the heat balance equation. The ambient temperature (Ta) ranged from 54.7 degrees C (I) to 35.7 degrees C (IV) and the relative humidity ranged from 17% (I) to 63% (IV). EHL ranged from 173.5 W.m-2 (IV) to 277.8 W.m-2 (I) at min 30 of encapsulation. R + C ranged from -129 W.m-2 (IV) to -230 W.m-2 (I) at that time and Tb averaged 37.6(+/- 0.3) degrees C (IV) and 38.1(+/- 0.2) degrees C (I). The average time of encapsulation ranged from 61.8(+/- 0.2) degrees C (I). The average time of encapsulation ranged from 61.8(+/- 13.2) min (IV) to 38.4(+/- 5.0) min (I). A multiple linear regression equation to predict tolerable encapsulation was developed. These data show that tolerable encapsulation is severely limited in hot environments which have a marked solar heat load. A preliminary study (n = 2) indicated that encapsulation time in 54.7 degrees C/17%rh could be extended by some 23 min by covering the WRAP with wetted towels, thereby decreasing body heat storage by enhancing EHL from the surface of the WRAP.

Body Temperature Regulation↗
PubMed1987

Cutaneous blood flow and local sweating after systemic atropine administration.

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.

Adult↗
PubMed1987

Local sweating and cutaneous blood flow during exercise in hypobaric environments.

The effect of acute hypobaric hypoxia on local sweating and cutaneous blood flow was studied in four men and four women (follicular phase of menstrual cycle), who exercised at 60% of their altitude-specific peak aerobic power for 35 min at barometric pressures (PB) of 770 Torr (sea level), 552 Torr (2,596 m), and 428 Torr (4,575 m) at an ambient temperature of 30 degrees C. We measured esophageal temperature (Tes), mean skin temperature (Tsk, 8 sites), and local sweating (ms) from dew-point sensors attached to the skin at the chest, arm, and thigh. Skin blood flow (SkBF) of the forearm was measured once each minute by venous occlusion plethysmography. There were no gender differences in the sensitivity (slope) or the threshold of either ms/Tes or SkBF/Tes at any altitude. No change in the Tes for sweating onset occurred with altitude. The mean slopes of the ms/Tes relationships for the three regional sites decreased with increasing altitude, although these differences were not significant between the two lower PBS. The slope of SkBF/Tes was reduced in five of the eight subjects at 428 Torr. Enhanced body cooling as a response to the higher evaporative capacity of the environment is suggested as a component of these peripheral changes occurring in hypobaric hypoxia.

Adult↗
PubMed1987

Human thermoregulation after atropine and/or pralidoxime administration.

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.

Adult↗
PubMed1986

Effect of nerve block on response of forearm blood flow to local temperature.

To determine the role of neurotransmitter in the response of forearm blood flow (ABF) to local (forearm) skin temperature (Tsk) we measured ABF of six subjects at Tsk from 25 to 40 degrees C before (control) and after brachial plexus block (BPB). Control experiments were conducted in an ambient temperature of 27-29 degrees C, adjusted to minimize the subject's overall thermal sensation. Tsk was regulated by blowing a controlled-temperature airstream through a plastic bag enclosing the arm. We first lowered Tsk to 25 degrees C and after 20 min began to measure ABF with Whitney strain gauges. We then raised Tsk by 2.5 degrees C steps to 40 degrees C and measured ABF every 30 s for at least 10 min at each level of Tsk. Mean ABF rose from 1.1 ml X 100 ml-1 X min-1 at Tsk of 25 degrees C to 2.1 ml X 100 ml-1 X min-1 at 32.5 degrees C to 13.7 ml X 100 ml-1 X min-1 at 40 degrees C in control experiments and from 2.8 to 4.4 to 14.8 ml X 100 ml-1 X min-1 after BPB. The effect of Tsk on ABF was highly significant (P less than 0.0001) but the effect of BPB was not (P approximately equal to 0.2). At thermoneutrality, the effect of Tsk on ABF is largely independent of neural activity, since this effect is unaffected by nerve block.

Adult↗
PubMed1986

Role of changes in insulin and glucagon in glucose homeostasis in exercise.

This experiment was performed to determine if plasma glucose homeostasis is maintained in normal human volunteers during light exercise (40% maximal oxygen consumption [VO2 max]) when changes in insulin and glucagon are prevented. Hormonal control was achieved by the infusion of somatostatin, insulin, and glucagon. Glucose kinetics and oxidation rates were determined with stable isotopic tracers of glucose, and by indirect calorimetry. Two different rates of replacement of insulin and glucagon were used; in one group, insulin was clamped at 19.8 +/- 2.6 microU/ml (high-insulin group), and in the other group insulin was clamped at 9.2 +/- 1.3 microU/ml (low-insulin group). Glucagon was maintained at 261 +/- 16.2 and 124 +/- 6.4 pg/ml, respectively, in the high-insulin and low-insulin groups. Without hormonal control, plasma glucose homeostasis was maintained during exercise because the increase in glucose uptake was balanced by a corresponding increase in glucose production. When changes in insulin and glucagon were prevented, plasma glucose concentration fell, particularly in the high-insulin group. Glucose uptake increased to a greater extent than when hormones were not controlled, and glucose production did not increase sufficiently to compensate. The increase in glucose uptake in the hormonal control groups was associated with an increased rate of glucose oxidation. When euglycemia was maintained by glucose infusion in the hormonal control subjects, the modest increase in glucose production that otherwise occurred was prevented. It is concluded that during light exercise there must be a reduction in insulin concentration and/or an increase in glucagon concentration if plasma glucose homeostasis is to be maintained. If such changes do not occur, hypoglycemia, and hence exhaustion, may occur.

Blood Glucose↗
PubMed1986

Effects of atropine on thermoregulatory responses to exercise in different environments.

The thermoregulatory effects of atropine (2 mg im) were examined in six heat-acclimated subjects during exercise in three environments, which provided different evaporative capacities, but similar heat stress as indicated by the wet bulb, globe temperature index (WBGT). Subjects walked in environments of Ta = 42.3 degrees C, Tdp = 14.6 degrees C, WBGT = 29.1 degrees C (HD); Ta = 33.9 degrees C, Tdp = 23.5 degrees C, WBGT = 28.9 degrees C (WM); Ta = 30.4 degrees C, Tdp = 23.8 degrees C, WBGT = 27.4 degrees C, (WW) after atropine and saline injections. In comparison to saline, atropine elevated rectal temperature (Tre) (p less than 0.05) in HD. Additionally, atropine elevated (p less than 0.01) mean skin temperature (Tsk), and heart rate (HR) in all three environments relative to saline. Whole body sweating rate (msw) was 45% lower (p less than 0.01) in each environment after atropine relative to saline. Exercise time was reduced from saline values (p less than 0.05) by 26.5 min in the HD after atropine. Within the atropine treatments, Tre was higher (p less than 0.05) in HD (0.6 degrees C) than WW, and HR was higher (p less than 0.05) in HD (23 b X min-1) and WM (14 b X min-1) than WW. Tsk was higher (p less than 0.01) in WM than WW (1.2 degrees C) and in HD than WM (1.5 degrees C). Exercise time was 26.5 min longer (p less than 0.05) in WW than HD in the atropine experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗