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Biomedical subjects

J T Maher

Publications and source records attributed to J T Maher.

At least 37 records · Page 2Linked to original sources
PubMed1977

Recurrent heat exposure: enzymatic responses in resting and exercising men.

Heat acclimatization was induced in a group of healthy male test subjects by repetitive treadmill walking (5.6 km-h-1, 49 degrees/27 degrees C dry/wet bulb, 90 min-day-1, 7 days). A second group of men, paired for maximal O2 consumption and body weight, remained sedentary under identical environmental conditions. Total plasma protein increased significantly after 45 (P less than 0.05) and 90 (P less than 0.025) min of exercise on the first day of heat exposure, yet after 7 days no increments occurred. Even after heat acclimatization was achieved (day 7), plasma levels of creatine phosphokinase increased during the 90-min walk in the heat (time O vs. 90, P less than 0.025), as was also the case on day 1 (P less than 0.05). Levels of lactate dehydrogenase, glutamate-oxaloacetate transaminase, and glutamate-pyruvate transaminase were not significantly affected by exercise in the heat either before or after heat acclimatization. No correlations could be drawn between base-line enzyme levels and state of physical conditioning.

Acclimatization↗
PubMed1976

Measurement of cardiac output by electrical impedance at rest and during exercise.

A comparison was made between cardiac output values determined by the dye dilution and electrical impedance methods in ten subjects at rest and during graded exercise on a bicycle ergometer. The cardiac output values determined by the two methods were linearly related and significantly (P less than 0.001) correlated (r = 0.90). Movement artifact associated with exercise at maximum or near-maximum work loads caused severe distortion of the dZ/dt wave form and prevented calculation of impedance cardiac output at these levels of work. Use of the lowest value of L (distance between mean value of L in the impedance stroke volume equation (SV = p(L2/ZO2) (dZ/dt)mt), resulted in nearly identical values for the least-squares line and equalvalue line of impedance and dye cardiac outputs. Although absolute values of cardiac output determined by the two methods were not identical in all subjects the changes in cardiac output were nearly identical during the different levels of exercise. The data support the validity of the impedance method as a noninvasive, atraumatic measure of cardiac output at rest and during graded exercise.

Adult↗
PubMed1976

Sustained venoconstriction in man supplemented with CO2 at high altitude.

Venoconstriction occurs at high altitude. This study sought to determine whether hypoxia or hypocapnia is the cause of the venoconstriction. Five male subjects were exposed to 4,000-4,400 m (PB 440-465 mmHg) with supplemental 3.77 +/- 0.02% CO2 in a hypobaric chamber for 4 days. Similar alveolar O2 tensions were obtained in four control subjects exposed to 3,500-4,100 m (PB 455-492 mmHg) without CO2. A water-filled plethysmograph was used to determine forearm flow and venous compliance. Systemic blood pressure was measured with the cuff procedure. Catecholamines were measured in 24-h urine collections. Venous compliance fell at high altitude in both groups and was less (P less than 0.01) than control values. Forearm flow and resistance were unaltered at altitude in the group with CO2 supplementation while forearm flow decreased and resistance increased in the hypocapnic group at 72 h of exposure. Urinary catecholamines increased in the group with CO2 and remained unaltered in the hypocapnic group. It is concluded that hypoxia is responsible for decreasing venous compliance, and hypocapnia for increasing resistance and decreasing flow. Group differences observed in urinary catecholamines may be explained by differences in arterial pH.

Adolescent↗
PubMed1976

Human coagulation abnormalities during acute exposure to hypobaric hypoxia.

Multiple coagulation studies were carried out in eight healthy young men at sea level (SL) and after 1, 24, and 48 h at a simulated altitude of 4,400 m. Platelet aggregation, as induced by ADP, epinephrine, and collagen, was not significantly altered by high-altitude (HA) exposure. Mean 2,3-diphosphoglycerate, a physiological inhibitor of platelet aggregation, rose (P less than 0.001) after 24 h at HA and remained elevated while no changes in circulating catecholamines were observed. Platelet count, factor 3 availability, and membrane lipid peroxide formation were likewise unaltered at HA, as were prothrombin and thrombin times and protamine paracoagulation test. However, mean partial thromboplastin time was significantly shortened (P less than 0.01) after 1 and 24 h at HA, recovering to SL control by 48 h. Fibrinogen and factor VIII levels also fell (P less than 0.01 and P less than 0.02) after 1 h at HA but returned to the preexposure values by 24 h. Fibrin degradation products were transiently detectable in three subjects at HA. Thus, although normal platelet function did not appear to be modified by short-term exposure to simulated high altitude, evidence for a coagulopathy was obtained.

Acute Disease↗
PubMed1976

Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2.

Hypobaric hypoxia causes hypocapina and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O2 tension of 55 torr for 5 days with 3.77% CO2 added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2 tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2 tension being 39 torr. By contrast, three men at high altitude without CO2 supplementation (PB=455 torr; alveolar PO2=56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial PO2 (48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2 but in the group without CO2 catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2 added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.

Adult↗
PubMed1976

Increased 2,3-diphosphoglycerate during normocapnic hypobaric hypoxia.

The effect of 96 h of exposure to hypobaric hypoxia with and without 3.8% CO2 supplementation was studied in two groups of subjects. Five subjects (CO2) were exposed to 440-465 mm Hg barometric pressure (4000-4400 m), and 4 subjects (no-CO2) were exposed to 455-492 mm Hg (3500-1400 m) in order to produce similar levels of resting end-tidal PO2. After 24 h, 2,3-DPG levels of both groups significantly increased and remained elevated. The CO2 group had higher levels than the non-CO2 group after 48 and 72 h. Concurrent measurements of P50 showed similar changes over the same time course. Mean corpuscular hemoglobin concentrations remained normal for 48 h and then decreased in both groups, the CO2 group showing the larger decrease. We conclude that altitude exposure may produce an increase in 2,3-DPG without the presence of respiratory alkalosis previously thought necessary.

Adolescent↗
PubMed1975

Cardiovascular responsiveness to beta-adrenergic stimulation and blockade in chronic hypoxia.

Previous studies have shown that exposure to high altitude results in an initial increase in heart rate, followed by a return to sea-level values within several days; circulating catecholamines rise progressively during this time. Nine conscious dogs were studied in normoxia (N) and after 10 days' exposure to 445 torr (CH). The mean (plus or minus SE) hematocrit was higher in CH (50 plus or minus 2 vs. 42 plus or minus 1%) while Pa-o2 (53 plus or minus 1 vs. 97 plus or minus 2 torr) and PaCO2 (27 plus or minus 1 vs. 35 plus or minus 1 torr) were lower than in N. A 3.5-fold increase in plasma norepinephrine above the N value was found in CH. Arterial pH, heart rate (HR), and mean femoral arterial pressure (MAP) did not differ significantly in N and CH. Isoproterenol (ISO), 0.5 mug/kg iv, produced an average increase in HR of 92 plus or minus 9 beats/min in N, but only 66 plus or minus 8 beats/min in CH (P smaller than .02). Reduction in MAP after ISO were similar. Pretreatment with propranolol, 0.15 mg/kg iv, reduced HR equally in N and CH without affecting MAP, but diminished the HR response to ISO significantly more in CH than in N. The attenuated chronotropic response to beta-adrenoceptor stimulation following chronic hypobaric hypoxia suggests a relative cardiac refractoriness secondary to an increased level of sympathetic activity.

Adrenergic beta-Agonists↗
PubMed1975

Aldosterone dynamics during graded exercise at sea level and high altitude.

Hormonal responses to graded exercise of eight low altitude residents were examined at sea level (SL) and after 1 (acute) and 11 (chronic) days at 4,300 m (HA). Caloric, water, and electrolyte intakes were controlled, as were temperature and humidity. Blood was sampled at rest and during light and moderate upright bicycle exercise (20 min at 40% and 75% of maximal O2 uptake, respectively). Mean VO2 max at HA was 27% lower than at SL. Resting plasma levels of aldosterone (Aldo), renin, and angiotensin II (A II) were significantly lower (P smaller than 0.05) on day 1 at HA compared to SL, but returned to SL values by day 11. Plasma cortisol values at rest were similar at SL and HA and were not significantly altered by light or moderate exercise. Renin, A II, and Aldo rose progressively with increasing workload in each environment. With acute HA, renin and Aldo were lower than at either SL or chronic HA. The chronic HA levels tended to approximate SL findings, implying adaptation. The data suggest that aldosterone is predominantly under the control of the renin-angiotensin system during graded exercise at sea level and that the response of this system is altered on acute high-altitude exposure.

Acclimatization↗
PubMed1975

Changes in serum and sweat magnesium levels during work in the heat.

Serial changes in serum magnesium (Mg2+) were assessed in unacclimatized males during treadmill exercise in a hot (49 degrees/27 degrees C, dry/wet bulb) environment. Eight subjects walked at 5.6 km/h on a 0% grade, and at 90 min of exercise had a mean heart rate of increase of 70 plus or minus 5 (S.E.) beats/min, rise in rectal temperature of 2.1 degrees plus or minus 0.1 degrees C, and a weight loss of 2.07 plus or minus 0.10 kg. There was a significant (p less than 0.01) decrease in mean serum Mg2+ concentration (control: 1.87 plus or minus 0.06 mEq/I; 45 min: 1.81 plus or minus 0.07; 90 min: 1.72 plus or minus 0.08). The Mg2+ concentration in sweat samples collected over 90 min of work in the heat averaged 0.28 mEq/I (range 0.13 to 0.45). Thus, in normal man, exercise in an hot, dry environment resulted in a fall in serum magnesium which was not wholly explicable on the basis of sweat loss of this ion.

Adolescent↗
PubMed1975

Acute mountain sickness: increased severity in eucapnic hypoxia.

This study examined the hypothesis that prevention of hypocapnia and alkalosis would ameliorate the symptoms of acute mountain sickness (AMS). Five subjects were exposed to simulated high altitude for 4 d with 3.8% CO2 added to the chamber to maintain normocapnia. Four other subjects were exposed for 4 d to hypobaric hypoxia without CO2 supplementation, and became hypocapnic. Barometric pressure was lower in the group with added CO2 so that alveolar oxygen tensions (55-60 mm Hg) would not be different. The severity of symptoms was clearly greater in normocapnic than in hypocapnic subjects. Thus, prevention of hypocapnia did not alleviate AMS symptoms. The efficacy of CO2 addition in reducing symptoms, as reported by earlier workers, was probably the result of induced hyperventilation and partial relief of hypoxia. Indeed, in the present study with two comparably hypoxic groups, CO2 addition augmented the sysptoms, possibly by causing increased cerebral vasodiladation and spinal fluid pressure.

Acute Disease↗