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Biomedical subjects

R F Grover

Publications and source records attributed to R F Grover.

At least 19 recordsLinked to original sources
PubMed1990

The coronary stress of skiing at high altitude.

Skiing, which may involve strenuous exercise in the cold at high altitude, could place considerable stress on the coronary circulation. To explore this possibility, we obtained by telemetry electrocardiograms on 149 men during recreational skiing at altitudes above 3100 m (10 150 ft). Tachycardia was impressive; heart rate exceeded 80% of predicted maximum in two thirds of the subjects. Five men developed abnormal ST-segment depression during or immediately after exercise. All five were older than 40 years, so in this age group the incidence of ST abnormalities was 5.6%. This is not greater than the incidence among asymptomatic men during submaximal exercise at low altitude. The high level of physical fitness of men who ski may have offset the added stress of cold and hypoxia. Hence, for physically fit older men, mountain skiing does not appear to pose a greater coronary stress than does comparable exercise at low altitude among men of only average physical fitness without known heart disease.

Adult↗
PubMed1979

Postnatal changes in response of canine neonatal pulmonary arteries to histamine.

Postnatal development of histamine receptors in the canine pulmonary circulation was examined utilizing histamine cumulative dose-response curves of pulmonary arteries isolated from neonatal and adult dogs. The maximal contractile response to histamine was relatively low at birth (avg 0.069 g) and increased with postnatal age, reaching a maximum in the adult (avg 1.10 g). H2-receptor blockade with metiamide increased the contractile response to histamine during the first 2 wk of life (avg 0.38 g), suggesting H2-receptor dominance over H1-receptors in the newborn. Maximal developed tension, in response to KCl, gradually increased with postnatal age, suggesting progressive maturation of the smooth muscle response. In contrast to pulmonary arteries, isolated tracheal segments from puppies aged 1-5 days demonstrated large contractile responses (avg 5 g). Histamine (in microgram/g of wet wt of lung tissue) was absent in the lungs from 3rd trimester fetal dogs and rapidly increased over the first 2 wk of life, reaching a maximum in the adult. It is concluded that 1) the response of pulmonary arteries to histamine changes during the first 2 wk of life; 2) this change may reflect a decrease in H2-receptors and an increase in H1-receptors; 3) the contractile ability of pulmonary vascular smooth muscle increases with postnatal age; and 4) histamine is unavailable for physiological responses in the fetal dog pulmonary circulation.

Animals↗
PubMed1979

Pregnancy-induced pulmonary hypertension in cows susceptible to high mountain disease.

Observations in several species suggest that pulmonary vascular reactivity may be reduced during pregnancy. We tested this hypothesis in two groups of unanesthetized cows, one "susceptible" and one "resistant" to high mountain or brisket disease. At the altitude of residence (1,524 m), mean pulmonary arterial pressure was elevated during pregnancy by 18% and total pulmonary vascular resistance by 32% in susceptible but not in resistant cows. During acute exposure to simulated altitudes of 2,120--4,550 m, pulmonary arterial pressure was increased by 16% and total pulmonary resistance by 28% during pregnancy in susceptible cows. The pulmonary pressor response to a 5 microgram/kg bolus of prostaglandin FIalpha was not different during pregnancy in either group. Resistant cows hyperventilated while pregnant, raising arterial partial pressure of oxygen (PaO2) by 6 Torr both at 1,524 m and, on the average, by 7 Torr at altitudes of 2,120--4,550 m. Susceptible cows increased their PaO2 less than did the resistant cows during pregnancy. The results indicated that pregnancy was associated with a greater rise in pulmonary arterial pressure and total pulmonary vascular resistance during acute hypoxia and failed to elicit as great a ventilatory response in susceptible than in resistant cows.

Altitude↗
PubMed1979

Accentuated hypoxemia at high altitude in subjects susceptible to high-altitude pulmonary edema.

To investigate the hypotheses that activated coagulation, catecholamine release, or arginine vasopressin release are involved in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured these variables in seven subjects susceptible to HAPE and in nine control subjects at an altitude of 1,600 m, and after 6 and 12 h at a simulated altitude of 4,150 m. Each subject was studied twice, once after 3 days of placebo medication and once after 3 days of premedication with aspirin and dipyridamole. At high altitude, HAPE-susceptible subjects showed significantly exaggerated hypoxemia and a slightly higher end-tidal carbon dioxide partial pressure that did not account fully for the hypoxemia. Fibrinolytic activity was significantly accelerated in both groups at high altitude, whereas other coagulation measurements, catecholamines and arginine vasopressin levels, and pulmonary function tests were not significantly changed. Similar findings were obtained after both placebo and platelet-inhibitor premedication. The results indicate that none of the three hypothesized mechanisms, i.e., activated coagulation, excessive catecholamine release, or antidiuresis, would account for HAPE susceptibility. Instead, HAPE-susceptible subjects exhibited exaggerated hypoxemia associated with relative hypoventilation and a widened alveolar-arterial gas pressure difference.

Adolescent↗
PubMed1979

Cardiac function in goats exposed to carbon monoxide.

To investigate the possibility that prolonged carbon monoxide (CO) exposure would depress myocardial function, six chronically instrumented, unsedated goats were exposed to 160--200 ppm CO for 2 wk, resulting in a mean carboxyhemoglobin saturation of 20%. Cardiac index and stroke volume remained unchanged during and after exposure. Hematocrit and hemoglobin concentration started increasing on the 10th day of exposure, this increase reached statistical significance (P less than 0.05) on the 6th postexposure day. Contractility (Vmax) of the left ventricular myocardium and heart rate were unchanged during exposure to CO, but both were significantly (P less than 0.05) decreased at some time during the 1st wk after removal from CO. If there was a decrease in intrinsic myocardial function during CO exposure, it may have been masked by increased sympathetic activity. The mechanism(s) that might produce the decrease in heart rate and contractility after removal from CO are not obvious. Possible explanations are discussed.

Animals↗
PubMed1978

Impaired oxygenation during sleep in excessive polycythemia of high altitude: improvement with respiratory stimulation.

Although polycythemia of high altitude is usually due to excessive hypoxemia, in some patients the hematocrit is elevated out of proportion to the degree of hypoxemia measured awake. One possible explanation is that severe hypoxemia occurs during sleep in these subjects. We therefore monitored oxygen saturation (SaO2), breathing pattern, and electroencephalogram (EEG) during sleep in five normal high-altitude residents and in five patients with excessive polycythemia. The polycythemic patients were studied as part of a placebo--drug double-blind crossover trial of the respiratory stimulant drug medroxyprogesterone acetate (MPA). The polycythemic patients while taking placebo were much more hypoxemic during sleep than the normals (all-night mean SaO2: 79.4 +/- 1.7% versus 87.8 +/- 1.7%, p less than 0.01). Abnormalities in breathing patterns were observed in all the subjects, especially during REM stage sleep. In polycythemic subjects, this resulted in precipitous hypoxemia with SaO2 as low as 50%--70%. Severe hypoxemia was not observed in control subjects despite similar abnormalities in breathing. Significant improvement in nocturnal SaO2 occurred when the polycythemic patients were taking MPA, mean SaO2 rising from 79.4 +/- 1.7% to 83.7 +/- 0.7%, p less than 0.05. Of probably greater importance, MPA largely prevented the precipitous drops in SaO2, mean lowest SaO2 rising from 64.6 +/- 4.7% to 76.0 +/- 2.1% p less than 0.05. The severe decreases in SaO2 during sleep may explain elevations in hematocrit that are out of proportion to the awake SaO2 in man at high altitude. The therapeutic effect of MPA in this condition may be due to amelioration of sleep hypoxemia.

Adult↗
PubMed1978

Decreased pulmonary vascular responses in dogs with increased pulmonary blood flow.

We wished to determine whether high pulmonary blood flow alters the pulmonary vascular responses to the vasoconstrictors, hypoxia and prostaglandin F2alpha (PGF2alpha). Acute or chronic left pulmonary artery (PA) occlusion was performed in dogs in order to create high pulmonary blood flow conditions. Right lung pulmonary vascular resistance (PVR) during normoxia was reduced by both acute and chronic left PA occlusion, suggesting passive vasodilatation. Increases in right lung PVR induced by hypoxia (10--15% O2) and PGF2alpha (0.8-4 microgram kg-1 min-1) were attenuated both in acute and chronic left PA occluded dogs. Since the reductions in responsiveness were similar with acute and chronic increases in blood flow, the attenuating effect of high blood flow was not dependent upon morphologic changes in the vasculature. Pulmonary vascular responsiveness was probably reduced in these animals due to their dilated pulmonary vascular beds, consequent to the increased blood flow, thereby decreasing the effectiveness of smooth muscle contraction.

Animals↗
PubMed1978

Potentiation of hypoxic pulmonary vasoconstriction by ethyl alcohol in dogs.

Pulmonary and systemic hemodynamics and arterial blood gases were measured in anesthetized and mechanically ventilated dogs before and after oral or intravenous administration of ethanol. Increases in mean pulmonary artery pressure and pulmonary vascular resistance occurred. Platelet antiserum-induced thrombocytopenia inhibition of prostaglandin synthesis with meclofenamate, or alpha-adrenergic blockade did not alter the pulmonary pressor response to ethanol. However, the increase in resistance following ethanol was abolished by hyperoxia and potentiated by hypoxia. Thus, it appears that the effect of ethanol is to augment hypoxic pulmonary vasoconstriction, whereas ethanol per se has no independent pulmonary pressor activity.

Administration, Oral↗
PubMed1978

Cold-induced pulmonary hypertension in cattle.

The frequency with which cattle develop right-heart failure during the winter at high altitude suggested that cold might contribute to hypoxic pulmonary hypertension. Indeed in a preliminary study conducted out-of-doors during early Spring, two calves with known hyperreactive pulmonary vessels showed elevated pulmonary arterial pressures attributed to their prior exposure to nighttime cold (-5 degrees C). In a second study five hyperreactive calves had increases in mean pulmonary arterial pressure from 29 to 45 Torr (+ 55%) during 48 h of exposure to cold (0 to -5 degrees C) in a climatic chamber. Three calves with less reactive lung vessels increased their pressures from 25 to 36 Torr (+ 44%). In a more complete study, six calves selected as potential hyperresponders showed increases in pulmonary arterial pressure (+ 60%), blood flow (+ 18%), and vascular resistance (+ 38%) during 48 h of cold exposure. Arterial PO2 decreased (-10 Torr) and PCO2 rose (+6 Torr) suggesting hypoventilation. Oxygen breathing returned pulmonary pressures and resistance to near control values, suggesting that cold had induced a hypoxic pulmonary vasoconstriction and an increased blood flow. Thus, a cold produced pulmonary hypertension in cattle at the modest altitude of 1,524 m and the pressor responses were greater in calves with more reactive lung vessels.

Altitude↗
PubMed1978

Exercise ventilation correlates positively with ventilatory chemoresponsiveness.

To determine the relationship of ventilatory responsiveness to hypoxia and hypercapnia to exercise hyperpnea, these responses and steady-state exercise ventilation (VE) were measured in 16 athletes during light (1/3 VO2 max) and heavy (2/3 VO2 max) exercise. Both the hypoxic and hypercapnic ventilatory responses correlated positively with VE per unit metabolic rate (VE/VCO2) at both exercise levels (P less than 0.05). The contribution of the hypoxic response to normoxic exercise VE was quantified by comparing VE in normoxia to VE during a brief (1 min) exposure to high O2 (PAO2 = 200 Torr). High O2 reduced normoxic exercise VE by a mean of 20% at either exercise intensity. Among individuals this reduction was directly dependent upon the intensity of the hypoxic response, and ranged from 7 to 42% of normoxic VE. After the variable reduction of normoxic VE by hyperoxia, all correlations of ventilatory response with exercise VE were lost except for the correlation of hypercapnic response with heavy exercise VE/VCO2. These findings indicate that the extent of VE in light or heavy exercise is modified by the strength of the hypoxic ventilatory response, and that the hypercapnic response independently correlates with VE during heavy exercise.

Adult↗
PubMed1978

Diagnosis of airflow obstruction at high altitude.

Using predicted sea level values for spirometry done at high altitude, underestimation of airway obstruction may result. We therefore established spirometric normal values for an altitude of 3,100 m for white men.

Adolescent↗
PubMed1978

Excessive polycythemia of high altitude: role of ventilatory drive and lung disease.

Persons residing at high altitude who develop excessive polycythemia are more hypoxemic than normal high-altitude residents. We investigated the causes of hypoxemia in 20 patients with excessive polycythemia residing at an altitude of 3,100 m. Lung disease evidenced by abnormal spirometric features and results of a respiratory questionnaire was present in 10 of 20 patients and resulted in increased alveolar-arterial difference for PO2 [(A-a)PO2]. The excessive hypoxemia in the patients with normal lungs was not due to increased (A-a)PO2. We measured ventilatory responses to hypoxia and to hypercapnia to determine whether blunting of these responses was a cause of this excessive hypoxemia. We found, however, that chemical drives to breathe, although blunted, were the same in patients with polycythemia as in high-altitude control subjects. However, an abnormal breathing pattern was observed; the polycythemic patients had a smaller tidal volume and a greater ratio of dead space to tidal volume than did the normal subjects. In addition, the polycythemic patients had increased minute ventilation on breathing 100 percent O2, whereas the normal subjects did not. Thus, hypoxic depression of ventilation may have been present. Our findings suggested that blunted chemical drives are not causative in this disease, and that some other cause of hypoxemia must be present.

Altitude↗