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Biomedical subjects

A Tucker

Publications and source records attributed to A Tucker.

At least 109 records · Page 6Linked to original sources

Spectra of molecular changes induced in DNA of Drosophila spermatozoa by 1-ethyl-1-nitrosourea and X-rays.

Mutations induced in Drosophila spermatozoa at the alcohol dehydrogenase Adh locus by 1-ethyl-1-nitrosourea (ENU) were compared to X-ray-induced mutations using genetic tests for complementation, southern blotting, western blotting and northern blotting. 8 of 10 ENU-induced mutations complemented all known adjacent loci and were presumed to be intragenic. In contrast, 8 of 30 X-ray-induced mutations were intragenic. Southern blot analysis showed that 2 of 7 intragenic mutations induced by X-rays were altered at the Adh locus, whereas all 8 intragenic ENU mutants appeared normal. Western blot analysis showed 4 of 7 intragenic mutants induced by X-rays produced a detectable polypeptide; 1 of the 4 had normal molecular weight and charge. In contrast, 7 of the 8 intragenic mutants induced by ENU produced a polypeptide of normal molecular weight and charge. One ENU and two X-ray-induced mutants, which had normal southern blots and no detectable polypeptide, produced normal molecular weight mRNA by northern blots. The interpretation of these results is that in spermatozoa X-rays induce primarily deletions that either produce deficiencies of the Adh locus or nonsense mutations within the locus, whereas ENU induces primarily missense mutations. This forward mutation assay based on loss of enzymatic activity efficiently recovered a broad spectrum of mutations ranging from missense to intragenic deletions and multi-locus deficiencies. Only 3 of these 40 mutations produced a polypeptide detectable as an electrophoretic variant.

Alcohol Dehydrogenase↗

Metabolic and heart rate responses to submaximal arm lever and arm crank ergometry.

Previous studies have shown that arm cranks and arm levers, working as propulsion mechanisms for nonambulatory individuals, may have mechanical and physiologic advantages over standard handrim wheelchairs. This study evaluated physiologic responses to arm lever and arm crank ergometry using identical workloads. An arm lever ergometer (ALE) was constructed and adapted to an arm crank ergometer (ACE) so that equal workloads could be applied with both ergometers. Fifteen able-bodied men and 15 able-bodied women exercised at a low (15 watts) and a high (45 watts) workload, with a three-minute rest interval. While exercising at each level, oxygen consumption (VO2), minute ventilation (VE), and heart rate (HR) were monitored. When low workloads with ALE and ACE were compared, no significant differences (p greater than 0.05) were demonstrated in any of the variables for men or women. For the men, at the high workload, the ALE elicited significantly lower (p less than 0.05) VO2 (by 9.8%), HR (by 6.3%), and VE (by 7.5%), than did the ACE. For the women, at the high workload, VO2 was significantly lower (p less than 0.05) (by 7.6%) with the ALE, as was VE (by 7.5%), but HR, although 3.3% lower with the ALE, was not significantly different (p greater than 0.05) from the ACE. These data suggest that the ALE is physiologically less stressful than the ACE at high workloads. Arm levers may, therefore, provide an advantage for handicapped persons when they propel themselves in wheelchairs.

Arm↗

Maximal respiratory pressures and pulmonary function in male runners.

To determine the effects of long term exercise on respiratory muscle strength, maximal inspiratory (Pl max) and expiratory (PE max) pressures, pulmonary volumes and capacities and anthropometric parameters were measured in a group of 101 male runners aged 16 to 58 years. The runners exhibited significantly (p less than 0.05) lower PE max (202 +/- 41 cm H2O and significantly greater residual lung volumes (RV) (2.08 +/- 0.49 L) than predicted values for normal subjects of similar height and age. Forced vital capacities were not different (p greater than 0.05) from values reported for normal non-smoking populations. These data suggest that running may cause a non-pathological increase in RV, perhaps mediated by reductions in expiratory muscle strength. Additionally, current RV regression equations developed for normal subjects may be inappropriate for use in running populations.

Adolescent↗

Hypoxic moderation of systemic hypertension in the spontaneously hypertensive rat.

The mechanism by which chronic, moderate, hypobaric hypoxia attenuates systemic systolic blood pressure (SBP) in the spontaneously hypertensive rat (SHR) was investigated in a three-part study. In experiment 1, 10 wk of hypoxia (3,658 m altitude) commencing in 7-wk-old rats was partially effective in preventing the rise in SBP [hypoxic SHR (SHR-H) 154 mmHg vs. normoxic SHR (SHR-N) 180 mmHg; P less than 0.01]. When hypoxia was initiated in 5-wk-old SHR (experiments 2 and 3), protection against hypertension was nearly complete (experiment 2: SHR-H 122 mmHg vs. SHR-N 175 mmHg; P less than 0.001; experiment 3: 135 vs. 152 mmHg, respectively; P less than 0.05). Elevations in O2 consumption (VO2) and rectal temperature (Tre) in SHR vs. normotensive [Wistar-Kyoto (WKY)] rats provided evidence that the SHR is a hypermetabolic animal. Thyroid hormonal indices suggested that SHR changed from a low to high thyroid status at a time that rapid blood pressure elevation occurred; however, hypoxia did not influence thyroid status. Acute, significant decrements in VO2 and Tre in SHR-H (experiments 2 and 3) accompanied the attenuation of SBP by hypoxia, whereas large decrements in VO2 and SBP did not occur in hypoxic WKY. Timely administration of moderate hypoxia protects against the development of hypertension in the SHR. This protection may relate to a metabolic adaptation made by the hypoxic SHR.

Animals↗

Severe pulmonary hypertension and arterial adventitial changes in newborn calves at 4,300 m.

Some human newborns have a syndrome characterized by irreversible pulmonary hypertension and severe hypoxemia and by medial hypertrophy and adventitial thickening of pulmonary arteries. We considered that newborn calves made severely hypoxic might reproduce features of the human disease. When 2-day-old calves were placed at 4,300 m simulated altitude, pulmonary arterial pressure was increased and could be reversed by 100% O2. However, after 2 wk at 4,300 m, pulmonary arterial pressures were suprasystemic and there was right-to-left shunting probably through the foramen ovale and a patent but restrictive ductus arteriosus. Suprasystemic pulmonary pressure and hypoxemia persisted with 100% O2 breathing. Morphometrical examination of the lung arteries showed a markedly thickened adventitia with cellular proliferation and collagen and elastin deposition. There was increased medial thickness and distal muscularization of the pulmonary arteries associated with decreased luminal diameter. The rapid development of severe pulmonary hypertension and poor responsiveness to O2 was associated with increased arterial wall thickness, particularly involving the adventitia. Thus the pulmonary arterial circulation in these calves, which were placed at high altitude for 2 wk, exhibited features resembling persistent pulmonary hypertension in newborn infants.

Altitude Sickness↗

The thyroid and hypoxic moderation of systemic hypertension in the spontaneously hypertensive rat.

Surgically thyroidectomized (TX), sham-operated euthyroid (EU), or thyroidectomized with dietary hormone replacement (RPL), 8-week-old male spontaneously hypertensive rats were subjected to 4 weeks of either of two altitude treatments: normoxia (N; lab altitude = 1520 m) or hypobaric hypoxia (H; simulated altitude = 3658 m). Systolic blood pressure (SBP) was attenuated in all hypoxic and in TX-N rats (p less than 0.05). Thyroidectomy reduced oxygen consumption, rectal temperature, and hormonal indices of thyroid function, as well as attenuating hypoxia-induced polycythemia and right ventricular hypertrophy. Thyroidectomy decreased the sensitivity of aortic rings to KCl and isoproterenol with no differences between EU-N and EU-H or between TX-N and TX-H apparent. Vessel responsiveness in RPL-H was consistent with the hypothyroid status indicated by hormonal measurement, while RPL-N vessel responsiveness was characteristic of euthyroid vessels. Since EU-H rats were euthyroid, with similar vascular responses to EU-N, hypoxia-induced attenuation of SBP does not require hypothyroid-like vascular alterations. Thus, hypoxia and thyroidectomy appear to mitigate systemic hypertension by different mechanisms.

Altitude↗

Low acute hypoxic ventilatory response and hypoxic depression in acute altitude sickness.

Persons with acute altitude sickness hypoventilate at high altitude compared with persons without symptoms. We hypothesized that their hypoventilation was due to low initial hypoxic ventilatory responsiveness, combined with subsequent blunting of ventilation by hypocapnia and/or prolonged hypoxia. To test this hypothesis, we compared eight subjects with histories of acute altitude sickness with four subjects who had been asymptomatic during prior altitude exposure. At a simulated altitude of 4,800 m, the eight susceptible subjects developed symptoms of altitude sickness and had lower minute ventilations and higher end-tidal PCO2's than the four asymptomatic subjects. In measurements made prior to altitude exposure, ventilatory responsiveness to acute hypoxia was reduced in symptomatic compared to asymptomatic subjects, both when measured under isocapnic and poikolocapnic (no added CO2) conditions. Diminution of the poikilocapnic relative to the isocapnic hypoxic response was similar in the two groups. Ventilation fell, and end-tidal PCO2 rose in both groups during 30 min of steady-state hypoxia relative to values observed acutely. After 4.5 h at 4,800 m, ventilation was lower than values observed acutely at the same arterial O2 saturation. The reduction in ventilation in relation to the hypoxemia present was greater in symptomatic than in asymptomatic persons. Thus the hypoventilation in symptomatic compared to asymptomatic subjects was attributable both to a lower acute hypoxic response and a subsequent greater blunting of ventilation at high altitude.

Adult↗

Attenuation of alpha-adrenergic responsiveness in hypoxic SHR.

Chronic exposure to hypoxia reduces the severity of hypertension in SHR. This study explored the possibility that hypoxic moderation of spontaneous hypertension is caused by a decrease in vascular responsiveness. In vitro studies were conducted with thoracic aortic rings obtained from SHR and Wistar-Kyoto (WKY) rats maintained under hypoxic (H; simulated altitude = 3658 m) and normoxic (N; laboratory altitude = 1520 m) conditions. Vessels were removed prior to the rapid development of hypertension (5 weeks of age; 3 days of altitude exposure), during the rapid hypertension-development stage (10 weeks of age; 5 weeks of altitude exposure), and during the established hypertension stage (18 to 20 weeks of age; 11 to 13 weeks of altitude exposure). Dose-response curves were obtained using a non-specific vasoconstrictor (KCl) and an alpha-adrenergic agonist, phenylephrine. At all ages, WKY vessels developed greater maximal contraction to vasoconstrictor stimuli, whereas vessels from the two older groups of SHR were more sensitive (more responsive at lower dosages) to KCl. Hypoxia caused significant (p less than 0.05) attenuation of the contractile responses to phenylephrine in young "pre-hypertensive" SHR, while similar, though less marked, attenuation of phenylephrine responsiveness was evident in young WKY-H. Chronically-reduced responsiveness to phenylephrine was found in vessels from SHR-H but not WKY-H. The lack of hypoxia-induced changes in vessel response to the non-specific vasoconstrictor, KCl, suggests a specific hypoxic attenuation of adrenergic vascular responsiveness. Thus, hypoxia may protect against the development of spontaneous hypertension through attenuation of alpha-adrenergic vasoconstrictor mechanisms.

Analysis of Variance↗

Pulmonary vascular responsiveness in cold-exposed calves.

The pulmonary vascular responses to acute hypoxia and to infusions of histamine and 5-hydroxytryptamine (5-HT) were recorded in unanesthetized standing bull calves under neutral (16-18 degrees C) and cold (3-5 degrees C) temperature conditions. Cold exposure alone resulted in a significant increase in pulmonary arterial wedge pressure from 10.2 +/- 3.5 to 15.9 +/- 4.9 Torr (1 Torr = 133.322 Pa). Resistance to blood flow between the pulmonary wedge and the left atrium significantly increased from 0.50 +/- 0.51 to 1.21 +/- 0.78 mmHg . L-1 . min-1 (1 mmHg = 133.322 Pa) with cold exposure. This apparent pulmonary venoconstrictor response to cold exposure was further evaluated to determine if hypoxia, histamine, or 5-HT responsiveness was altered by cold exposure. Twelve minutes of hypoxia increased pulmonary arterial and systemic arterial pressures, heart rate, and respiratory rate similarly in cold and neutral temperatures. Cold exposure did not alter the dose-related reductions of systemic arterial and pulmonary arterial pressures in response to histamine. Similarly, the decreases in systemic arterial pressure and heart rate and increases in pulmonary arterial and left atrial pressures in response to 5-HT were not significantly different in cold and neutral conditions. It was concluded that acute, mild cold exposure results in an increase in resistance to blood flow in the pulmonary venous circulation without a general increase in pulmonary vascular reactivity, as measured by responses to hypoxia, histamine, and 5-HT.

Animals↗

Interaction between cold and altitude exposure on pulmonary circulation of cattle.

Hereford calves were exposed in a temperature-controlled hypobaric chamber to environmental temperatures of -2 to 1 degree C (cold) at altitudes of 1,524 m (resident altitude) and 3,048 m 1) to characterize the effects of cold exposure on the pulmonary circulation; 2) to examine the role of cold-induced hypoventilation on the pulmonary circulation; and 3) to examine the interaction between cold and hypoxia on the pulmonary circulation. Cold exposure produced a significant increase in pulmonary arterial pressure (Ppa), pulmonary arterial wedge pressure (Ppaw), and pulmonary vascular resistance (PVR) at both 1,524 and 3,048 m without affecting cardiac output. Concomitantly, cold exposure caused reductions in minute ventilation, respiratory rate, end-tidal O2 tension (PETO2), and arterial O2 tension (PaO2). Tidal volume, end-tidal CO2 tension, and arterial CO2 tension increased. Neither arterial pH nor O2 consumption changed during cold exposure. These results indicated that both pulmonary arterial and venous vasoconstriction were responsible for the pulmonary hypertension associated with cold exposure. Acute exposure to 3,048 m during cold exposure produced increases in Ppa and PVR that were similar to those elicited by cold exposure at 1,524. It was concluded that altitude exposure neither attenuated nor potentiated the effect of cold exposure on the pulmonary circulation; rather, altitude and cold exposure interacted additively. O2 administered during cold exposure to restore PETO2 and PaO2 to control values partially restored Ppa and PVR to control values. This suggested that a portion of the pulmonary hypertension associated with cold exposure was due to hypoxic pulmonary vasoconstriction elicited by the cold-induced alveolar hypoventilation.

Altitude↗

Headache at high altitude is not related to internal carotid arterial blood velocity.

The cause of headache in persons going to high altitude is unknown. Relatively severe hypoxemia in susceptible subjects could induce large increases in cerebral blood flow that then could initiate the headache. Thus we measured noninvasively, by Doppler ultrasound, changes in internal carotid arterial blood velocity (velocity) in 12 subjects in Denver (1,600 m) and repeatedly up to 7 h at a simulated altitude of 4,800 m (barometric pressure = 430 Torr). Six subjects, selected because of prior history of high-altitude headache, developed comparatively severe headache at 4,800 m, and four subjects, without such history, remained well. Two subjects developed moderate headache. Velocity at 4,800 m did not correlate with symptom development, arterial O2 saturation, or end-tidal PCO2. Also, neither velocity nor blood pressure was consistently elevated above the Denver base-line values. During measurements of hypercapnic ventilatory response in Denver, velocity increased linearly with end-tidal PCO2, confirming that our Doppler method could demonstrate an increase. Also, 30 min of isocapnic or poikilocapnic hypoxia caused small increases in velocity (+8 and +6%) during the base-line measurement at low altitude. Although even a small increase in cerebral perfusion could contribute to headache symptoms at high altitude, cerebral blood flow does not appear to play a primary role.

Adult↗

Canine renal vascular response to bilateral carotid occlusion during hypoxia.

Chloralose-urethane anesthetized dogs were utilized to determine if hypoxemic potentiation of the baroreceptor-mediated increase in renal sympathetic nerve activity (RSNA) results in sufficient renal vascular vasoconstriction to reduce renal blood flow (RBF) during bilateral carotid occlusion (BCO). Additionally, hypercapnia and mechanical ventilation were randomly combined with hypoxemia during BCO to determine if further augmentation of renal vasoconstriction could be accomplished. BCO resulted in a similar increase in blood pressure (renal perfusion pressure) in all periods. RBF was not reduced significantly by BCO during any period even though renal vascular resistance was significantly increased by BCO during each period. When hypoxemia was combined with hypercapnia and mechanical ventilation simultaneously, there was a greater percentage increase in renal resistance with BCO. During BCO, when renal perfusion pressure was returned to control values by suprarenal aortic constriction, RBF remained unchanged and renal resistance decreased to control values. These results indicate that the BCO-induced increase in RSNA is relatively moderate and, even when potentiated by hypoxemia, hypercapnia, and mechanical ventilation, is not sufficient to reduce RBF in the presence of an increase in blood pressure and renal autoregulation.

Animals↗

Hypoxic pressor responses in lungs from rats acutely exposed to simulated high altitude.

Male Sprague-Dawley rats were exposed to 6, 3 or 1 h of simulated high altitude (380 Torr). The isolated perfused lung of each animal was challenged with 4 sequential periods of hypoxia, angiotensin II (AII), and 5-hydroxytryptamine (5-HT) following altitude exposure. Isolated perfused lungs of low altitude control rats were similarly challenged. The acute hypoxic vasoconstrictor response was significantly reduced in animals exposed to 3 and 6 h of high altitude compared to low altitude control animals. The hypoxic pressor response was not significantly different from control in animals exposed to 1 h of simulated altitude. Pressor responses to AII and 5-HT following altitude exposure were not significantly different from controls.

Altitude↗

Pulmonary vascular changes in young and aging rats exposed to 5,486 m altitude.

Young (YNG) and middle-aged (MA) male rats were exposed to 5,486 m for durations ranging from 1 to 42 days to determine the effect of age on the progression of polycythemia, right ventricular hypertrophy (RVH), lung vascular muscularization, and pulmonary vascular responsiveness. Other rats were exposed for 42 days at 5,486 m and were then allowed to recover at 1,520 m for periods up to 42 days. The progression and subsequent regression of polycythemia and RVH with altitude exposure were similar for YNG and MA rats. However, YNG rats exhibited vascular muscularization during the altitude exposure, characterized by hypertrophy of smooth muscle cells, whereas MA rats exhibited little or no change in vascular morphology. Lungs from both altitude-exposed YNG and MA rats exhibited blunting of acute hypoxic pulmonary vasoconstriction upon exposure to 5,486 m, with more severe blunting apparent in MA rats. Pressor responses to angiotensin II (AII) were potentiated in lungs from high altitude rats, particularly in the YNG rats, and this increased responsiveness persisted during the recovery period. A positive correlation was found in YNG rats between the degree of vascular muscularization and the pressor response to AII, suggesting that increased muscle mass was partially responsible for the potentiated AII responses. However, MA rats did not exhibit the same correlation for AII, and neither YNG nor MA rats exhibited increased responsiveness to 5-hydroxytryptamine. The results indicate that age influences the morphologic responses to altitude exposure and vascular responsiveness to AII, but does not affect the polycythemic response or the degree of RVH.

Aging↗

Pulmonary and systemic vascular responses to tolazoline in neonatal and mature calves.

Tolazoline was infused intravenously (2 mg/kg over 2 minutes) in awake neonatal and mature calves. In normoxic pulmonary normotensive neonatal calves, tolazoline induced minimal hemodynamic changes, except for an immediate bradycardia. Tolazoline caused increases in systemic arterial pressure and vascular resistance and a bradycardia in normoxic normotensive mature calves. Calves were also made hypoxic, by breathing 12% O2 by facemask, in order to produce pulmonary hypertension. In hypoxic pulmonary hypertensive neonatal calves, tolazoline induced transient pulmonary vasodilation, a reduction in systemic arterial pressure, and marked bradycardia. Similarly, tolazoline caused reductions in pulmonary and systemic arterial pressure and bradycardia in hypoxic pulmonary hypertensive mature calves. Pentobarbital anesthesia in neonatal calves induced marked hemodynamic changes but did not alter the cardiovascular responses to tolazoline. A significant correlation was found between the baseline pulmonary arterial pressure and the magnitude of the pulmonary depressor response to tolazoline when all interventions were evaluated. Thus, tolazoline induced transient pulmonary vasodilation in pulmonary hypertensive calves but simultaneously caused profound transient bradycardia, particularly in neonatal calves.

Aging↗

Skeletal muscle capillarity during recovery from chronic hypoxic exposure.

Young male Sprague-Dawley rats were randomly assigned to one of three groups (Chronically Hypoxic, N = 15; Age-Control, N = 15; Weight-Control, N = 15) and studied immediately following a 36-day exposure at a simulated altitude of 5846m or after recovery periods of one, three or seven days. Following preincubation at pH 3.8, cross-sections of soleus muscle were stained by the calcium ATPase method and analyzed for six indices of skeletal muscle capillarity: capillary density (CD), fiber density, number of capillaries around each fiber (CAF), Capillary/fiber ratio (C:F), fiber cross-sectional area (FCSA), and fiber diameter. No differences in skeletal muscle capillarity were observed in chronically hypoxic rats at the termination of exposure or during the seven day recovery period. The Chronically Hypoxics differed significantly (p less than or equal to .05) from both control groups in three different measures of physiologic stress, but showed a definite trend toward recovery in the post-exposure period. This recovery was most apparent in body weight comparisons. The Chronically Hypoxics weighed less than the Age-Controls immediately following the exposure period but gained rapidly during the first three days post-exposure. These rapid body weight increases in rats recovering from chronic exposure to hypoxia suggest that age-controls should not be excluded in favor of weight-controls in similar studies.

Age Factors↗