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Biomedical subjects

H V Forster

Publications and source records attributed to H V Forster.

At least 127 records · Page 7Linked to original sources
PubMed1980

Hemoglobin affinity for oxygen during short-term exhaustive exercise.

We assessed hemoglobin affinity for oxygen (standard P50: pH 7.40, PCO2 40 Torr, temperature 37 degrees C) in 3 series of studies of 16 male subjects who performed exhaustive treadmill exercise of 10 min duration. Standard P50 was significantly elevated (0.7--2.5 Torr) during the last minute of and for 30 min following exercise. Exercise while carboxyhemoglobin (HbCO) was acutely elevated to 5% did not affect std P50 any differently than exercise alone. 2,3-Diphosphoglycerate (2,3-DPG) was significantly elevated after exercise, but not during or 30 min postexercise, and it correlated significantly with P50 in 2 studies (r, 0.43--0.68). ATP (mumol/100 ml) was significantly elevated only 3 min postexercise. Serum [Na+], [K+], [Cl-], osmolarity, and hemoglobin (Hb) concentration were significantly elevated during exercise with [Na+] osmolarity, and [Hb] remaining significantly elevated postexercise. There was no significant correlation between std P50 and any of these variables. Multiple correlation regression analysis between P50 and 2,3-DPG, ATP, and [Na+] yields a coefficient of 0.86. We conclude this type of exercise is unique in causing a small change in std P50 that appears to be mediated by several factors.

Adult↗
PubMed1980

Recovery of peripheral chemoreceptor function after denervation in ponies.

Resting ventilation (PaCO2) and ventilatory responses to acute hypoxia and to intravenous NaCN were assessed over a 4-yr period following cutting of the carotid sinus nerves and stripping the adventitia of the aortic arch. The data indicated essentially complete loss of peripheral chemoreceptor function immediately after surgery and hypoventilation during normoxia (delta PaCO2 = +8.7 Torr). There was a time-dependent, partial recovery of peripheral chemoreceptor function between 2 and 22 mo after surgery. Approximately 10% of the ventilatory response to iv NaCN returned, and 30-40% of the normal response to acute hypoxia was restored. Resting PaCO2 was no longer significantly elevated above normal by 22 mo after surgery. Four years after surgery these animals were unable to sustain normal ventilatory acclimatization to chronic hypoxia just as in an earlier study in the same ponies. Experiments carried out under anesthesia showed that recovered peripheral chemoreceptor sensitivity was not present in the carotid chemoreceptor area. However, sectioning of the aortic nerve caused the animals to again hypoventilate during acute hypoxia, and it nearly eliminated the ventilatory response to NaCN, but normal eucapnic ventilation was retained. We conclude that in the pony aortic chemoreceptors become functional in a time-dependent manner following carotid body denervation.

Acid-Base Equilibrium↗
PubMed1979

Role of cerebrospinal fluid [H+] in ventilatory deacclimatization from chronic hypoxia.

Once ventilatory acclimatization begins in sea level residents sojourning at high altitude, abrupt restoration of normal oxygen tensions will not restore ventilation to normal. We have investigated the role of cerebrospinal fluid (CSF) [H(+)] in this sustained hyperventilation by measuring CSF acid-base status in seven men (lumbar) and five ponies (cisternal) in normoxia, first at sea level and then periodically over 13-24 h of "deacclimatization" after 3-5 d in hypoxia (P(B) = 440 mm Hg). After 1 h deacclimatization, hyperventilation continued at a level only slightly less than that obtained in chronic hypoxia (+1-2 mm Hg Pa(CO2)), whereas CSF pH was either equal (in man) or alkaline (in pony, +0.02, P < 0.01) to sea level values. Between 1 and 12-13 h deacclimatization in all humans and ponies Va fell progressively (Pa(CO2) increased 4-7 mm Hg) and CSF pH became increasingly more acid (-0.02 to -0.05, P < 0.01). Between 12 and 24 h of normoxic deacclimatization in ponies, Pa(CO2) rose further toward normal, coincident with an increasing acidity in CSF (-0.02 pH). Similar negative correlations were found between changes in arterial pH and Va throughout normoxic deacclimatization. We conclude that [H(+)] in the lumbar or cisternal CSF is not the mediator of the continued hyperventilation and its gradual dissipation with time during normoxic deacclimatization from chronic hypoxia. These negative relationships of Va to CSF [H(+)] in normoxia are analogous to those previously shown during acclimatization to hypoxia.

Acclimatization↗
PubMed1978

Cerebrospinal fluid acid-base balance during muscular exercise.

Ventilation, metabolism, arterial blood gases, and blood and cerebrospinal fluid (CSF) acid-base status were measured in exercise studies on seven ponies during mild, moderate, and near-maximal treadmill exercise. CSF and arterial blood were sampled via indwelling catheters. Generally measurements were made during the 3rd, 6th, and 9th minute of steady-state exercise, with CSF sampled only during the 9th minute. Alveolar ventilation (VA) and metabolic rate (VO2) increased proportionately during exercise below the anaerobic threshold, but above this threshold, VA increased at a faster rate than VO2. The similarity of these response to those observed in man suggests the pony is a suitable animal model for study of exercise hyperpnea. No change in CSF acid-base balance occurred with light-to-moderate work; however, with near-maximal work a fall in CSF carbon dioxide partial pressure due to hyperventilation caused CSF to become alkaline (pH = 7.380) relative to rest (pH = 7.330). CSF lactate increased slightly with exercise but had no effect on CSF [HCO3-], which remained constant from rest to severe exercise. We conclude that it is unlikely the hyperpnea at any intensity of exercise results from an increased H+ stimulation at the medullary chemoreceptor.

Acid-Base Equilibrium↗
PubMed1978

Physiological response to aerosol propellants.

Acute exposures to isobutane, propane, F-12, and F-11 in concentrations of 250, 500, or 1000 ppm for periods of 1 min to 8 hr did not produce any untoward physiological effects as determined by the methods employed which included serial EKG's and continuous monitoring of modified V5 by telemetry during exposure. Repetitive exposures to these four propellants were also without measurable untoward physiological effect with the exception of the eight male subjects repetitively exposed to 1000 ppm, F-11, who did show minor decrements in several of the cognitive tests. Of particular importance is the observation that none of the subjects showed any decrement in pulmonary function or alteration in cardiac rhythm as the result of exposure to concentrations of the gases or vapors far greater than encountered in the normal use of aerosol products in the home.

Adolescent↗
PubMed1977

Acute and repetitive human exposure to isobutane.

Eight adult volunteers of both sexes were exposed to isobutane in a controlled-environment chamber for the purpose of monitoring their physiological responses to a series of gas concentrations ranging from 250 to 1,000 ppm. First, the response to exposure periods of 1 min, 2 min, 1 h, 2 h, and 8 h were studied. There being no untoward responses to these acute exposures, the eight volunteers were exposed repetitively to isobutane at concentrations of 500 ppm, 1, 2 or 8 h per day, five days per week for two weeks. Then exposures to two mixtures of isobutane and propane for 1, 2 or 8 h per day for two days were studied. During the investigation all subjects were kept under comprehensive medical surveillance. No untoward subjective responses or abnormal physiological responses occurred during or following these exposures. Special emphasis was placed on evaluating the cardiac and pulmonary response to these exposures through the use of continuous ECG telemetry and serial computerized spirometric measurements. The following serial laboratory studies were unaltered by the exposures: complete blood count, urinalysis, serum alkaline phosphatase, SGOT, LDH, serum bilirubin, blood sugar, serum calcium, serum phosphorus, BUN, spontaneous electroencephalogram, visual evoked response, a battery of cognitive tests, and an ACTH stimulation test.

Adrenal Cortex↗
PubMed1977

Effect of sojourn at 3200-m altitude on spinal reflexes in young adult males.

Studies of the H reflex and the Achilles tendon reflex (ATR) were performed in 12 healthy males under six conditions: 1) sea level control, 2) during the first 1-3 h at altitude while normoxic conditions were maintained, 3-5) at 6, 24 and 72 h of hypoxia, and 6) after Ve acclimatization at altitude in 5-14 d. After altitude acclimatization, the peak-to-peak amplitude of the H reflex and the ATR response was significantly elevated over control. A trend toward decreased amplitudes of both the ATR and the H reflex was observed at 6 h after the onset of hypoxia. There was no significant alteration in latency of the H reflex under any test condition. These findings suggest that sojourn at altitude by sea level residents induces changes in spinal motor reflexes. These changes are most probably mediated by altered high central modulation of the cord.

Acclimatization↗
PubMed1976

Hypoventilation in ponies after carotid body denervation.

Seven ponies were subjected to carotid body denervation (CD) and two ponies were sham operated (S). Measurement of arterial blood gases and arterial blood and cerebrospinal fluid (CSF) acid-base balance were made prior to and 1,2,4,9, and 17 wks after surgery in unanesthetized animals. Resting ventilation and ventilatory responsiveness to hypoxia and NaCN infusion were assessed prior to and 2,9, and 17 wks after surgery. Alveolar hypoventilation in the CD ponies was marked 1-2 wk after surgery when VE and VA were reduced 40% and 10%, respectively, from control and PaCO2 was 12-15 mmHg above control. However, the effect was not nearly as great 4, 9, and 17 wk after surgery when the PaCO2 stabilized at approximately 6 mmHg above control PaCO2. Arterial blood pH was normal in the hypercapnic CD ponies, but CSF pH remained acid relative to normal throughout the 17-wk period. Changes in ventilatory responsiveness to hypoxia and NaCN tended to parallel changes in resting ventilation. These findings suggest: 1) the carotid bodies are essential in ponies to maintain normal ventilation: 2) in CD ponies peripheral chemosensitivity is partially regained at some unestablished locus; and 3) pH compensating mechanisms in chronically hypercapnic ponies function relatively better in blood than in CSF.

Acid-Base Equilibrium↗
PubMed1976

Ventilatory control in peripheral chemoreceptor-denervated ponies during chronic hypoxemia.

The present study was designed to provide further insight into the role of the carotid and aortic chemoreceptors in ventilatory (VE) acclimatization during sojourn at altitude. Measurements were made: 1) on 10 ponies near sea level (SL, 740 Torr) under normal conditions, 2) on 6 of these at SL following chemoreceptor denervation (CD), and 3) subsequently on all 10 during 4 days of hypobaric hypoxia (PaO2 = 40-47 Torr). CD resulteo in hypoventilation at SL (deltaPaCO2 = d8 Torr, P less than 0.05), and it prevented hyperventilation normally observed with injection of NaCN and acute exposure to hypoxia (less than 1 h). In contrast, hyperventilation was evident in normal ponies during acute hypoxia (deltaPaCO2 = -6.7 Torr). Ventilation increased in both groups between the 2nd and 8th h of hypoxia (deltaPaCO2 from 1 h = -4 Torr, P less than 0.05). This change, a common characteristic of acclimatization, persisted throughout 4 days of hypoxia in the normal ponies. However, in the CD ponies this change was evident consistently only through the 12th h and after the 44 h hyperventilation was no longer evident. We conclude that the peripheral chemoreceptors are essential in ponies for normal VE acclimatization to this degree of hypoxemia. Two additional findings in CD ponies suggest the presence of a CNS inhibitory influence on the VE control center during chronic hypoxemia. First, acute hyperoxygenation on the 4th day of hypoxemia induced hyperventilation (deltaPaCO2 = -5 Torr, P less than 0.05). Second, again on the 4th day and during hyperoxygenation, VE responsiveness to CO2 and doxapram HCl was greater than at sea level.

Acclimatization↗
PubMed1975

Cerebrospinal fluid alkalosis during high-altitude sojourn in unanesthetized ponies.

Unanesthetized adult female ponies were studied near sea level (250 m) and during sojourns to 3400 m (N=6) and 4300 m (N=7) altitude. The pH, PCO2, and PO2 of arterial blood and pH and PCO2 of cerebrospinal fluid (CSF) were measured under conditions of acute (1 hr) and chronic (1-45 days) hypoxia. Cerebrospinal fluid was sampled from the cisterna magna of the awake pony and arterial blood withdrawn from an indwelling arterial catheter. In both groups of animals, PaCO2 decreased slightly after 1 hr of hypoxia (delta PaCO2= - 0.6 mm Hg at 3400 m; - 3.9 mm Hg at 4300 m), decreased further after 1-5 days at high altitude (delta PaCO2= - 7.2 mm Hg at 3400 m; - 12.3 mm Hg at 4300 m) and then increased significantly after 6 days of chronic hypoxia (delta PaCO2= + 4.1 mm Hg at 3400 m; + 4.7 mm Hg at 4300 m). Although PaO2 decreased markedly during acute hypoxia, subsequent changes in PaCO2 at high altitude did not alter PaO2 from that observed during acute hypoxia (PaO2=52 mm Hg at 3400 m; 41 mm Hg at 4300 m). The pH of CSF increased during acute hypoxia (delta pH= + 0.013 unit at 3400 m; + 0.033 unit at 4300 m) and became more alkaline after 1-2 days at high altitude (delta pH= + 0.031 unit at 3400 m; + 0.064 unit at 4300 m). At 4300 m, CSF pH remained alkaline to control values throughout sojourn. Under these conditions of chronic hypocapnic hypoxia, CSF pH was imperfectly regulated and regulated in a magnitude equal to (3400 m) or less than (4300 m) arterial blood. Furthermore, the similarity of relative changes in CSF [HCO3-] and arterial [HCO3-] during chronic hypoxia may indicate a passive regulation of CSF [HCO3-] rather than local 'CSF-specific' mechanisms as previously proposed.

Acclimatization↗
PubMed1975

Effects of moderate hypoxemia and hypocapnia on CSF [H+] and ventilation in man.

The effects of 26 h of normoxic hypocapnia (PaCO2, 31 MMHg) vs. 26 h of hypocapnia plus hypobaric hypoxia (PaCO2 32, PaO2 57 mmHg) were compared with respect to: a) CSF acid-base status; and b) the spontaneous ventilation (at PIO2 145 mmHg) which followed the imposed (voluntary) hyperventilation. For each condition of prolonged hypocapnia, PaCO2 was held constant throughout and pHa and [HCO3-]a were constant over the final 6-10 h. We assumed that measured changes in lumbar CSF acid-base status paralleled those in cisternal CSF. Spontaneous hyperventilation followed both normoxic and hypoxic hypocapnia but was significantly greater following hypoxic hypocapnia. In the CSF, pH compensation after 26 h of hyperventilation was incomplete (similar to 45-50%), was similar to that in arterial blood, and was unaffected by a superimposed hypoxemia. These data were inconsistent with current theory which proposes the regulation of CSF [HCO2] via local mechanisms and, in turn, the mediation of ventilatory acclimatization to hypoxemia and/or hypocapnia via CSF [H+]. Alternative mediators of ventilatory acclimatization were postulated, including mechanisms both dependent on and independent of "chemoreceptor" stimuli.

Acid-Base Equilibrium↗
PubMed1975

HbO2 dissociation in man during prolonged work in chronic hypoxia.

In healthy human sojourners to 3,100 m we studied exercise-induced shifts in HbO2 dissociation: their regulation in femoral venous blood and their net effect on estimated capillary PO2 (PC-O2) in working skeletal muscle. Prolonged heavy work effected an increase of 10.3 plus or minus 0.9 mmHg in in vivo P50 (7.30 PH-v, 41 degrees C-v, and 45 Pv-CO2); due entirely to the additive effects of increased venous temperature and [H+]. The rightward curve shift during work at 3,000 m, compared to that at 250 m, produced a similar increase in in vivo P50 but a reduced net effect on PC-O2, because Cv-02 at 3,100 m was reduced similar to 2 ml/100 ml to the lower converging portions of the curve. The lower Cv-O2 (and Pv-O2) at 3,100 M was attributable to a small decrease in total systemic blood flow. The net effect of the rightward curve shift during exercise on mean to end-capillary PO2 was positive in most cases (+1 to +8 mmHg PCO2). However, it was shown that the levels of mean to end-capillary PO2 (28-13 mmHg), which would have been obtained during exercise in the absence of any rightward curve shift, were more than adequate to sustain a steady state of aerobic energy production in working skeletal muscle. These data do not support the concept of a significant contribution to oxygen delivery to working skeletal muscle from in vivo shifts in HbO2 dissociation, during either acclimatization to high altitude or during prolonged muscular work.

Acclimatization↗
PubMed1975

Incomplete compensation of CSF [H+] in man during acclimatization to high altitude (48300 M).

This study has assessed the regulation of arterial blood and cerebrospinal fluid acid-base status in seven healthy men, at 250 m altitude and after 5 and 10-11 days sojourn at 4,300 m altitude (PaO2 = 39 mmHg day 1 to 48 mmHg day 11). We assumed that observed changes in lumbar spinal fluid acid-base status paralleled those in cisternal CSF, under these relatively steady-state conditions. Ventilatory acclimatization during the sojourn (-14 mmHg PaCO2 at day 11) was accompanied by: 1) reductions in [HCO3-] (-5 to -7 meq/1) which were similar in arterial blood and CSF; 2) substantial, yet incomplete, compensation (70-75%) of both CSF and blood pH; and 3) a level of CSF pH which was maintained significantly alkaline (+0.05 +/- 0.01) to normoxic control values. These data at 4,300 m confirmed and extended our previous findings for more moderate conditions of chronic hypoxia. It was postulated that the magnitude and time course of pH compensation in the CSF during chronic hypoxia and/or hypocapnia are determined by corresponding changes in plasma [HCO2-].

Acclimatization↗
PubMed1975

Effect of sojourn at 4,300 m altitude on electroencephalogram and visual evoked response.

The purpose of the present study was to determine the effect of sojourn at high altitude on cerebral electrical activity. Electroencephalographic (EEG) and visual evoked responses (VER) were recorded from seven healthy males under the following conditions: 1) during the first 2-3 h at 4,300 m altitude when Pao2 was maintained at 90 mmHg (control condition), 2) during the first 2-3 h of hypoxia (Pao2 = 40 mmHg), and 3) at 24- to 48-h intervals during the first 9-12 days of hypoxia. Electrode placement was according to the 10-20 International Electrode System. The VER was recorded from an electrode at the inion referred to the left ear. We found no significant changes from control cerebral electrical activity during the first 2-3 h of hypoxia. One subject's VER amplitude was greater than control on the 2nd and 3rd days of hypoxia and a similar change from control was consistently evident in a second subject beginning the 5th day of hypoxia. These changes suggest cortical depression. After the 5th day changes occurred in the remaining subjects which would be consistent with cortical excitation. In three subjects, EEG frequency was increased, amplitude decreased, and/or spiking became evident. In four subjects VER amplitude was reduced. Our findings provide support for the hypothesis that certain behavioral and physiological changes induced by sojourn at altitude could be caused by alterations in central nervous system function.

Acclimatization↗