Biomedical subjects

J V Weil

Publications and source records attributed to J V Weil.

At least 127 records · Page 7Linked to original sources

PubMed1975

Ventilatory control in myxedema and hypothyroidism.

Alveolar hypoventilation is known to occur in myxedema. To clarify the role of hypoxic ventilatory drive and hypercapnic ventilatory drive in thyroid hormone insufficiency states, 10 patients with myxedema and seven with hypothyroidism (thyroid ablation) were studied before and after thyroid replacement. An index developed for hypoxic ventilatory drive was markedly reduced in myxedema: 17 plus or minus 4.7 (S.E.M.) (normal, 126 plus or minus 8.7) (P smaller than 0.01) and increased to 78 plus or minus 12.6 (p = 0.02) with thyroid hormone replacement. In the hypothyroid group this index was also depressed as compared to normal at 67 plus or minus 20 (p smaller than 0.01) and increased to 114 plus or minus 19 (p smaller than 0.02) with replacement. An index for hypercapnic ventilatory drive was depressed in myxedema, 0.69 plus or minus 0.01), but was not significantly depressed in hypothyroidism. With thyroid hormone replacement this index did not significantly increase in either group. We conclude that both myxedema and hypothyroid states produce depression of hypoxic ventilatory drive that is responsive to replacement therapy. This alteration in ventilatory control may contribute to the hypoventilation seen in myxedema.

Adult↗

PubMed1975

Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome.

Most patients with extreme obesity do not exhibit alveolar hypoventilation, but an intriguing minority do. The mechanism(s) of this phenomenon remain unknown. A disorder in ventilatory control has been suggested as a major factor in the pathogenesis of the obesity-hypoventilation syndrome. Accordingly, hypoxic and hypercapnic ventilatory drives were measured in 10 patients with the typical symptoms of the syndrome: obesity, hypersomnolence, hypercapnia, hypoxemia, polycythemia and cor pulmonale. Hypoxic ventilatory drive, measured as the shape parameter A, averaged 21.9 +/- 5.35, approximately one-sixth that in normal controls, A = 126 +/- 8.6 (P less than 0.01). The ventilatory response to hypercapnia also was markedly reduced, the slope of the response averaging 0.51 +/- 0.005, or about one-third the normal value of 1.83 +/- 0.13 (P less than 0.01). This decreased responsiveness in hypoxic and hypercapnic ventilatory drive was consistent throughout the group. The depression in ventilatory drive found in the obesity-hypoventilation syndrome may be causally related to the alveolar hypoventilation manifested by these patients.

Adult↗

PubMed1975

Sleep physiology at high altitude.

All night sleep EEG, EKG, and respiration were recorded from six young men during 2 nights at sea level and 4 nonconsecutive nights at high altitude (14.110 ft., 4301 m). Sleep at high altitude was chraacterized initially by a significant decrease in Stages 3 and 4, a significant increase in the number of arousals, and a trend towards more time spent awake. In terms of actual time spent sleep, however, a relatively good night's sleep was obtained, which suggests that the objective sleep disturbance was not commensurate with the marked subjective complaints of sleeplessness. Periodic respiration during sleep was frequent at high altitude, was quickly terminated by oxygen administration, was not clearly related to the increased number of arousals, and usually was not seen during REM periods. Heart rate was increased during sleep at high altitude. All measures tended to return towards sea level means during 12 days at altitude. We suggest that the marked increase in the number of arousals may account for the disparity between the subjective reports and objective measures of sleep disturbance at high altitude. Although the objective sleep disruption is probably related in some fashion to hypoxemia, it is unclear whether hypoxemia itself or the alkalosis commonly present shortly after arrival at altitude is the major factor.

Adult↗

PubMed1975

Effect of ethanol on the ventilatory responses to oxygen and carbon dioxide in man.

1. Hypoxic and hypercapnic ventilatory drives were measured in eight healthy male subjects before and after ingestion of ethanol, in a dose of 17 mmol/kg body weight. 2. A significant decrease in hypoxic ventilatory drive was observed at 20 min after ethanol (P less than 0.05). A significant depression in hypercapnic drive was observed at 70 min after indigestion of ethanol (P less than 0.05). The mean peak blood ethanol (24mmol/1) occurred at 20 min, at which time the lowest mean hypoxic drive was recorded. 3. Ethanol in moderate doses produced a depression of both hypoxic and hypercapnic ventilatory drives in normal subjects. This suggests that ethanol may play a role in the precipitation of acute respiratory failure in certain patients in whom the ventilatory drive is already impaired, as in chronic airways obstruction.

Carbon Dioxide↗

PubMed1975

Effect of pentobarbitone on hypoxic ventilatory drive in man: Preliminary study.

The effect of an intramuscular injection of pentobarbitone 2 mg/kg on the hypoxic ventilatory drive was measured in 10 volunteers. Five subjects showed significant depression of the ventilatory response to hypoxia 30 min after administration. This depression persisted for 90 min. The other five subjects showed no change from control responses. The two groups appeared to differ in their levels of physical fitness as measured by differences in resting heart rate and maximal oxygen uptake.

Adult↗

PubMed1975

Hypoxic ventilatory drive in dogs during thiopental, ketamine, or pentobarbital anesthesia.

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in seven chronically tracheostomized dogs awake and during anesthesia with pentobarbital (30 mg/kg, iv), ketamine, or thiopental (10 and 15 mg/kg, respectively, followed by infusion). Isocapnic hypoxic ventilatory drive (HVD) was expressed as the parameter A such that the higher the A, the greater the hypoxic drive. HVD(A) was significantly reduced from 259 +/- 28 (mean +/- SEM) in awake dogs, to 96 +/- 14 after pentobarbital, 161 +/- 27 after thiopental, and 213 +/- 23 after ketamine. Hypercapnic ventilatory drive (HCVD) as measured by S (slope of the VE-PACO2 response curve) was significantly reduced from 1.3 +/- .32 in awake dogs to 0.4 +/- .13 after pentobarbital, 0.5 +/- .12 after thiopental, and 0.6 +/- .11 after ketamine. In addition, hypercapnia-induced augmentation of hypoxic drive was markedly diminished by the two barbiturates but was unaffected by ketamine. Therefore, ketamine at this dose level afforded greater protection during exposure to hypoxia than did barbiturates. (Key words: Ventilation, hypoxic response; Hypoxia, ventilation; Oxygen, ventilatory response; Carbon dioxide, ventilatory response; Anesthetics, intravenous, ketamine; Anesthetics, intravenous, thiopental; Hypnotics, barbiturates, pentobarbital.)

Anesthesia, Intravenous↗

PubMed1975

Hypoxic ventilatory depression in dogs.

It is well known that hypoxia, acting mainly through peripheral chemoreceptors, is an important ventilatory stimulus. It is also known that under certain circumstances hypoxia can lead to ventilatory depression, perhaps through its effect on the central nervous system. This study, utilizing dogs, was carried out to determine the degree of hypoxia required to produce ventilatory depression and to study the effects of chloralose anesthesia, variations in blood carbon dioxide tension, and peripheral chemoreceptor denervation on hypoxic ventilatory depression. In the awake, intact dog, ventilatory depression did not occur until the Pao2 = 18.6 plus or minus 0.8 mmHg (SEM). This value was not significantly different from that observed in chloralose anesthetized dogs, Pao2 = 18.7 plus or minus 0.43 mmHg. Hyper- and hypocapnia had no significant effect on the Pao2 at which ventilatory depression occurred. Denervation of either aortic or carotid chemoreceptors produced a very small change in the Pao2 of ventilatory depression, increasing it from 18.6 plus or minus 0.58 to 20.8 plus or minus 0.93 mmHg. Denervation of both aortic and carotid chemoreceptors produced a further small increase (Pao2 = 21.8 plus or minus 0.76 mm Hg). In peripheral chemoreceptor-denervated animals, hypoxia produced no significant change in ventilation until the ventilatory depression point was reached. These studies indicate that in the dog hypoxic ventilatory depression occurs only during severe hypoxia and ventilatory depression occurs only during severe hypoxia and is uninfluenced by chloralose anesthesia, hyper- or hypocapnia, and only slightly affected by chemoreceptor denervation.

Anesthesia, Inhalation↗

PubMed1975

Normal values for hypoxic and hypercapnic ventilaroty drives in man.

To better determine the range of normal values of hypoxic and hypercapni ventilatroy drives in man, these drives were measured in 40 males and 4 females between 21 and 51 yr of age. The average hypoxic drive, expressed as parameter A, was 186 plus or minus 12.8 (SEM). The average hypercapnic drive, expressed as the slope S, was 2.69 plus or minus 0.19. The range of values for these individuals was large and could not be accounted for by variations in maximal oxygen uptake, age, or sex. However, positive correlations were found between these drives and height and weight, and a positive correlation was found between hypoxic and hypercapnic drive.

Adult↗

PubMed1975

Depression of hypoxic and hypercapnic ventilatory drives in severe asthma.

Because of the previous finding of an attenuated hypoxic ventilatory drive in a teenager with severe asthma, the ventilatory responses to hypoxia and hypercapnia were examined during remission in 16 patients with the history of severe asthma. Spirometric and body plethysmographic pulmonary functions were normal or nearly normal just prior to ventilatory drive testing. The ventilatory responses to progressive isocapnic hypoxia and to hyperoxic hypercapnia were studied. Both hypoxic and hypercapnic drives were significantly depressed in the asthmatic patients. Factors known to blunt the ventilatory drives were not present in this group of patients. Hence, the etiology of these changes is unclear. In some patients, these depressed respiratory drives might contribute to hypoventilation, to severe hypoxemia, and to respiratory failure during severe asthma.

Adolescent↗

PubMed1975

Symptomatic and puomonary response to acute phlebotomy in secondary polycythemia.

A double-blind study of the effects of phlebotomy was carried out in 18 patients with polycythemia secondary to severe hypoxemic lung disease. Eleven subjects underwent a single phlebotomy of 10 percent of their blood volume, and eight patients serving as controls underwent a sham procedure. Eight of the phlebotomized subjects, but none of the controls, reported subjective clinical improvement (P less than 0.005). Subjects who noted improvement after venesection had higher hematocrit readings than those who did not (P less than 0.02). Symptomatic relief seemed to be most dramatic in those with clinical evidence of congestive heart failure. In contrast to this clear-cut subjective improvement, phlebotomy did not alter objective indices of airway obstruction, lung elastic recoil, pulmonary gas exchange, or exercise tolerance in either the phlebotomized or the control group. Thus, although phlebotomy produced subjective benefit in the majority of patients studied, it was not associated with objective improvement in lung function or exercise tolerance.

Adult↗

PubMed1975

Progesterone for outpatient treatment of Pickwickian syndrome.

Ten patients with the Pickwickian syndrome, characterized by obesity, hypoxemia, hypercapnia, polycythemia, and cor pulmonale, underwent long-term treatment as outpatients with medroxyprogesterone acetate. Although there was no significant weight change in the group, PaO2 rose 12.6 +/- 2.7 mm Hg (SEM) from 49 +/- 2.6 mm Hg to 62 +/- 2.3 mm Hg (P less than 0.001), while PaCO2 fell 13 +/- 2.6 mm Hg from 51 +/- 1.9 mm Hg to 38 +/- 1.2 mm Hg (P less than 0.001). Hematocrit fell from 56 +/- 2.5% to 50 +/- 1.2%, a mean fall of 6% (P less than 0.01), during medroxyprogesterone acetate therapy. In the 2 patients who had cardiac catheterization before and during medroxyprogesterone acetate therapy, mean pulmonary arterial pressure fell 13 and 19 mm Hg. There were no recurrences of cor pulmonale during treatment. These effects on arterial blood gas values and clinical state were sustained during therapy. On withdrawal of medroxyprogesterone acetate during 1-month period, arterial oxygen and carbon dioxide tensions deteriorated to their previous pretreatment values. Reinstitution of medroxyprogesterone acetate caused improvement in both the oxygen and carbon dioxide tensions. We conclude that sublingual medroxyprogesterone acetate therapy is useful in the management of the Pickwickian syndrome.

Adult↗

PubMed1975