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Biomedical subjects

K Wasserman

Publications and source records attributed to K Wasserman.

At least 235 records · Page 13Linked to original sources
PubMed1976

Role of the carotid bodies in the heart rate response to breath holding in man.

To investigate the role of the carotid bodies in regulating the bradycardia of breath holding in man, we studied heart rate (HR) responses to prolonged breath holding (BH) in five asymptomatic asthmatic patients whose carotid bodies had been resected (CBR). Seven normal subjects served as controls. BH experiments were randomly initiated with single breaths of 100%, 21%, or 12% 92. During BH with 21% O2, normal subjects displayed the typical bradycardia; this response, however, was attenuated with the other O2 concentrations. In contrast, the CBR subjects manifested BH tachycardia which was inversely proportional to the O2 tension. HR increased in be CBR group by 5%, 31%, and 45% during BH with 100%, 21%, and 12% O2, respectively. These results demonstrate that the bradycardia of BH in normal man is under the influence of the carotid bodies. During BH and in the absence of carotid bodies, an O2 tension-dependent tachycardia is unveiled.

Adult↗
PubMed1976

Effect of beta-adrenergic blockade during exercise on ventilation and gas exchange.

The ventilatory effects of beta-adrenergic blockade during steady-state exercise were studied in eight normal subjects using intravenous propranolol hydrochloride (0.2 mg/kg). Heart rate decreased in all subjects by an average of 17%. Coincident with the phase of decreasing heart rate was a significant decrease in both minute ventilation (VE) and CO2 output (VCO2), averaging 9.6 and 9.2%, respectively. Both functions returned to prepropranolol levels after heart rate had reached its reduced steady-state value. The change in VE was significantly correlated with the change in VCO2 (r = 0.85, P less than 0.005), and was associated with negligible changes in endtidal CO2 tensions and ventilatory equivalents for CO2. We interpret these studies as showing that the transient isocapnic hypopnea concomitant with an acute reduction in cardiac output was secondary to a transient decrease in CO2 flux (cardiac output x mixed venous CO2 content). This decrease in VE appears to be induced by the acute decrease in cardiac output ("cardiodynamic hypopnea"), in fashion similar to the previously described cardiodynamic hyperpnea.

Adolescent↗
PubMed1975

A sinusoidal load generator for use in cycle ergometry.

We have modified an electromagnetically braked cycle ergometer to provide a sinusoidally varying work load. This was accomplished by applying a low-frequency sinusoidal voltage at the inputs of the electromagnets using a sinusoidal potentiometer, whose shaft was driven by a variable-speed motor, and a voltage-programmable power supply to amplify the signal. The frequency range is currently 0.0017-0.3 Hz. This technique for sinusoidal work loads allow the period, amplitude, and mean position to be easily changed from a console, even during a test if required.

Electronics↗
PubMed1975

Regulation of arterial PCO2 during intravenous CO2 loading.

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by "conventional" airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite "sensitivity" when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.

Animals↗
PubMed1975

Effect of carotid body resection on ventilatory and acid-base control during exercise.

To investigate the role of the carotid bodies in exercise hyperpnea and acid-base control, normal and carotid body-resected subjects (CBR) were studied during constant-load and incremental exercise. There was no significant difference in the first-breath ventilatory responses to exercise between the groups; some subjects in each reproducibly exhibited abrupt responses. The subsequent change in Ve toward steady state was slower in the CBR group. The steady-state ventilatory responses were the same in both groups at work rates below the anaerobic threshold (AT). However, above the AT, the hyperpnea was less marked in the CBR group. Ve and acid-base measurements revealed that the CBR group failed to hyperventilate in response to the metabolic acidosis of either constant-load or incremental exercise. We conclude that the carotid bodies 1) are not responsible for the initial exercise hyperpnea, 2) do affect the time course of Ve to its steady state, and 3) are responsible for the respiratory compensation for the metabolic acidosis of exercise.

Acid-Base Equilibrium↗
PubMed1975

Advances in the treatment of pulmonary alveolar proteinosis.

Our currecnt technique for lung lavage is described. This technique can be safely and effectively applied to patients with pulmonary alvelar proteinosis who require therapy. Normal saline alone is as effective a solution as one containing heparin and acetylcysteine. Chest percussion during lung lavage considerably enhances the yeild of each lavage and thus shortens the time required for the procedure. Lung lavage results in remarkable clearing of the chest roentgenogram and reversal of the physiologic defects and symptoms of the patient by the following day. In our experience this improvement lasts for at least one year.

Acetylcysteine↗
PubMed1975

Diffusing capacity, specific diffusing capacity and interpretation of diffusion defects.

Six pathophysiologic mechanisms of a reduced single breath CO diffusing capacity are discussed and the usefulness of relating carbon monoxide (CO) uptake to the functioning alveolar volume (DL/VA, specific diffusing capacity) is illustrated for several pulmonary diseases. In patients with emphysema and pulmonary emboli (pulmonary vascular occlusive disease), reduced CO uptake is associated with significantly reduced DL/VA and is compatible with reduction of pulmonary capillary bed. In patients with pulmonary alveolar proteinosis, improvement in CO uptake and DL/VA follows lung lavage and suggests that lung units partially filled with proteinaceous material are responsible for hypoxemia, reduced CO uptake and reduced DL/VA. In most cases of radiation fibrosis, sarcoidosis and miscellaneous interstitial fibrosis, reduced CO uptake is associated with a normal DL/VA and suggests that loss of alveolar units, both capillaries and alveoli, has occurred. New regression equations for DL and DL/VA are established for children and adults. DL/VA is linearly related to height and independent of age and sex, while different predictive equations must be used for DL for the 5 through 17 and 18 through 76 age groups. The new regression equations for DL show better correlation in adults we studied over 50 years of age than previous regression equations which use a constant reduction of 2 to 3 ml CO per minute per mm of mercury for each 10 years of adult aging.

Adolescent↗