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Biomedical subjects

A P Fishman

Publications and source records attributed to A P Fishman.

At least 109 records · Page 6Linked to original sources
PubMed1977

Normalization of the blunted ventilatory response to acute hypoxia in congenital cyanotic heart disease.

Patients with congenital cyanotic heart disease have a blunted ventilatory response to hypoxia, but the permanence of the blunting is disputed. To determine how early the blunted ventilatory response develops and whether it is reversible, we studied three groups of children and young adults: five (seven to 13 years of age) with acyanotic heart disease, eight (seven to 16) with cyanotic congenital heart disease (arterial oxygen saturation, 55 to 83 per cent), and 13 (seven to 17) whose cardiac defects were repaired (arterial oxygen saturation, 93 to 98 per cent). The ventilatory response to acute hypoxia was subnormal in the hypoxemic children in that their ventilation showed little increase when arterial oxygen saturation fell by 10 to 20 per cent, compared to a 150 to 300 per cent increase in the control subjects. This characteristic even appeared in a seven-year-old patient, indicating that the disorder occurs in early life. The appearance of blunted ventilatory response is delayed when hypoxia from birth is less severe. After operation, with return of the arterial hypoxemia to normal, the response was in the normal range. We conclude that the blunted response is reversible.

Adolescent↗
PubMed1977

Electrophysiological and anatomical observations on the heart of the African lungfish.

Electrophysiological and histological observations were made on the heart of the African lungfish. Impulse origin and propagation were studied using simultaneously recorded epicardial and pericardial electrograms. The primary pacemaker site in the lungfish was found to be at the sinus venosus at its junction with the left cardinal vein. Under a variety of circumstances, pacemaker function shifted to other sites. In response to stress, probably under vagal influence, the regular and rapid sinus venosus rate was generally superseded by an irregular and slower atrial pacemaker. Heart rate and sinoatrial and atrioventricular conduction times varied with changes in temperature [Q10=3.77, 2.55, and 5.46, respectively]. Although alterations in impulse formation and conduction did occur, the site of impulse formation and the patterns of conduction between heart chambers were usually fixed, implying the existence of an organized conduction system. Nonetheless, extensive histological study failed to disclose either organized nodal structures or specialized conduction pathways.

Africa, Central↗
PubMed1977

Analysis of lung ventilation in the aestivating lungfish Protopterus aethiopicus.

During aestivation, the breathing pattern of the lungfish changed from the usual aquatic pattern of a single breath followed by prolonged apnea to the pattern of alternating tachypnea and apnea that characterizes Cheyne-Stokes breathing. As aestivation continued, the number of breaths per tachypneic period increased gradually to reach a steady level at about the 3rd mo. During the bouts of tachypnea, minute ventilation increased because of the increase in respiratory frequency even though tidal volumes decreased. Ventilation of the lungs during aestivation appeared to involve the same mechanism as during life in water, i.e., a buccal force pump. The breathing cycle began with the aspiration of air into the mouth as the buccal cavity enlarged. Lung deflation then occurred abetted by contraction of the abdominal muscles. Lung inflation followed and involved the "swallowing" of air form the posterior buccal region into the lungs. Cycles of deflation and partial inflation of the lungs were repeated 8-40 times (tachypneic period). At the end of the tachypneic cycle, after the last deflation, a series of larger buccal force-pump maneuvers reinflated the lungs before the start of the apneic period.

Adaptation, Physiological↗
PubMed1976

Measuring the quality of medical care. A clinical method.

We outline the implementation of a new method of measuring the quality of medical care that counts cases of unnecessary disease and disability and unnecessary untimely deaths. First of all, conditions are listed in which the occurrence of a single case of disease or disability or a single untimely death would justify asking, "Why did it happen?" Secondly, we have selected conditions in which critical increases in rates of disease, disability, or untimely death could serve as indexes of the quality of care. Finally, broad categories of illness are noted in which redefinition and intensive study might reveal characteristics that could serve as indexes of health. We describe how these inth of the general population and the effects of economic, political, and other environmental factors upon it, and to evaluate the quality of medical care provided both within and without the hospital to maintain health and to prevent and treat disease.

Female↗
PubMed1976

Permeability of pulmonary vascular endothelium.

Three aspects of transendothelial exchange in the lungs are considered: stretching of interendothelial junctions of pulmonary microvessels by increase in pulmonary capillary pressures; selective stretching of interendothelial junctions of bronchial venules in response to histamine, bradykinin and endotoxin; active transport of peptides across the body of the endothelial cell after enzymic action at or near the luminal surface of the endothelial cell. Stretching of interendothelial junctions between the cells lining the pulmonary capillaries was demonstrated using a variety of macromolecular tracers under controlled haemodynamic conditions. Selective leakage of bronchial venules, the systemic venules of the lungs, was shown using colloidal carbon as a tracer. Transendothelial transport of peptides across the pulmonary capillary lining involved the use of electron microscopic autoradiography after intravenous administration of radioactively-labelled lipoproteins. Different mechanisms appear to provide routes of entry into the perivascular interstitial spaces of the lungs.

Animals↗
PubMed1976

Metabolism of 125I-labeled lipoproteins by the isolated rat lung.

The capacity of the isolated perfused rat lung to metabolize the protein moieties of serum lipoproteins was assessed using homologous (rat) and heterologous (human) plasma lipoproteins. The protein and lipid moieties of the plasma lipoproteins were labeled in vivo with Na[125I]. In selected cases the lipoprotein peptides were labeled in vivo with 14C- or 3H-labeled amino acids. Uptake of lipoprotein label during perfusion was monitored by measure of losses in perfusate label and by rises in pulmonary tissue labeling as shown by radioassay and by light and electron microscope radioautography. Lipoprotein degradation was assessed by fractionation of perfusate and lung tissue radioactive material into trichloroacetic acid (TCA)-isoluble, TCA-soluble, and ether-ethanol-soluble fractions. When heparin was included in the perfusion medium, there was selective degradation of the protein portion of very low density lipoprotein (VLDL) in the perfusate and concomitant uptake of radioactive label by the lungs. Low density lipoprotein (LDL)) was neither taken up nor catabolized by the isolated rat lung in the absence or presence of heparin. By light and electron microscopy, the label was localized over the interalveolar septa, predominantly the capillary endothelium. Disappearance of TCA-insoluble radioactivity from the perfusate was associated with the generation of both TCA-soluble iodide and noniodide radioactivity. Greater than 50% of the radioactive label taken up by the lungs was found in the delipidated TCA-insoluble fraction. This study provides in vitro evidence for pulmonary catabolism of VLDL apolipoproteins and uptake of peptide catabolic products of VLDL by the lung.

Animals↗
PubMed1976

Electromyographic response of respiratory muscles during elastic loading.

The response of respiratory motor neurons to graded elastic loading was assessed in anesthetized dogs by recording the electromyogram (EMG) from the diaphragm (ED) and the intercostal muscle (EIC). Elastic loads were applied for 1-20 breaths. The effects of changes in PCO2 on respiratory motor neuron output was assessed by applying loads during the course of CO2 rebreathing. On the first loaded breath, ED and EIC increased reflexly due chiefly to prolongation of inspiration. Vagotomy or vagal cooling to block the Hering-Breuer reflex eliminated the increase in ED and diminished the increase in EIC. During the second to fifth breath, the level of EMG activity was disproportionately high for the level of PCO2, suggesting an additional reflex component over and above the reflex activity present on the first loaded breath.

Animals↗
PubMed1976

Effects of hypercapnia on mouth pressure during airway occlusion in conscious man.

The effects of hypercapnia and inspiratory flow-resistive loading on mouth pressure during periods of arrested airflow were studied in conscious human subjects to determine the usefulness of inspiratory muscle force in the assessment of respiratory neural efferent activity. Hypercapnia increased the peak end-inspiratory mouth pressure (Ppeak) during complete airway occlusion and the pressures at 100, 200, and 300 ms after the onset of inspiration (P100, P200, P300). During rebreathing without added mechanical loads, P100 and Ppeak increased linearly with the electrical activity of the diaphragm and changes in P100 and Ppeak during hypercapnia correlated well with ventilatory responses to PCO2 (DELTA V/DELTA PCO2) suggesting that occluded mouth pressures are reliable measures of respiratory activity. In individuals with the greatest reduction in delta V/DELTA PCO2 during inspiratory flow-resistive loading, changes in P100 and Ppeak with PCO2 increased only minimally. In contrast, there was a much greater increase in occluded mouth pressures with hypercapnia in the presence of mechanical loading when inspiratory flow-resistive loading failed to depress delta V/DELTA PCO2. In all subjects, occluded mouth pressures were greater at any given PCO2 during mechanical loading than during free breathing. Mechanical loading resulted in augmented respiratory neural efferent activity unexplained by alterations in chemical stimulation.

Adult↗
PubMed1976

Effects of hypercapnia and flow-resistive loading on tracheal pressure during airway occlusion.

To determine whether the isometric force of concentration of the inspiratory muscles could be used to assess respiratory efferent neural activity, the tracheal pressure generated by the inspiratory muscles during airway occlusion (occluded tracheal pressure) was measured during progressive hypercapnia in anesthetized dogs breathing normally and breathing against added flow-resistive loads. Hypercapnia increased the peak end-inspiratory tracheal pressure and the occluded tracheal pressures generated 100, 200, and 300 ms after the onset of inspiration. The duration of the occluded inspiratory effort generally remained unchanged and the configuration of the pressure tracing was not affected. During normal breathing occluded tracheal pressures increased linearly with tidal volume and with the electrical activity of the diaphragm and the external intercostal muscles both before and after vagotomy. Inspiratory flow-resistive loading reduced the ventilatory response to CO2 but did not affect occluded tracheal pressures at any given PCO2 or the change in pressures with hypercapnia both before and after vagotomy. Similarly, expiratory flow-resistive loading failed to affect occluded tracheal pressures. These results suggest that occluded tracheal pressures measure respiratory efferent neural activity and can be used as indices of CO2 responsivity even during mechanical loading in anesthetized animals.

Airway Obstruction↗
PubMed1976

Effect of hypoxia on the pressure developed by inspiratory muscles during airway occlusion.

The effect of progressive isocapnic hypoxia on the pressure generated by the inspiratory muscle during airway occlusion was studied in 10 awake subjects during normal and obstructed breathing. Isocapnic hypoxia was produced by rebreathing a gas mixture of 6% CO2 in air while the expired gas was passed through a CO2 scrubber so as to maintain PACO2 constant (42.6 mmHg +/- 2.2 SE). Occlusion of the airway was performed randomly for a single breath at FRC. In all 10 subjects maximal pressure (Ppeak) and the pressures measured 100, 200, 300, and 400 ms after the onset of inspiration increased during hypoxia. Furthermore, good correlation was noted between the occlusion pressure response to hypoxia (delta P/DELTA[1/PO2-32]) and simultaneous changes in ventilatory response to hypoxia (delta VI/DELTA[1/PO2-32]). The occlusion pressure response to hypoxia therefore seems to be a reliable measure of respiratory center output. When rebreathing was repeated during inspiratory resistive loading, the occlusion pressure at any given PO2 and delta P/DELTA(1PO2-32) measured in the first 400 ms of inspiration increased in 9 of 10 subjects. Since PACO2 and PAO2 during both control and loaded experiments were the same, the increase in occlusion pressure in the presence of flow-resistive loading appeared to represent a neurally mediated increase in inspiratory motoneuron activity.

Adult↗
PubMed1976

Control of breathing in uremia: ventilatory response to CO2 after hemodialysis.

The mechanisms responsible for the transient respiratory alkalosis which follows clinical hemodialysis were evaluated by studying the ventilatory response to carbon dioxide in chronic uremic patients, and in unanesthetized normal and chronic uremic goats. A significant increase in sensitivity to CO2 was found in acidotic uremic patients immediately (within 30 min) following hemodialysis (P less than 0.01). Sensitivity to CO2 returned to the predialysis value within 24 h. Lung volume and maximal breathing capacity were unchanged. A similar increase in sensitivity to CO2 was seen in nonacidotic uremic goats following hemodialysis. In the goats, these changes in sensitivity could not be explained by changes in cerebrospinal fluid acid-base status. Adding sufficient urea to the dialysate to prevent a fall in plasma urea concentration, eliminated this increase in sensitivity to CO2 in both uremic patients and goats. These results suggests that the transient respiratory alkalosis following hemodialysis is due to an increase in the sensitivity of the ventilatory response to carbon dioxide and is a consequence of dialysis-induced osmotic disequilibrium.

Adolescent↗