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Biomedical subjects

A P Fishman

Publications and source records attributed to A P Fishman.

At least 127 records · Page 7Linked to original sources
PubMed1975

Abnormal breathing patterns.

In health, breathing is regular and the respiratory rate is sufficiency constant to be useful as a vital sign of health and disease. This regularity depends on a complex interplay of chemical and neural control systems that operate automatically to reset the rate and depth of breathing as changes occur in posture and activity, to adjust the level of ventilation so that changes in gas tensions and pH in the blood and in the brain intersitial fluid are exceedingly modest despite wide swings in metabolic rate and in environmental conditions, and to coordinate ventilation and circulation so that the requirements of individual tissues for O2 delivery and CO2 removal are satisfied. Two broad categories of disorders can result from malfunction of these systems (Table 1): (1) disproportionate ventilation (too high or too low) for the level of metabolic activity, thereby producing severe abnormalities in blood gas tensions or in acid-base balance, and (2) an irregular breathing pattern without eliciting gross changes in blood gas tensions or in acid-base balance. Because of the complexity of the control system, each of these categories represents a final common pathway that can be produced in different ways. In this presentation, we will attempt to describe the general features that characterize the operation of the control system and some new technics that make it possible to trouble-shoot the malfunctioning system in order to identify the mechanism(s) responsible for the abnormality in breathing pattern.

Animals↗
PubMed1975

Hemodynamic consequences of delayed ventriculoconal conduction in the frog Rana catesbeiana.

We investigated the function of the conus arteriosus in the bullfrog Rana catesbeiana using a combination of anatomical and physiological techniques. Although there is a normal delay in ventriculoconal conduction and we could induce a spectrum of ventriculoconal conduction disturbances by manipulating the region of the ventriculoconal junction, we found no histological evidence of specialized conducting myocardial tissue in this region. The performance of the conus arteriosus was explored during various disturbances of ventriculoconal conduction and also during hemodynamic disturbances produced by hemorrhage and afterloading. The conus was found to contribute little to forward flow under ordinary circumstances, but its contribution increased greatly during bleeding or partial occlusion of the truncus. In contrast to the conclusion of others, no evidence could be adduced to support the idea that the conus serves as a depulsating chamber. Disparities in previous reports concerning the operation of the conus as a booster pump are attributed to special experimental circumstances.

Animals↗
PubMed1975

Effects of mechanical loading and hypercapnia on inspiratory muscle EMG.

The electromyograms of the diaphragm and an external intercostal muscle were analyzed to see if the effects of hypercapnia on inspiratory muscle electrical activity could be distinguished from those of mechanical loading and to determine whether changes in inspiratory muscle electrical activity were a sueful measure of CO2 response during mechanical loading. Anesthetized dogs were studied: 1) during progressive hypercapnia without mechanical loading, 2) during flow-resistive and elastic loading at constant PCO2, and 3) during progressive hypercapnia and mechanical loading. Both mechanical loading and hypercapnia increased total inspiratory diaphragmatic and intercostal muscle electrical activity. However, inspiratory duration was increased by mechanical loads but reduced by hypercapnia. Because of these changes in inspiratory duration, the average rate of diaphragmatic electrical activity remained unaffected by mechanical loading before and after vagotomy but was increased by hypercapnia. In contrast, both hypercapnia and mechanical loading increased the average rate of intercostal muscle electrical activity. There was a greater increase in both total and average rate of intercostal muscle electrical activity during hypercapnia in the presence of mechanical loading than during unloaded breathing. However, the change in total and average rate of diaphragmatic electrical activity with PCO2 was unaffected by added mechanical loads. These results suggest that diaphragmatic but not intercostal muscle electrical activity can be used as an index of CO2 response even during mechanical loading.

Airway Resistance↗
PubMed1975

Changes in strength of lung inflation reflex during prolonged inflation.

Recovery from respiratory inhibition produced by the lung inflation reflex was studied in anesthetized dogs, paralyzed and ventilated with a respiratory pump. During constant ventilation the lungs were periodically inflated using positive end-expiratory pressure, while the respiratory motor output was monitored in the phrenic nerve. Inhibition of the phrenic discharge was followed by gradual recovery throughout 8-min inflation periods despite constant blood gases. Recording afferent potentials in a vagus nerve indicated that adaptation of pulmonary stretch receptors contributed to the initial recovery of the phrenic discharge, but this recovery continued after the receptor discharge had stabilized. The phrenic discharge also recovered after initial inhibition in two situations which avoided stretch receptor adaptation: a) when the stretch receptor discharge from the separate lungs was alternated in an overlapping manner by asynchronous pulmonary ventilation, and b) during continuous electrical stimulation of a vagus nerve. Phrenic activity was temporarily increased above its control value after periods of lung inflation, asynchronous ventilation and vagal stimulation. It is concluded that the lung inflation reflex gradually attenuates during prolonged stimulation due to both stretch receptor adaptation and changes within the central pathways.

Adaptation, Physiological↗
PubMed1975

The effect of anemia on the ventilatory response to transient and steady-state hypoxia.

The effects of anemia upon the ventilatory responses to transient and steady-state hypoxia were studied in unanesthetized goats. Responses to transient hypoxia (inhalation of several breaths of nitrogen) were considered to reflect peripheral chemoreceptor and non-chemoreceptor influences of hypoxia upon ventilatory control. In all goats, severe anemia (hemoglobin 3.1-4.8 g/100ml) markedly heightened the responses to transient hypoxia (from a mean of 0.27 to a mean of 0.75 liter/min/percent fall in SaO2). This phenomenon was substantially reversed by alpha-adrenergic blockade (phenoxybenzamine, 5 mg/kg). In contrast, the ventilatory responses to steady-state hypoxia were unaffected by severe anemia. These data suggest that severe anemia enhances the peripheral chemoreceptor-mediated response to hypoxia through a mechanism involving the alpha-adrenergic system. It also appears that a ventilatory depressant effect of hypoxia which is not mediated by the peripheral chemoreceptors is also enhanced by severe anemia, thereby preventing an increase in the steady-state ventilatory response to hypoxia. Finally, experiments involving variation in oxygen affinity of hemoglobin suggested that O2 tension rather than O2 availability in arterial blood is the major determinant of peripheral chemoreceptor activity.

Administration, Intranasal↗
PubMed1974

Bronchial venular leakage during endotoxin shock.

The pulmonary effects of endotoxin shock were investigated in dogs by a combination of anatomic and physiologic technics. Shock was produced in 14 dogs by injecting Escherichia coli lipopolysaccharide intravenously. Three dogs in hypovolemic shock and 6 untreated dogs served as controls. Colloidal carbon was injected intravenously to detect sites of pathologic increase in vascular permeability. During the first hour of endotoxin shock, bronchial venules allowed carbon and blood elements to traverse their walls, whereas no leakage of these large particles or ultrastructural changes could be detected in the alveolar walls. Only after the first hour was bronchial venular leakage accompanied by focal degenerative changes in the alveolar endothelium, focal interstitial edema in the alveolar septum and sequestration of damaged leukocytes in the alveolar capillaries. In contrast to these observations in endotoxin shock, control dogs in hypovolemic shock did not show bronchial venous leakage. Our findings suggest that the leakage of bronchial venules may be involved in the pathogenesis of pulmonary interstitial edema caused by endotoxin shock.

Animals↗