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Biomedical subjects

A P Fishman

Publications and source records attributed to A P Fishman.

At least 163 records · Page 9Linked to original sources
PubMed1970

The effects of abnormal sympathetic nervous function upon the ventilatory response to hypoxia.

THE VENTILATORY RESPONSE TO HYPOXIA WAS STUDIED IN TWO GROUPS OF SUBJECTS WITH ABNORMAL SYMPATHETIC NERVOUS CONTROL: (a) human subjects with familial dysautonomia (Riley-Day syndrome), and (b) unanesthetized goats treated with an alpha-adrenergic blocking agent (phenoxybenzamine). The ventilatory response to hypoxia was evaluated in two ways: (a) from the slope of the relationship between ventilation and alveolar P(Co2) ([unk]V(E)-P(ACo2) slope) during the rebreathing of hypoxic and hyperoxic gases, and (b) from the change in ventilation produced when hypoxia was abruptly relieved. The ventilatory and circulatory responses of the unanesthetized, phenoxybenzamine-treated goats were qualitatively similar to those of dysautonomic patients. In contrast to the sustained stimulation of ventilation produced by hypoxia in normal subjects, hypoxia either did not change, or decreased, the [unk]V(E)-P(ACo2) slope of dysautonomic patients and phenoxybenzamine-treated goats; CO(2)-free hypoxia produced a fleeting hyperventilation, which was followed by apnea when hypoxia was abruptly relieved. Unlike normal subjects, the dysautonomic patients and phenoxybenzamine-treated goats became hypotensive while hypoxic. The results indicate that peripheral chemoreceptor reflex responses to hypoxia are preserved in subjects in whom sympathetic nervous responses are impaired. However, the central nervous depression of ventilation by hypoxia is enhanced simultaneously. The inordinate central depression is attributed to the inability of the dysautonomic subjects and goats to maintain systemic blood pressure and, consequently, cerebral blood flow during hypoxia, thereby aggrevating central nervous hypoxia.

Animals↗
PubMed1969

Hemoglobin as a tracer in hemodynamic pulmonary edema.

Stroma-free hemoglobin is an electron-opaque molecule useful as a tracer for the ultrastructural stuty of pulmonary capillary permeability. After this tracer was infused into the isolated pulmonary lobe of the dog, the endothelial junctions of the capillaries, as revealed by electron microscopy, act like distensible pores, thus allowing the tracer to escape when the pulmonary artery pressure was raised above 50 millimeters of mercury.

Animals↗
PubMed1969

Traube-Hering waves in the pulmonary circulation of the dog.

Although the pulmonary blood vessels receive an ample supply of nerves, it has been difficult to prove that these nerves operate in the regulation of the pulmonary circulation. In the present study, using the isolated lobe of the lung perfused in situ, waves in pulmonary arterial pressure were induced and were shown, as in the case of Traube-Hering waves in the systemic circulation, to be nervous in origin.

Animals↗
PubMed1968

The release of a bradykinin-like pulmonary vasodilator substance in foetal and new-born lambs.

1. Exposure to glass of whole blood from anaesthetized foetal lambs (at 0.6-0.95 of term) causes the rapid development of a potent pulmonary vasodilator agent.2. The formation of the vasodilator agent on exposure to glass, its disappearance with time, and the inhibition of its production by soya bean trypsin inhibitor, suggest that it is bradykinin.3. Small doses of bradykinin ( approximately 1 ng/kg) cause pulmonary vasodilatation on close arterial injection. Neither this, nor the vasodilatation caused by glass-exposed whole blood, are affected by agents which block the vasodilator actions of acetylcholine, isoprenaline or histamine.4. Exposure of foetal plasma and/or red cells to glass rarely caused the development of a pulmonary vasodilator agent. Maternal plasma was always active. Injection of the buffy coat from foetal blood caused pulmonary vasodilatation.5. The capacity of plasma from sheep at different ages to produce kinin(s) was examined by assay on the isolated rat's uterus. In the foetus activity was very low; it increased with age.6. In adolescent lambs 5-14 weeks after birth injection of approximately 10 ng/kg bradykinin into the pulmonary artery caused only a trifling vasodilatation; this was greater when pulmonary vasoconstriction was induced by lung collapse, hypoxaemia and hypercapnia.7. The possible physiological consequences of these findings are discussed.

Aging↗
PubMed1968

Respiratory adjustment to chronic metabolic alkalosis in man.

This study examined the ventilatory adjustment to chronic metabolic alkalosis induced under controlled conditions in normal human volunteers. Metabolic alkalosis induced by buffers (sodium bicarbonate, trishydroxymethylamine methane) or ethacrynic acid was associated with alveolar hypoventilation, as evidenced by a rise in arterial Pco(2), a fall in arterial Po(2), a reduced resting tidal volume, and a diminished ventilatory response to CO(2) inhalation. Alveolar hypoventilation did not occur when metabolic alkalosis was induced in the same subjects by thiazide diuretics or aldosterone despite comparable elevations of the arterial blood pH and bicarbonate concentration.The different ventilatory responses of the two groups could not be ascribed to differences among individuals comprising each group, pharmacological effects of the alkalinizing agents, differences in the composition of the lumber spinal fluid, changes in extracellular fluid volume, or sodium and chloride balance.The differences in ventilatory adjustments were associated with differences in the patterns of hydrogen and potassium ion balance during the induction of alkalosis. Alveolar hypoventilation occurred when hydrogen ions were buffered (sodium bicarbonate, trishydroxymethylamine methane) or when renal hydrogen ion excretion was increased (ethacrynic acid). Alveolar hypoventilation did not occur when induction of similar degrees of extracellular alkalosis was accompanied by marked potassium loss and no demonstrable increase in external hydrogen loss (thiazides and aldosterone).These observations suggest that respiratory depression does not necessarily accompany extracellular alkalosis but depends on the effect of the mode of induction of the alkalosis on the tissues involved in the control of ventilation.

Journal Article↗