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Biomedical subjects

J A Dempsey

Publications and source records attributed to J A Dempsey.

At least 19 recordsLinked to original sources
PubMed1979

Hodgkin's disease: evaluation of staging procedures for abdominal involvement.

Results of preoperative assessment procedures and subsequent staging laparotomy are evaluated in 32 consecutive patients who presented with extra-abdominal Hodgkin's disease which was not already known to be in an advanced stage. Disease was found in the abdominal cavity of 10 of the 27 patients who presented with disease above the diaphragm, and of two of the five patients in whom disease presented in the inguinal nodes. In patients who initially presented with disease above the diaphragm, the spleen was involved in all 10 cases where abdominal disease was detected. Lymphography was not found to be reliable as a diagnostic aid in doubtful cases. Neither liver nor spleen scans were found to be helpful in assessment of these patients.

Abdominal Neoplasms↗
PubMed1979

Human pulmonary resistance: effect of frequency and gas physical properties.

We have investigated a new technique that could be specific for detecting small airway diseases. We measured resistance in nine subjects, evaluating the effect of breathing 80% He-20%O2, air, and 80% SF6-20% O2 at different flow rates (0.25--1.01 l/s) and frequencies (4--12 Hz). To test the sensitivity and specificity of this new technique, we used intravenous histamine infusion to cause peripheral constriction. During histamine infusion six of nine subjects showed the following changes: 1) dynamic compliance decreased; 2) subjects developed frequency dependence of compliance, and 3) there was no significant change in pulmonary resistance or Rrs (respiratory resistance) at 4 Hz. These data suggested a time-constant discrepancy in the periphery due to histamine infusion. These six subjects also developed frequency dependence of resistance (delta Rrs from 4 to 12 Hz), which was significant when breathing air (-22 +/- 6%) and maximal when we used He-O2 (-32 +/- 3%). We conclude that He-O2 can improve the specificity of frequency dependence of Rrs for detecting events occurring in the peripheral airways.

Adult↗
PubMed1979

Role of cerebrospinal fluid [H+] in ventilatory deacclimatization from chronic hypoxia.

Once ventilatory acclimatization begins in sea level residents sojourning at high altitude, abrupt restoration of normal oxygen tensions will not restore ventilation to normal. We have investigated the role of cerebrospinal fluid (CSF) [H(+)] in this sustained hyperventilation by measuring CSF acid-base status in seven men (lumbar) and five ponies (cisternal) in normoxia, first at sea level and then periodically over 13-24 h of "deacclimatization" after 3-5 d in hypoxia (P(B) = 440 mm Hg). After 1 h deacclimatization, hyperventilation continued at a level only slightly less than that obtained in chronic hypoxia (+1-2 mm Hg Pa(CO2)), whereas CSF pH was either equal (in man) or alkaline (in pony, +0.02, P < 0.01) to sea level values. Between 1 and 12-13 h deacclimatization in all humans and ponies Va fell progressively (Pa(CO2) increased 4-7 mm Hg) and CSF pH became increasingly more acid (-0.02 to -0.05, P < 0.01). Between 12 and 24 h of normoxic deacclimatization in ponies, Pa(CO2) rose further toward normal, coincident with an increasing acidity in CSF (-0.02 pH). Similar negative correlations were found between changes in arterial pH and Va throughout normoxic deacclimatization. We conclude that [H(+)] in the lumbar or cisternal CSF is not the mediator of the continued hyperventilation and its gradual dissipation with time during normoxic deacclimatization from chronic hypoxia. These negative relationships of Va to CSF [H(+)] in normoxia are analogous to those previously shown during acclimatization to hypoxia.

Acclimatization↗
PubMed1979

Serotonin and the control of ventilation in awake rats.

In awake, unrestrained, intact rats, reserpine, para-chlorophenylalanine, 6-fluorotryptophan, and para-chloroamphetamine depleted whole brain serotonin and produced a substantial and sustained hyperventilation as evidenced by a 5--9 torr drop in PaCO2. Administration of 5-hydroxytryptophan to rats treated with para-chlorophenylalanine partially alleviated the hyperventilation. No change in ventilation was observed after alpha-methyltyrosine. 5,7-Dihydroxytryptamine produced contradictory results. On the basis of these pharmacological studies, we propose that some serotonin-mediated nerve transmissions might function under physiological conditions to inhibit the central nervous system output which controls normal breathing.

5,7-Dihydroxytryptamine↗
PubMed1979

The brain's role in exercise hyperpnea.

Three aspects concerning the role of the central nervous system in the control of exercise hyperpnea are reviewed. First, the integration of sensory input stresses the concept of multiple sites of integration--with the end result that both adequate gas exchange and near-optimal mechanical response of the lung and chest wall are achieved during exercise. Secondly, the potential role of the "central" [H+] chemoreceptor is discussed--in terms of the mechanisms available for the protection of brain ECF [H+] and the stimulus-response characteristics of this important chemical sensor and a critical analysis of how it may be evaluated. Finally, the question of forebrain influences on exercise hyperpnea and the "sensation" of ventilatory effect is discussed, with particular emphasis on the multi-purpose regulation of breathing in athletic endeavors.

Brain↗
PubMed1978

Role of H1 and H2 receptors in increased small airways resistance in the dog.

The relative importance of H1 and H2 receptors to central and peripheral airways resistance in the anesthetized intact dog lung were determined through the use of pharmacologically specific antagonists during graded intravenous infusions of histamine. The indirect effects of infused histamine were also tested via alpha and beta adrenergic blockade (alpha + beta blk) and post-ganglionic parasympathetic blockade (vagal blk). We measured pulmonary resistance (RL), dynamic compliance (Cdyn), thoracic gas volume (Vtg), and partitioned oscillatory pulmonary resistance (RLosc) into a peripheral (Rp) and central component with an intrabronchial catheter. Infused histamine caused a significant increase in RL, primarily the result of the increase in Rp, with substantial dose-dependent reductions in Cdyn, and increases in Vtg. These effects were not altered by vagal blk, were increased by alpha + beta blk, and were completely prevented by H1 receptor blockade, but not by H2 receptor blockade. We conclude that histamine infusion causes bronchoconstriction in the canine lung, primarily in peripheral airways (less than 3 mm diameter), by its direct action on H1-type receptors.

Airway Resistance↗
PubMed1978

Rat as a model for humanlike ventilatory adaptation to chronic hypoxia.

Oxygen uptake (VO2), expired volume (VE), and arterial blood gases were studied in awake, unrestrained rats over 14 days of hypobaric hypoxia (4,300 m altitude) and upon return to acute normoxia. Control data (at 250 m) showed (mean +/- 95% confidence limits (CL)) arterial oxygen pressure (Pao2) = 85.5 +/- 1.1; arterial carbon dioxide pressure (PaCO2) = 39.8 +/- 0.5; arterial pH pHa) = 7.430 +/- 0.009; VE = 78 +/- 3; VO2 = 2.36 +/- 0.09 ml.min-1.100 g-1; and dead space volumetidal volume ratio (VD/VT) = 0.37 +/- 0.04. During 14 days at 4.300 m the rat showed: a) a constant PaO2 (50-52 Torr); b) a time-dependent hyperventilation (e.g., PaCO2 = 30.2 +/- 1.1 at 1 h of hypoxia, 24.7 +/- 1.3 at day and 21.9 +/- 1.0 at 14 days); c) an increase in VE (85% of control) due to both frequency (33%) and VT (40%); d) a continued but reduced hyperventilation upon acute return to normoxia after 5 h to 14 days at 4,300 m; e) a 24% fall in VO2 after 1 h of hypoxia which returned to control by 4 days at 4,300 m; and f) a rise in pHa to 7.52 after 5 h of hypoxia, which fell to 7.45 by 14-day hypoxia. The rat's marked ventilatory response and changing VO2 during acute hypoxia clearly differs from the human response to sojourn at 4,300 m. However, the progressive and sustained hypocapnia during hypoxic exposure and the continued hyperventilation with acute normoxia in the rat provided essential, perhaps unique characteristics for an animal model of human ventilatory acclimatization.

Adaptation, Physiological↗
PubMed1978

Ventilatory response to medroxyprogesterone acetate in normal subjects: time course and mechanism.

The time course of ventilatory adaptation to medroxyprogesterone acetate (MPA) and potential mediators of this response in plasma and lumbar CSF were determined in five healthy adult males. A significant decrease in arterial PCO2 (PACO2) at rest and exercise was noted within 48 h of drug administration with the maximum effect reached within 7 days and amounting to a 5-Torr decrement in PACO2. Blood and lumbar cerebrospinal fluid pH because significantly alkaline to control as soon as the ventilatory resporse was noted and remained alkaline during the treatment period. The ventilatory and dP/dt max response to exogenous CO2 was unchanged but their response to moderate exercise was increased after MPA. MPA-rlated materials were detected in both the plasma and CSF as soon as the ventilatory response was noted. The increase in CSF MPA-related materials approximated the unbound fraction determined in plasma. We conclude that [H+] in plasma and CSF is a function rather than a cause of ventilator acclimatization to MPA. MPA-related materials are capable of crossing the blood-brain barrier and could potentially exert their ventilatory stimulant effect by some central mechanism.

Adult↗
PubMed1976

Dependence of CSF on plasma bicarbonate during hypocapnia and hypoxemic hypocapnia.

We have previoulsy shown pH compensation to be similar in CSF and arterial blood during chronic hypoxemic hypocapnia in man and pony, and postulated that the compensatory reduction in CSF [HCO3] was dependent upon corresponding changes in [HCO3]a. We tested this hypothesis in anesthetized, paralyzed dogs by determining the effects of 7 or 14 hours of hypocapnia (PaCO2 20 and 30 mm Hg), hypoxemia (PaO2 30, 38 and 48 mm Hg) and hypocapnic hypoxemia on CSF acid-base status. [hco3]a was either permitted to fall normally or was held near control levels by NaHCO3 infusion. In hypocapnia and hypoxemic hypocapnia, the decrease in [HCO3] and % pH compensation in CSF were less than or equal to that in arterial blood. Most (51-89%) of the compensatory decrease in CSF [HCO3] was prevented by preventing the corresponding reduction in [HCO3]a. This dependence of changes in CSF on plasma [HCO3] required a concurrent decrease in CSF PCO2, but was largely independent of variations in plasma pH. A minor but significant portion of the decrease in CSF [HCO3] was achieved independently of corresponding changes in [HCO3]a. The contribution of this local mechanism to CSF [HCO3] regulation increased with increasing severity of hypocapnia or hypoxemia and was usually associated with a selective increase in CSF lactate. It was concluded that [HCO3] regulation in the CSF during hypoxemic hypocapnia was primarily dependent upon, and therefore limited by, the concomitant decrease in plasma [HCO3].

Acid-Base Equilibrium↗
PubMed1976

Acute alterations in stroke volume during exercise at 3,100 m altitude.

Following 3 weeks exposure to an altitude of 3,100 m, the cardiac output response to upright submaximal exercise was examined in 3 healthy subjects breathing ambient air and breathing 60% oxygen. The procedure allowed acute alteration of the 2 conditions within a single testing period of 30 min, 60% oxygen breathing either preceding or following breathing ambient air. Cardiac output was also measured in two of the subjects during maximal exercise under these two conditions. Administration of the high oxygen inspirate during exercise had little effect on the level of cardiac output but resulted in an immediate bradycardia and a dramatic increase of approximately 16% in stroke volume. Stroke volumes during maximal exercise were also increased by approximately 10% by the administration of high oxygen. It is suggested that the condition of decreases exercise stroke volume which develops with chronic exposure to altitude may be largely the result of diminished myocardial contractility stemming from a condition of myocardial hypoxia.

Altitude↗
PubMed1975

Cerebrospinal fluid alkalosis during high-altitude sojourn in unanesthetized ponies.

Unanesthetized adult female ponies were studied near sea level (250 m) and during sojourns to 3400 m (N=6) and 4300 m (N=7) altitude. The pH, PCO2, and PO2 of arterial blood and pH and PCO2 of cerebrospinal fluid (CSF) were measured under conditions of acute (1 hr) and chronic (1-45 days) hypoxia. Cerebrospinal fluid was sampled from the cisterna magna of the awake pony and arterial blood withdrawn from an indwelling arterial catheter. In both groups of animals, PaCO2 decreased slightly after 1 hr of hypoxia (delta PaCO2= - 0.6 mm Hg at 3400 m; - 3.9 mm Hg at 4300 m), decreased further after 1-5 days at high altitude (delta PaCO2= - 7.2 mm Hg at 3400 m; - 12.3 mm Hg at 4300 m) and then increased significantly after 6 days of chronic hypoxia (delta PaCO2= + 4.1 mm Hg at 3400 m; + 4.7 mm Hg at 4300 m). Although PaO2 decreased markedly during acute hypoxia, subsequent changes in PaCO2 at high altitude did not alter PaO2 from that observed during acute hypoxia (PaO2=52 mm Hg at 3400 m; 41 mm Hg at 4300 m). The pH of CSF increased during acute hypoxia (delta pH= + 0.013 unit at 3400 m; + 0.033 unit at 4300 m) and became more alkaline after 1-2 days at high altitude (delta pH= + 0.031 unit at 3400 m; + 0.064 unit at 4300 m). At 4300 m, CSF pH remained alkaline to control values throughout sojourn. Under these conditions of chronic hypocapnic hypoxia, CSF pH was imperfectly regulated and regulated in a magnitude equal to (3400 m) or less than (4300 m) arterial blood. Furthermore, the similarity of relative changes in CSF [HCO3-] and arterial [HCO3-] during chronic hypoxia may indicate a passive regulation of CSF [HCO3-] rather than local 'CSF-specific' mechanisms as previously proposed.

Acclimatization↗