Evaluation of abnormal lung function.
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Biomedical subjects
Publications and source records attributed to J R Gillespie.
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Hematocrit and plasma protein concentration in healthy dogs and monkeys (Macaca arctoides) awake and anesthetized with halothane-oxygen and halothane-nitrous oxide oxygen were compared during conditions of spontaneous and controlled ventilation. Both hematocrit and plasma protein concentration decreased within 15 minutes following anesthetic induction. This decrease persisted throughout constant- or variable-depth anesthesia and did not vary appreciably with ventilation, anesthetic dose, or introduction of nitrous oxide. Plasma volume, determined by a dye dilution technique, concomitantly increased. This increase is compatible with the directional changes in hematocrit and plasma protein.
Single-breath carbon monoxide diffusing capacity (DLco), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) were measured in 24 beagle dogs aged 289-3,882 days. DLco and Vc were a function of age and alveolar volume (Va). Vc decreased with age resulting in changes in DLco. Changes in Vc may have been due to pulmonary morphological changes or to an exaggerated decrease in pulmonary blood flow in old dogs in response to 20-30 cmH-2O transpulmonary pressure. There was no age-related change in Dm.
Respiratory function in newborn foals is discussed with particular reference to the important part played by functional residual capacity and chest wall compliance in maintaining blood gaseous exchange within normal limits.
The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.
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We measured simultaneously, by single breath methods, pulmonary capillary blood flow (Q(c)), carbon monoxide diffusing capacity (DL(CO)), and isotopic oxygen ((18)O(18)O) diffusing capacity (DL(18) (O2)) in five normal males during conditions of rest and moderate exercise at mixed venous O(2) tensions (PO(2) 33-44 mm Hg). During moderate exercise at a work load of 100 W. pulmonary capillary blood flow increased from 6.9+/-1.5 to 12.9+/-3.4 min(-1) and DL(18) (O2) increased from 25+/-4 to 43+/-3 ml.min(-1).mm Hg(-1), whereas DL(CO) showed no significant change (45+/-5 to 49+/-10 ml.min(-1).mm Hg(-1)). DL(18) (O2) increased proportionally to Q(c) (r = 0.74), where DL(CO) did not (r = 0.08). The greater increase in DL(18) (O2) during exercise can be explained by a more homogeneous diffusion/perfusion (DL(O2)/Q(c)) distribution in the individual respiratory exchange units during exercise. This improved distribution of DL(O2)/Q(c) acts to help prevent an increase in alveolar-arterial O(2) tension difference from developing despite the decrease in pulmonary erythrocyte transit times that occur during exercise. The insignificant rise in DL(CO) with exercise under these hypoxic breathholding conditions may result from pulmonary vasomotor responses to short-term hypoxia or from relative insensitivity of DL(CO) to moderate levels of exercise.
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