Journal of applied physiology
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Comparative Study
Diminished hypoxic ventilatory responses in near-miss sudden infant death syndrome.
The ventilatory response to hypoxia and to hypercarbia was assessed in 36 near-miss sudden infant death syndrome (N. M SIDS) and 23 control infants. Base-line measurements during non-REM sleep documented no significant difference in respiratory frequency, alveolar CO2 and O2 partial pressure (PAco2 and PAo2) or tidal volume between the N-M SIDS and control infants. ⋯ For both groups, the increase in ventilation with hypoxia appeared linear within the PAo2 range assessed (65-115 Torr) and was therefore expressed as the slope of the delta VI/PAo2 plot (ml.kg-1 min-1 per Torr PAo2). The slope of the hypoxic ventilatory response was significantly less in the N-M SIDS than in the control group, -8.3 +/- 1.0 VS. -19.9 +/- 1.5, respectively (p less than 0.001). In summary, in comparison to control infants, N-M SIDS infants as a group have a significantly smaller increase in VI in response to hypoxia as well as to hypercarbia.
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Transdiaphragmatic pressure (Pdi) was measured at functional residual capacity (FRC) in four normal seated subjects during supramaximal, supraclavicular transcutaneous stimulation of one phrenic nerve (10, 20, 50, and 100 Hz--0.1 ms duration) before and after diaphragmatic fatigue, produced by breathing through a high alinear inspiratory resistance. Constancy of chest wall configuration was achieved by placing a cast around the abdomen and the lower one-fourth of the rib cage. Pdi increased with frequency of stimulation, so that at 10, 20, and 50 Hz, the Pdi generated was 32 +/- 4 (SE), 70 +/- 3, and 98 +/- 2% of Pdi at 100 Hz, respectively. ⋯ Recovery for high stimulation frequencies was complete at 10 min, but at low stimulation frequencies recovery was slow: after 30 min of recovery, Pdi at 20 Hz was 31 +/- 7% of the control value. It is concluded that diaphragmatic fatigue can be detected in man by transcutaneous stimulation of the phrenic nerve and that diaphragmatic strength after fatigue recovers faster at high than at low frequencies of stimulation. Furthermore, it is suggested that this long-lasting element of fatigue might occur in patients with chronic obstructive lung disease, predisposing them to respiratory failure.
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An objective and accurate measurement and characterization of breath sounds was carried out by a fast-Fourier-transform frequency-domain analysis. Normal vesicular breath sounds, picked up over the chest wall of 10 healthy subjects showed a characteristic pattern: the power of the signal decreased exponentially as frequency increased. ⋯ The maximal frequencies of inspiratory and expiratory breath sounds, picked up over the base of the right lung, were (in Hz +/- SD) 446 +/- 143 and 286 +/- 53 (P less than 0.01), over the base of the left lung 475 +/- 115 and 284 +/- 47 (P less than 0.01), over the interscapular region 434 +/- 130 and 338 +/- 77 (P less than 0.05), and over the right anterior chest 604 +/- 302 and 406 +/- 205 (P less than 0.05). Breath sounds picked up over the trachea were characterized by power spectra typical to a broad spectrum sound with a sharp decrease of power at a cut-off frequency that varied between 850 and 1,600 Hz among the 10 healthy subjects studied.
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Bronchial inhalation challenges to Ascaris suum, citric acid, and methacholine were performed in eight Basenji-Greyhound (BG) crossbreed dogs, five of which were reactive to Ascaris antigen aerosols (AAA). Responses to aerosol challenges were measured as changes in pulmonary resistance (RL) and dynamic compliance (Cdyn) and were compared to responses obtained in five mongrel dogs. ⋯ Methacholine responses were elicited at 10-30 times lower concentrations in BG dogs than in mongrels; 10% citric acid, which failed to elicit any response in mongrels, increased RL 5- to 10-fold in BG dogs. We conclude that the BG dog demonstrates nonspecific bronchial hyperreactivity, as in human asthma.
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Previously we found that raising cerebrospinal fluid pressure (PCSF) caused pulmonary vasoconstriction mediated by adrenal catecholamines. To localize the site of this vasoconstriction we used the outflow occlusion technique to divide changes in the pulmonary arteriovenous pressure gradient (Pa-v) into upstream and downstream pressure drops. Experiments were conducted in 10 dogs in which the animal's left lower lung lobe was denervated and perfused at constant flow and outflow pressure with blood pumped from the dog's pulmonary artery. ⋯ Thus, it appears that elevated PCSF caused primarily pulmonary venoconstriction. Similar results were obtained with norepinephrine and epinephrine infusion. This is consistent with previous studies, indicating that adrenal catecholamines are responsible for the increase in Pa-v in response to PCSF in this preparation.