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Biomedical subjects

T M Berman

Publications and source records attributed to T M Berman.

6 recordsLinked to original sources
PubMed1981

Attenuated responses to CO2 and hypoxia in parents of threatened sudden infant death syndrome infants.

Ventilatory and heart rate responses to hypercapnia and hypoxia were measured in the following three groups: group I, controls (n equals 15); group II, parents of threatened sudden infant death syndrome (SIDS) infants (n equals 10); and group III, parents of SIDS infants (n equals 17). We found significantly reduced heart rate responses to carbon dioxide and hypoxia in group II (1.4 plus or minus 1.9 percent and 16.0 plus or minus 4.0 percent; mean plus or minus SEM) compared with controls (7.1 plus or minus 1.4 percent and 26 plus or minus 2.4 percent; P less than .025). Ventilatory responses to hypoxia in groups II and III were not significantly different from controls. Two group II mothers had a greatly reduce ventilatory response to carbon dioxide. Four other parents in group II had abnormally low heart rate responses to hypoxia or carbon dioxide. We concluded that parents of threatened SIDS infants had reduced heart rate responses to carbon dioxide and hypoxia and may have reduced ventilatory responses to carbon dioxide.

Adult↗
PubMed1980

Increased hypoxic ventilatory drive due to administration of aminophylline in normal men.

We evaluated the effects of intravenous administration and five days of oral administration of aminophylline on hypoxic and hypercapnic ventilatory drives in seven normal men. Serum levels of theophylline were 13.2 micrograms/ml +/- 1.0 micrograms/ml (mean +/- SD) after intravenous administration of aminophylline and 8.8 micrograms/ml +/- 1.7 micrograms/ml after oral administration of aminophylline. Aminophylline had no effect on the slope of the line for carbon dioxide response or on hypoxic ventilatory drive, measured at resting alveolar carbon dioxide tension (PACO2). Hypoxic ventilatory drive was significantly increased (P < 0.025) after intravenous administration of aminophylline when the PACO2 was raised to the control level before aminophylline. Intravenously administered aminophylline shifted the intercept of the line for carbon dioxide response from 40.7 +/- 2.3 to 32.9 +/- 4.6 mm Hg (P < 0.005) and lowered the resting PACO2 from 38.3 +/- 1.8 to 33.7 +/- 2.1 mm Hg (P < 0.005). Similar but smaller changes were seen after oral administration of aminophylline. There was a significant correlation between end-tidal carbon dioxide tension and the serum level of theophylline (P < 0.001), indicating that aminophylline stimulates ventilation in a dose-dependent fashion. This increase in ventilation is due in part to an increase in hypoxic ventilatory drive.

Administration, Oral↗