Biomedical subjects

N Gibson

Publications and source records attributed to N Gibson.

13 recordsLinked to original sources

PubMed1988

Carbon dioxide reactivity of the cerebral circulation in extremely premature infants: effects of postnatal age and indomethacin.

Little is known about the vasoactivity of cerebral arterioles in extremely premature infants. We have assessed the effects of a small rise in PaCO2 of 1 kPa (7.5 mm Hg) on cerebral blood flow velocity measured by duplex Doppler ultrasound. Nineteen mechanically ventilated infants of 33 wk gestational age or less in whom direct arterial blood pressure monitoring was available, were studied on 45 occasions. There was a close relationship between increasing PaCO2 and increasing cerebral blood flow velocity (p less than 0.005) but on seven of 45 occasions the cerebral blood flow velocity fell with rising PaCO2. There was a 44% (median value) rise in cerebral blood flow velocity per 1 kPa rise in PaCO2 (5.9%/1 mm Hg) in 21 infants tested within 24 h of birth and this increased to a 53% (median value) rise (7%/1 mm Hg) in 20 infants tested after 24 h (p less than 0.001). Eleven infants had paired studies, the first within 24 h and a second at a median age of 48 h. There was a statistically significant increase in percentage reactivity when the later group was compared to those tested within 24 h (p less than 0.001). Carbon dioxide reactivity was also assessed before and after indomethacin infusion (0.2 mg/kg) on four occasions and there was a reduction in reactivity from a median value of 144 to 49.5%, 10 min after indomethacin. The extremely immature, ill infant is less sensitive to a small change in PaCO2 within 24 h of birth and after indomethacin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1987

Effect of smoking on functional activity of plasma alpha 1-protease inhibitor.

We determined the levels of alpha 1-protease inhibitor, the plasma trypsin-inhibiting capacity (TIC), and elastase-inhibiting capacity (EIC) in 29 nonsmokers and 30 smokers, who were healthy volunteers matched for age (mean age, 39 +/- 12 years [+/- SD]). The functional activity of plasma alpha 1-protease inhibitor (in micrograms of enzyme inhibited per microgram of alpha 1-protease inhibitor) was slightly but significantly lower in smokers, compared with nonsmokers, both for TIC and EIC (smokers' TIC and EIC were 88.0 +/- 16.2 percent (+/- SD) and 90.4 +/- 17.9 percent of the respective mean values in nonsmokers; p less than 0.05). Among smokers, there was a significant negative correlation (r = -0.37; p less than 0.05) between the average number of cigarettes smoked per day and the functional activity of plasma alpha 1-protease inhibitor; the seven subjects who smoked 40 or more cigarettes per day had significantly lower EIC and TIC than the remaining smokers. In 12 smokers tested before and after a two-hour period of intense smoking of eight cigarettes, there was a statistically significant decrease (p less than 0.05) in EIC one hour after smoking to 93.9 +/- 2.5 percent (+/- SE) of the initial value prior to smoking. It is concluded that there is a slight but significant decrease in the functional activity of plasma alpha 1-protease inhibitor in smokers, both for TIC and EIC.

Adult↗

PubMed1986

Putting men back in the picture. Sexism in nutrition and extension programmes.

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Decision Making↗

PubMed1986

Effect of smoking on plasma neutrophil elastase levels.

Plasma elastase is considered to indicate neutrophil elastase that has been released in vivo and has complexed with plasma inhibitors. Because smoking may play a pathogenetic role in emphysema by inducing elastase release in the lung, which may be reflected in the plasma elastase level, we evaluated the effect of smoking on plasma elastase in healthy men by using an enzyme-linked immunosorbent assay. No significant difference was found in plasma elastase levels between 30 smokers and 29 nonsmokers (103 +/- 23 [SD] ng/ml vs. 97 +/- 23 ng/ml). We found no significant change in plasma elastase level in eight heavy smokers when we compared morning with afternoon plasma samples taken about 7 hours later, while the subjects continued to smoke ad libitum in the interval. However, we found a significant rise in plasma elastase level in 12 healthy smokers who were tested after 8 hours of abstinence from smoking and then immediately and 1/2, 1, and 2 hours after intense smoking (eight cigarettes smoked over a period of 2 hours). Neutrophil count increased from a baseline of 3.8 +/- 0.7 X 10(3)/mm3 to 8.0 +/- 2.5 X 10(3)/mm3 at 1 hour, and 8.8 +/- 3.1 X 10(3)/mm3 at 2 hours. Plasma elastase level increased significantly (P less than 0.02) from a baseline of 111 +/- 30 ng/ml to 141 +/- 24 ng/ml at 1 hour after completion of smoking, but was not significantly different from baseline 2 hours after smoking (130 +/- 34 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Carboxyhemoglobin↗

PubMed1976