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Biomedical subjects

N P Randall

Publications and source records attributed to N P Randall.

5 recordsLinked to original sources
PubMed1999

Vascular trauma associated with routine spinal anaesthesia.

Samples of cerebrospinal fluid obtained from 130 patients undergoing spinal anaesthesia were examined microscopically. Subarachnoid puncture was performed using either a 25G Whitacre or 25G Quincke spinal needle. Two samples were collected from each patient and the red blood cell count of the second sample collected was taken as a measure of the vascular trauma associated with the procedure. Red blood cells were seen in 50 (38%) of these samples, of which 18 (14%) contained > 100 red blood cells.mm-3. Paraesthesia was felt by 11 (8.5%) patients and the occurrence of paraesthesia was associated with significantly raised red blood cell counts (p < 0.0001). There was also a correlation between the number of needle passes made at lumbar puncture and the red blood cell count in the sample (p < 0. 0001). Neither spinal needle type nor antiplatelet drug therapy influenced red blood cell counts (p = 0.66 and 0.37, respectively). These findings suggest that routine spinal anaesthesia is often complicated by minor degrees of vascular trauma, especially when paraesthesiae or technical difficulty occur at subarachnoid puncture.

Aged↗
PubMed1989

Effect of oral doxapram on morphine-induced changes in the ventilatory response to carbon dioxide.

A double-blind crossover volunteer trial has been carried out to determine if oral doxapram reduces the respiratory depression caused by morphine 0.12 mg kg-1 i.m. Doxapram was given to the subjects 90 min before the morphine and significantly reduced the displacement of the ventilatory response to carbon dioxide caused by the morphine. This occurred despite the fact that the plasma concentrations of doxapram were significantly lower when the subject had been given morphine than when a placebo injection had been administered. Doxapram alone in doses of 300 mg and 600 mg did not alter significantly the respiratory variables measured in this study.

Administration, Oral↗
PubMed1989

Doxapram and the neuromuscular junction.

We have studied the action of doxapram on neuromuscular transmission in the rat phrenic nerve-diaphragm preparation. Doxapram augmented neuromuscular transmission in a dose-related manner when a threshold concentration of 5 x 10(-5) mol litre-1 had been exceeded. The activity of the acetylcholinesterase in rat diaphragm has been examined also in the presence of doxapram. No inhibitory effect was seen in the concentration range which augmented neuromuscular transmission, thus excluding cholinesterase inhibition as the underlying mechanism. In contrast, in the presence of partial neuromuscular block, a dose-related depression of neuromuscular transmission with doxapram was revealed. This was greatest when the neuromuscular blocking agents possessed significant presynaptic activity (beta-bungarotoxin and tubocurarine). In this situation any facilitatory action of doxapram was severely reduced or abolished. In contrast, the facilitatory effects of doxapram were apparent in the presence of partial block produced by agents with less or no presynaptic activity (pancuronium and alpha-bungarotoxin). This study suggests that doxapram has a presynaptic facilitatory action at the neuromuscular junction. In the presence of partial neuromuscular block, an inhibitory action is revealed which may be post-junctional. The concentrations of doxapram at which these effects appear are approximately five times greater than those reached in plasma after a standard clinical dose.

Acetylcholinesterase↗
PubMed1987

The respiratory effects of oral ethyl loflazepate in volunteers.

A volunteer study was undertaken to assess the respiratory effects of ethyl loflazepate, a new benzodiazepine, and to correlate these with plasma concentrations of the active metabolites. Twelve volunteers were given placebo, 2 mg ethyl loflazepate, and 6 mg ethyl loflazepate on separate occasions. Respiration and plasma metabolite levels were assessed hourly for 8 h and at 24 h. The 6 mg ethyl loflazepate treatment produced a significant decrease (P less than 0.02) in the ventilatory response to carbon dioxide at 5 h. However this did not equate with a peak in plasma metabolite concentrations which were maintained at a plateau level from 4 to 24 h.

Adult↗