Biomedical subjects
Publications and source records attributed to I D Smith.
Vibrio cholerae, biotype El Tor, was isolated in a hospital laboratory in Kingston, Ont. in 1974. Confirmation and complete identification by the Ontario regional and provincial public health laboratories was obtained within 3 days. Institution of well established infection-control and public health measures prevented spread of the infection within the hospital and the community.
Relations among circadian rhythms in serum iron, glucagon and insulin and urinary cyclic AMP excretion differ drastically when diurnally active, nocturnally resting human adults consume all daily food for one week as breakfast only and for another week as dinner only - a finding of interest to diverse fields, e.g., for optimizing certain kinds of therapy or for a better utilization of calories.
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In an attempt to elucidate the roles of prostaglandin F2alpha and noradrenaline in exercise-induced asthma, plasma levels of these substances were measured at rest, during and after exercise in normal and asthmatic subjects. Changes in airways resistance were assessed by measuring the peak expiratory flow rate. Plasma levels of 15-keto-13,14-dihydro-prostaglandin F2alpha (a relatively stable metabolite of prostaglandin F2alpha) and noradrenaline, at rest, and the changes that occurred during and after exercise, were similar in both the normal and asthmatic subjects. Exercise-induced broncho-constriction occurred in all asthmatic subjects following exercise while no significant change occurred in the peak expiratory flow rates of the normal subjects. At this time, in both groups of subjects, the levels of 15-keto-13,14-dihydro-prostaglandin F2alpha were lower than at rest. The level of noradrenaline observed following exercise were lower than during exercise in all but one subject. It would appear that neither noradrenaline nor prostaglandin F2alpha (or its metabolites) play a significant role in the aetiology of exercise-induced asthma.
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The anti-inflammatory analgesic drugs, aspirin, indomethacin, phenylbutazone, mefenamic acid ibuprofen and flurbiprofen are shown to inhibit in a dose-dependent manner the force of contraction of isolated human pregnant myometrial strips which have been stimulated to contract by adding prostaglandin (PG) F2alpha to the tissue bath. These drugs and also flufenamic acid and salicin show a similar antagonism of the action of PGF2alpha with isolated rabbit non-pregnant myometrium. The ratio of the inhibitory concentration in vitro to the maximum plasma level after a normal dose in vivo suggests that phenylbutazone and possibly ibuprofen may be capable of inhibiting human uterine contractions in vivo. Patients who were treated with aspirin during induction of abortion using PGF2alpha during the second trimester of pregnancy showed no significant change in the induction-abortion interval compared with patients not taking aspirin.
Prostaglandin F-2alpha (PGF-2alpha) was administered via a Foley catheter over a 12 hour period to 8 healthy volunteers awaiting laparoscopic sterilisation. The amount of PGF-2alpha infused varied between 500 mu-g and 2000 mu-g every 2 hours for 6 doses. Plasma progestins and oestradiol 17beta, and urinary estrogens and pregnanediol were assayed throughout the study period. There was no evidence of luteolysis in any patient although vaginal bleeding of varying duration occurred in all women within 36 hours of administration of PGF-2alpha.
A group of five patients awaiting laparoscopic tubal diathermy were followed by daily assay of luteinising hormone (LH) and progesterone. Between five and eight days after the LH peak, prostaglandin F-2ALPHA (PGF-2ALPHA) was injected into either the corpus luteum or the ovarian stroma. Doses of 100 mu-g into the corpus tuteum, 1000 mu-g into the adjacent stroma and 500 mu-g into an indeterminate ovarian structure had no effect on peripheral plasma progesterone levels or uterine bleeding. An injection of 500 mu-g or 1000 mu-g given unequivocally into the corpus luteum produced a rapid and profound fall in plasma progesterone levels, the nadir coinciding with the onset of uterine bleeding which commenced 24 hours after the injection and persisted for more than seven days. Injection of 100 mu-g in the same volume of saline had no such effect. Despite continued bleeding plasma progesterone levels returned to normal luteal levels for three days and then fell again.
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