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Biomedical subjects

M Sinclair

Publications and source records attributed to M Sinclair.

At least 73 records · Page 4Linked to original sources
PubMed1983

Ventilatory effects during and after continuous infusion of fentanyl or alfentanil.

The opioid drugs fentanyl and alfentanil were infused at a constant rate as supplements to nitrous oxide in oxygen anaesthesia throughout the period of surgery. These infusions were continued into the period after operation for 1 h after the discontinuation of anaesthesia. Continuous infusion of alfentanil 20 micrograms kg-1 h-1 and fentanyl 3 micrograms kg-1 h-1 resulted in depression of the carbon dioxide response curve with a lesser effect on frequency and minute ventilation. One hour after discontinuing the infusions the degree of ventilatory depression was only marginally less with fentanyl, but considerably less with alfentanil, reflecting the shorter terminal half-life of that drug.

Adult↗
PubMed1980

Infants' orientation to lateral sounds from birth to three months.

Head turning to off-centered sound was videotaped monthly in a group of infants during their first 3 months of life. Infants turned reliably toward the sound at birth and at 1 and 3 months of age. They failed to respond reliably at 2 months due to an increase in no-turn responses. Potential explanations for the temporary decline in orientation responses to sound are discussed.

Auditory Perception↗
PubMed1979

The effects of flurazepam hydrochloride on brain electrical activity during sleep.

To further evaluate the effects of flurazepam on EEG during sleep, following 7 nights of placebo baseline, flurazepam (30 mg) was administered to 6 young adult poor sleepers for 10 additional nights while 6 other young adult poor sleepers continued to receive placebo capsules in a double-blind paradigm. Three placebo follow-up nights were recorded 2--3 weeks post-treatment. Twelve good sleepers received only placebo capsules for the first 7 nights. Delta waves, 0.5--2 c/sec, and sleep spindles were counted on-line by a phasic detector. Delta activity was also analyzed off-line by PDP-12 computer for only the first 4 h of sleep and involved a comparison over stages of sleep. Click-evoked K-complexes during NREM sleep were analyzed for 6 good sleepers and 11 poor sleepers. Repeated use of flurazepam caused a gradual decrease in delta amplitude and count, and a gradual increase in sleep spindle rate. The decrease in delta amplitude was seen in all sleep stages, but the decrease was significant only during SWS and stage 2. The decrease in delta amplitude was significant by the 3rd drug night, but the rate of amplitude decrease tended to slow with continued treatment. The decrease in delta count was less pronounced and more gradual over drug nights than the rate of decrease in amplitude. Flurazepam also significantly reduced evoked K-complex amplitude but did not affect latency. Sleep spindle rate was significantly increased by drug night 5. Results of this study indicate that the reduction of SWS with flurazepam during the initial drug nights is due primarily to the decrease in delta amplitude, but, with continued use, the decrease in delta count also contributes to the decrease in stage 4 sleep.

Adult↗
PubMed1976

An Alberta Cree Indian with a rare Duffy antibody, anti-Fy 3.

Anti-Fy3, found in the serum of an Fy(a-b-) Cree Indian woman believed to have been transfused 5 years previously, caused moderate hemolytic disease of the newborn in her eighth live-born baby. Only three examples of anti-Fy3 are know. It is striking that two were made by non-negro people, amongst whom Fy(a-b-) is extremely rare, and only one by a Negro, in whose people Fy(a-b-) is by far the commonest phenotype. This suggests that Fy(a-b-) may be a heterogeneous phenotype, with the negro version conferring some impediment to immunization by Fya, Fyb or Fy3 antigens. The rare allele Fyx is also present in the kindred of the propositus, and is shown to correspond to weak Fy3 as well as weak Fyb anitgen.

Alberta↗
PubMedDate not supplied

Acquired hemolytic anemia due to "auto"-anti-A or "auto"-anti-B induced by group O homograft in renal transplant recipients.

Three patients developed severe but self-limited hemolytic anemia within 2 weeks of renal transplantation. All three had received kidneys from cadaver donors who were blood group O. Two of the recipients were blood group B while the third was blood group A. There was no pretransplant preparation of the donors or the recipients. Preoperative crossmatch and antibody screen were negative; however, subsequent to the hemolytic episodes, group-specific blood was incompatible and the patients were transfused with group O crossmatch-compatible blood. Blood bank serological tests showed a positive direct antiglobulin test (DAT), and anti-A and anti-B were eluted from group A and B patients, respectively. There was no evidence of hemolysis despite the positive DAT at 37 days following transplantation in two of the three patients who were maintained on cyclosporine immunosuppression. Retrospective analysis of renal transplant records showed that these "autoantibodies" appeared in three of the four renal transplant recipients who were on an immunosuppressive regimen of cyclosporine , with or without prednisone, but not in the 21 recipients who received radiotherapy to the donor kidney in addition to cyclosporine or azathioprine (p = less than 0.001). The possible pathogenetic mechanism for "autoantibody" formation by donor kidney and the role of immunosuppressive agents are discussed.

ABO Blood-Group System↗
PubMedDate not supplied

Protection against hemolysis in ABO mismatched renal transplantation.

The kidneys from a blood group O cadaver donor were transplanted into two patients whose blood groups were B and A2B. The former developed a positive direct antiglobulin test (DAT) and hemolysis due to anti-B; the latter also developed a positive DAT, but due to anti-A. However, this second patient, unlike the first, did not have any hemolysis. Both patients were on the same immunosuppression regimen with cyclosporine. The possible protective roles of patients' ABO subgroup and blood group substances in plasma are discussed.

ABO Blood-Group System↗