Biomedical subjects

D M McKay

Publications and source records attributed to D M McKay.

58 records · Page 4Linked to original sources

PubMed1989

The effects of cholinergic and serotoninergic drugs on motility in vitro of Haplometra cylindracea (Trematoda: Digenea).

The spontaneous activity of the somatic muscle of the amphibian lung fluke, Haplometra cylindracea has been recorded in vitro, using an isometric force transducer system. Normal movement consisted of a continuous series of regular contractions which were maintained for over 4 h. Acetylcholine (ACh) inhibited motility at a concentration of 1 X 10(-3)M induced a flaccid paralysis. A similar response occurred with the cholinomimetric drugs, carbachol and nicotine, although in these instances the inhibition was less easily reversed by washing with frog Ringer. The inhibitory effect of ACh was blocked by d-tubocurarine but not by atropine. Serotonin (5-HT) caused an increase in the frequency and amplitude of contractions and the effect was blocked by methysergide. No uniform response was observed with 3-hydroxytryptamine (3-HT), but both reserpine and fluoxetine inhibited worm movement. Results suggest that the somatic musculature of the worm is controlled, at least in part, by an inhibitory cholinergic and an excitatory serotoninergic system.

Acetylcholine↗

PubMed1977

The effects of halothane on pregnant and nonpregnant human myometrium.

Strips of myometrium were obtained at operation from eight nonpregnant and ten pregnant patients. The tissues were immediately suspended in a muscle bath and induced to contract isometrically with K2SO4 in the presence and absence of halothane (0.5 to 2.0 vol per cent). The anesthetic produced significant dose-related depression of developed tension and rates of increase and decrease of tension in both pregnant and nonpregnant muscles. Time to peak tension was increased in the nonpregnant but not in the pregnant muscles. The depressant effect of the lower halothane concentrations (less than 1.1 vol per cent) was significantly greater in the pregnant muscles.

Adolescent↗

PubMedDate not supplied

Intestinal inflammation and the gut microflora.

The idea that the enteric microflora play a role in the pathogenesis or pathophysiology of inflammatory bowel disease (IBD) is not new. Indeed, identification of an infective cause for chronic IBD, and particularly for Crohn's disease, has been the focus of extensive research efforts. During the 1990s, there has been a noticeable re-emergence of interest in the link between bacteria and functional bowel disorders, and the value of antibiotic therapy to treat gut inflammatory disorders. A variety of experimental evidence from both laboratory model systems and clinical investigations is reviewed with respect to a pivotal role for enteric bacteria in gut inflammation. The voluminous scientific literature on this subject precludes any comprehensive synopsis of the area; instead, pertinent studies are cited to illustrate the ability of bacteria and their products to evoke or exacerbate gut inflammation.

Animals↗

PubMedDate not supplied

Inhibition of antigen-induced secretion in the rat jejunum by interferon alpha/beta.

Intestine from rats sensitized to egg albumin (EA) antigen responds to EA challenge with an increase in short-circuit current (Isc), indicative of predominantly chloride secretion. Here, we have examined the role of interferon alpha/beta (IFN alpha/beta) in the control of this event. Muscle-stripped jejunal segments from sensitized rats, mounted in Ussing chambers, displayed a reduced response to EA-challenge in the presence of IFN alpha/beta (100-1000 U/ml), when the cytokine was incubated with the tissue for > or = 60 min; serosal and luminal responses were significantly reduced by ca.32-47% and ca.50-80%, respectively. Preabsorption with an anti-IFN alpha/beta antibody abolished this inhibition. IFN alpha/beta did not influence the secretory response of the tissues to histamine, serotonin, bethanechol, or forskolin, suggesting that IFN alpha/beta does not affect the epithelium directly. IFN alpha/beta had no effect on Isc changes induced by electrical transmural stimulation of mucosal nerves in the tissue, nor did neuronal blockade with tetrodotoxin influence the action of IFN alpha/beta. These data indicate that the effect of IFN alpha/beta is not neuronally mediated. The normal anti-secretory actions of diphenhydramine (H1-antagonist) and piroxicam (cylooxygenase inhibitor) upon antigen-activation of mast cells, were not apparent in the presence of IFN alpha/beta. This suggests that IFN alpha/beta inhibits intestinal hypersensitivity by acting directly on mast cells. This hypothesis was confirmed by inhibition of antigen-induced release of the specific mucosal mast cell marker, rat mast cell protease II, in tissues treated with IFN alpha/beta. These findings suggest that IFN alpha/beta can function as an intestinal anti-inflammatory agent by stabilizing mucosal mast cells.

Animals↗