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Biomedical subjects

A Smythe

Publications and source records attributed to A Smythe.

25 records · Page 2Linked to original sources
PubMed1976

The rejection of islets of Langerhans following intrahepatic transplantation in the rat.

Pancreatic acinar tissue and islets of Langerhans have been isolated using a collagenase technique from Agus rats and transplanted separately into the liver of diabetic and nondiabetic isogeneic Agus and allogenic PVG/C rats. Livers were removed on days 1, 2, 4, 7 and 14 and examined histologically. Transplanted isogeneic islets showed no evidence of cellular infiltration and the beta cells appeared fully granulated. Transplanted allogeneic islets in non-diabetic recipients were surrounded by a mononuclear cellular infiltrate on day 2 and this became maximal by day 4. Although initially fully granulated, beta cells became degranulated on day 7 and by day 14 only small fragments of islet tissue remained. In allogeneic diabetic recipients the cellular infiltrate appeared less dense; beta cells appeared incompletely granulated from days 1 to 4 and a transient fatty degeneration occurred in the hepatic parenchuma around islets.

Animals↗
PubMed1975

The influence of exogenous PMS and HCG on the arachidonic acid content of the immature rat ovary.

The influence of exogenous PMS and/or HCG, on the arachidonic acid (C 20:4omega6) content of the immature rat ovary was examined. Changes in ovarian arachidonate content associated with hormone administration were assessed in total lipid extracts, and in several neutral and phospholipid fractions. Both relative percentage and absolute amounts of arachidonic acid in several lipids were measured as well as uptake of radioactivity into total lipid resulting from the administration of 3H-labeled arachidonic acid in vivo. On the basis of these studies, we conclude (1) PMS, with or without HCG promotes increased uptake of exogenous arachidonic acid into ovarian total lipids; (2) Arachidonic acid is a mojor fatty acid constituent from noncholine containing phosphatides at the onset of normal estrous (ca. 38 days) even in the animals which received no PMS or HCG; (3) Changes in ovarian arachidonic acid levels following gonadotropin administration are more striking in the two phospholipid fractions than in the two neutral lips examined; (4) PMS is associated with a rapid outpouring of ovarian lipid, accompanied by a high turnover of arachidonic acid which is enhanced or modified temporally by added HCG in vivo. These results provide the first quantitative evidence that gonadotropins may regulate prostaglandin biosynthesis in the ovary by their effects on the uptake, storage, or release of arachidonic acid, a major PG precursor, from specific ovarian lipids. While the data strongly suggest that the regulation of one or more ovarian esterases (cholesterol esterase, lipase, phospholipase) is the mechanism by which gonadotropins regulate PG biosynthesis, a direct action on PG synthetase is not ruled out.

Animals↗
PubMed1975

Pancreatic ischaemia; sensitivity and reversibility of the changes.

In the rat, pancreatic clamping producing warm ischaemic times ranging from 5 to 90 min gives rise to changes similar to those of an haemorrhagic pancreatitis. The severity of the changes is proportional to the time of ischaemia. After 1 to 1 1/2 h clamping 95 per cent of the glandular changes are reversible, and at 2 months the pancreas appears normal apart from localized areas of fibrosis. The islets of Langerhans remain morphologically normal even after 90 min ischaemia. The implications for islet cell transplantation are discussed.

Adipose Tissue↗
PubMed1972

A comparison of the excitatory and inhibitory effects of non-adrenergic, non-cholinergic nerve stimulation and exogenously applied ATP on a variety of smooth muscle preparations from different vertebrate species.

1. The responses to non-adrenergic, non-cholinergic nerve stimulation have been compared with those to exogenously applied ATP on seventeen different tissues from a number of vertebrate classes.2. Stimulation of all the mammalian gut preparations studied (with the exception of the guinea-pig ileum) after blockade of the effects of adrenergic and cholinergic nerve stimulation by guanethidine (3.5 muM) and hyoscine (1.3 muM) caused inhibition; exogenously applied ATP mimicked this inhibitory response.3. Stimulation of the guinea-pig ileum in the presence of hyoscine and guanethidine, usually caused a diphasic response, relaxation followed by contraction; exogenously applied ATP mimicked this response, in contrast to acetylcholine and noradrenaline which caused excitation and relaxation respectively.4. Stimulation of preparations of lower vertebrate gut and guinea-pig bladder in the presence of hyoscine and guanethidine caused contraction; exogenously applied ATP mimicked this contractile response.5. In each preparation the time course of the response to ATP was similar or identical to the response to non-adrenergic, non-cholinergic nerve stimulation.6. The results are consistent with the hypothesis that a purine nucleotide may be the transmitter substance released from non-adrenergic, non-cholinergic nerves supplying smooth muscle preparations from a number of vertebrate classes.

Acetylcholine↗
PubMed1972

Atropine resistant excitation of the urinary bladder: the possibility of transmission via nerves releasing a purine nucleotide.

1. The possibility that a purine nucleotide is involved in excitatory transmission to the urinary bladder has been tested. All the purine compounds tested which contained a pyrophosphate bond produced contraction, adenosine triphosphate (ATP) being the most potent. Adenosine and adenosine monophosphate caused relaxation.2. The response to ATP closely mimicked the nerve-mediated contraction, both being characterized by a rapid contraction which was not maintained. A lack of sensitivity to ATP was noted in some preparations of the rat urinary bladder.3. Both nerve-mediated contractions and contractions caused by ATP were blocked by quinidine, while the response to acetylcholine persisted.4. Nerve-mediated responses were depressed during tachyphylaxis produced by high concentrations of ATP. Tachyphylaxis did not occur when low concentrations were used. Possible explanations for these results are discussed.5. The results are consistent with the hypothesis that non-cholinergic excitatory nerves to the guinea-pig bladder release a purine nucleotide, but do not provide critical evidence for it.

Adenosine↗
PubMed1970

Evidence that adenosine triphosphate or a related nucleotide is the transmitter substance released by non-adrenergic inhibitory nerves in the gut.

1. Stimulation of the vagal non-adrenergic inhibitory innervation caused the release of adenosine and inosine into vascular perfusates from the stomachs of guinea-pigs and toads.2. Stimulation of portions of Auerbach's plexus isolated from turkey gizzard caused the release of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP).3. ATP, added to solutions perfused through the toad stomach vasculature, was broken down to adenosine, inosine and adenine.4. Of a series of purine and pyrimidine derivatives tested for inhibitory activity on the guinea-pig isolated taenia coli, ATP and ADP were the most potent.5. ATP caused inhibition of twelve other gut preparations previously shown to contain non-adrenergic inhibitory nerves. The inhibitory action of ATP was not prevented by tetrodotoxin.6. Quinidine antagonized relaxations of the guinea-pig taenia coli caused by catecholamines or adrenergic nerve stimulation. Higher concentrations of quinidine antagonized relaxations caused by ATP or non-adrenergic inhibitory nerve stimulation.7. When tachyphylaxis to ATP had been produced in the rabbit ileum, there was a consistent depression of the responses to non-adrenergic inhibitory nerve stimulation but not of responses to adrenergic nerve stimulation.8. It is suggested that ATP or a related nucleotide is the transmitter substance released by the non-adrenergic inhibitory innervation of the gut.

Adenine↗