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Biomedical subjects

C J Kirk

Publications and source records attributed to C J Kirk.

At least 109 records · Page 6Linked to original sources
PubMed1981

The stimulation of inositol lipid metabolism that accompanies calcium mobilization in stimulated cells: defined characteristics and unanswered questions.

It now appears to be generally agreed that the 'phosphatidylinositol response', discovered in 1953 by Hokin & Hokin, occurs universally when cells are stimulated by ligands that cause an elevation of the ionized calcium concentration of the cytosol. The initiating reaction is almost certainly hydrolysis of an inositol lipid by a phosphodiesterase. Phosphatidylinositol, phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate all break down rapidly under such circumstances. However, we do not yet know which of these individual reactions is most closely coupled to receptor stimulation, nor do we know where in the cell it occurs. With many stimuli, inositol phospholipid breakdown is closely coupled to occupation of receptors and appears not to be a response to changes in cytosol [Ca2+]: this provoked the suggestion that it may be a reaction essential to the coupling between activation of receptors and the mobilization of Ca2+ within the cell. In a few situations, however, it appears probable that inositol lipid breakdown can occur as a result of the rise in cytosol [Ca2+] that follows receptor activation: such observations gave rise to the alternative opinion that inositol lipid breakdown cannot be related to stimulus-response coupling at calcium-mobilizing receptors. It now seems likely that these two views are too rigidly polarized and that some cells probably display both receptor-linked and Ca2+-controlled breakdown of inositol lipids. Both may sometimes occur simultaneously or sequentially in the same cell.

Animals↗
PubMed1981

Phosphatidylinositol metabolism in rat hepatocytes stimulated by vasopressin.

In isolated rat hepatocytes, vasopressin evoked a large increase in the incorporation of [32P]Pi into phosphatidylinositol, accompanied by smaller increases in the incorporation of [1-14C]oleate and [U-14C]glycerol. Incorporation of these precursors into the other major phospholipids was unchanged during vasopressin treatment. Vasopressin also promoted phosphatidylinositol breakdown in hepatocytes. Half-maximum effects on phosphatidylinositol breakdown and on phosphatidylinositol labelling occurred at about 5 nM-vasopressin, a concentration at which approximately half of the hepatic vasopressin receptors are occupied but which is much greater than is needed to produce half-maximal activation of glycogen phosphorylase. Insulin did not change the incorporation of [32P]Pi into the phospholipids of hepatocytes and it had no effect on the response to vasopressin. Although the incorporation of [32P]Pi into hepatocyte lipids was decreased when cells were incubated in a Ca2+-free medium, vasopressin still provoked a substantial stimulation of phosphatidylinositol labelling under these conditions. Studies with the antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),8-arginine]vasopressin indicated that the hepatic vasopressin receptors that control phosphatidylinositol metabolism are similar to those that mediate the vasopressor response in vivo. When prelabelled hepatocytes were stimulated for 5 min and then subjected to subcellular fractionation. The decrease in [3H]phosphatidylinositol content in each cell fraction with approximately in proportion to its original phosphatidylinositol content. This may be a consequence of phosphatidylinositol breakdown at a single site, followed by rapid phosphatidylinositol exchange between membranes leading to re-establishment of an equilibrium distribution.

Animals↗
PubMed1981

Stimulation of inorganic-phosphate incorporation into phosphatidylinositol in rat thoracic aorta mediated through V1-vasopressin receptors.

Vasopressin stimulates the incorporation of [32P]Pi into phosphatidylinositol but not into other phospholipids in rat thoracic aorta strips. The relative abilities of three vasopressin analogues to stimulate phosphatidylinositol labelling in rat aorta are similar to their relative pressor potencies in vivo and to their relative potencies in stimulating the metabolism of rat hepatocytes, but very different from their relative antidiuretic potencies. The vasopressor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),8-arginine]vasopressin competitively inhibits [Arg8]vasopressin-stimulated phosphatidylinositol labelling in rat aorta with a pA2 of 8.1. It is concluded that the Ca2+-mobilizing vasopressin receptors (V1-receptors) of the rat aorta stimulate phosphatidylinositol metabolism, probably by enhancing phosphatidylinositol breakdown.

Animals↗
PubMed1979

The control by vasopressin of carbohydrate and lipid metabolism in the perfused rat liver.

Vasopressin-induced glucose release from the perfused livers of fed rats is diminished in the presence of insulin or following adrenal ablation. The reduced rate of glucose release following vasopressin treatment in the perfused livers of adrenalectomized rats was restored towards the control value by cortisol treatment in vivo. Vasopressin did not influence the total rate of fatty acid synthesis in the livers of fed rats perfused with medium containing glucose and two concentrations of lactate. The contribution of these precursors to hepatic fatty acid synthesis and CO2 production was similarly uninfluenced by vasopressin. Vasopressin casued a transient increase in the release of K+ by the perfused liver which was observed within 2 min of hormone administration. These results are discussed in relation to the possible mode of action of vasopressin in the liver.

Adrenal Glands↗
PubMed1979

The influence of vasopressin and related peptides on glycogen phosphorylase activity and phosphatidylinositol metabolism in hepatocytes.

The relative abilities of seven vasopressin-like peptides to activate hepatic glycogen phosphorylase and stimulate phosphate incorporation into phosphatidylinositol were compared. Although the individual peptides differed in their potencies, the concentrations required to stimulate phosphatidylinositol metabolism were always greater (about 10 times) than those needed to activate phosphorylase. The molecular specificity of the hepatic vasopressin receptor and the role of vasopressin-stimulated phosphatidylinositol turnover are discussed.

Animals↗
PubMed1979

The value of the electromagnetic flow probe in experimental and clinical microvascular anastomosis.

The Gould Statham Blood Flowmeter Model SP 2204 has been used to assess microanastomosis in 25 superficial femoral arteries of rabbits. When a pulsatile wave form has been achieved this correlates with a satisfactory anastomosis and vice versa. The digital read out of estimated volume flow past the anastomosis made by this instrument will need further evaluation. We are persisting with the electromagnetic flow probe in the assessment of our clinical microvascular anastomoses at operation.

Animals↗
PubMed1978

Intraoperative autotransfusion for elective aortic surgery.

Intraoperative autotransfusion using the Bentley ATS 100 was used in 23 patients requiring Dacron replacement of their abdominal aorta. An average 2000 ml of blood was reinfused and a total heparinization dose was given. The mean haemoglobin fell 2.8 g/dl and on average 2 pints of banked blood were given in the postoperative period. Coagulation studies performed before and after surgery showed minimal alteration. We feel that further evaluation of this system is essential so that an alternative is established for when banked blood is not available. The system is particularly useful at the present time for such emergencies as a leaking abdominal aortic aneurysm and severe trauma to the liver.

Aorta, Abdominal↗
PubMed1978

Oesophageal function in cirrhotic patients undergoing injection sclerotherapy for oesophageal varices.

Oesophageal function has been studied in three groups of cirrhotic patients: those without varices, those with varices and those with varices treated by injection sclerotherapy. Using the Honeywell Model 31 oesophageal motility probe and the Ingold combined stomach pH electrode, measurements were made of the lower oesophageal sphincter (LES) pressure and length, swallowing responses, reflux and clearance of acid. The presence of varices was associated with an increase in LES length and reduced lower oesophageal contraction pressure during swallowing and some failure of sphincter relaxation during swallowing. Sclerotherapy was associated with a reduction in the maximum LES pressure both at rest and during swallowing, and an impairment of acid clearance, but postural reflux of acid was not observed in any patient.

Deglutition↗
PubMed1976

Fatty acid synthesis in the perfused liver of adrenalectomized rats.

1. Fatty acid synthesis, measured in the perfused liver of fed adrenalectomized rats with 3H2O and 14C-labelled precursors, was less than in control sham-operated rats. 2. This defect was more extensive for synthesis of fatty acids incorporated into triacylglycerols than into phospholipids. 3. There was impairment in desaturation and export of newly synthesized fatty acid. 4. Fatty acid synthesis and desaturation were restored to normal rates 5h after treatment with cortisol in vivo. 5. Fatty acid synthesis was seasonally variable, being highest in the winter; the impairment after adrenalectomy was observed in all seasons. 6. In perfusions with oleate (0.7 mM), no further impairment in fatty acid synthesis was discerned in livers from adrenalectomized rats, in which the rate resembled that in control livers. 7. No defect in the incorporation of oleate into glycerides was discerned in livers from adrenalectomized rats. 8. Cortisol exerted no stimulatory effect on fatty acid synthesis when added to perfusion media. 9. The impairment in hepatic lipogenesis, demonstrable after adrenalectomy, shows that adrenal glucocorticoids promote hepatic capacity for fatty acid synthesis de novo, at least in intact non-diabetic rats. It is suggested that this effect is mediated by insulin, perhaps through direct action on the liver.

Adrenal Glands↗