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Biomedical subjects

J Marco

Publications and source records attributed to J Marco.

At least 199 records · Page 11Linked to original sources
PubMed1983

Influence of dimethylsulphoxide on the functional state of isolated rat hepatocytes.

The effect of dimethylsulphoxide upon respiration, glycolysis and gluconeogenesis in isolated rat hepatocytes was studied. The results show that the glycolysis pathway is strongly inhibited by the action of dimethylsulphoxide in the hepatocytes, with increased glucose uptake and reduced net flux. However, the alterations in respiration and the gluconeogenesis pathway are less pronounced, the only significant change being an increase in respiratory activity during the first 10 min of incubation with dimethylsulphoxide.

Animals↗
PubMed1983

Inhibitory effect of somatostatin-28 on pancreatic polypeptide, glucagon and insulin secretion in normal man.

We have compared the effects of equimolar doses of intravenous somatostatin-28 (SS-28) and somatostatin-14 (SS-14) (250 micrograms and 125 micrograms, respectively) on the secretion of pancreatic polypeptide (PP), glucagon and insulin evoked by a protein-rich meal in normal subjects. Both peptides reduced the fasting plasma levels of these hormones and completely abolished their responses to the alimentary stimulus; in addition, they caused an early decrease of plasma glucose followed by a hyperglycemic phase. As compared to SS-14, SS-28 elicited a longer-lasting inhibition of PP and insulin secretion and displayed greater hypo- and hyperglycemic effects. A somatostatin-like component, similar to SS-28, has been identified in pancreatic extracts as well as in peripheral plasma. Thus, it might be hypothesized that this peptide plays a role in the control of pancreatic hormone release.

Adult↗
PubMed1983

Stimulatory effect of vasoactive intestinal peptide on glycogenolysis and gluconeogenesis in isolated rat hepatocytes: antagonism by insulin.

We have studied the effect of Vasoactive Intestinal Peptide (VIP) on glycogenolysis and gluconeogenesis (as measured by the conversion of [U-14C]pyruvate into glucose) in hepatocytes isolated from fed rats. The influence of VIP on glycogen phosphorylase alpha and pyruvate kinase activities, as well as on cAMP levels, was also evaluated. In addition, the possible antagonism of insulin on these VIP-mediated effects was investigated. VIP enhanced both glycogenolysis and gluconeogenesis in a dose-dependent manner. At 10(-6) M VIP, both processes were increased 2-fold as compared to the basal values; the calculated half-maximal stimulatory concentrations were 2.5 x 10(-8) M and 4 x 10(-8) M, respectively. VIP also caused a dose-dependent activation of glycogen phosphorylase and inactivation of pyruvate kinase. At 10(-6) M VIP, glycogen phosphorylase a was increased 3-fold and pyruvate kinase activity was reduced by 46%. The addition of 10(-7) M VIP to the incubation medium caused a 2-fold increase of basal cAMP levels. All these VIP-mediated effects were markedly blocked by the presence of 10(-8) M insulin. As compared to glucagon (10(-7) M) the potency of an equimolar concentration of VIP, in terms of stimulation of gluconeogenesis, inactivation of pyruvate kinase, and activation of glycogen phosphorylase ranged from 35-45%. Our results indicate that VIP increases hepatic glucose output through the stimulation of both glycogenolysis and gluconeogenesis. These effects seem to be mediated by a cAMP-dependent mechanism.

Animals↗
PubMed1983

[Transluminal coronary angioplasty. Results of the multicenter study of the Working Group on Functional Cardiovascular Research of the French Society of Cardiology].

A multicentre study instituted by the "Functional Cardiovascular Investigations" working group of the French Cardiac Society assembled 219 cases files of patients who had undergone attempted transluminal angioplasty for coronary artery stenosis according to Gruntzig's protocol, between August 1979 and October 1981. The stenosis was catheterised in 179 cases (81 p. 100) and a good result was obtained in 152 patients (69 p. 100). One or more complications occurred in 25 patients (11 p. 100) including one death, 16 emergency aortocoronary bypass procedures (7,3 p. 100) and 7 myocardial infarctions (3,2 p. 100). Medium term follow-up of these patients showed an incidence of restenosis of between 16 p. 100 (24 patients with angina out of the 152 primary successes) and 32 p. 100 (25 of the 77 patients controlled by coronary angiography). The results of this multicentre trial are compared to those reported by the National Heart Lung and Blood Institute. We conclude that transluminal coronary angioplasty gives a good result which is maintained (in some patients after 2 dilatations) in 60 p. 100 of cases, with, however, a risk which is not negligeable: the indications for this procedure should therefore be restricted.

Adult↗
PubMed1983

[Treatment of coronary artery vasospasm during coronary arteriography].

Coronary spasm was first demonstrated by Gensini in 1962, and the diagnostic value of spontaneous spasm during coronary angiography is now generally accepted. In its absence, provocation tests with ergonovine or its derivatives form part of routine hemodynamic investigation for confirming the spastic nature of atypical chest pain or pain suggestive of Prinzmetal angina. The coronary spasm so induced gives rise to reduced coronary flow, an increase in coronary resistance and myocardial ischemia as shown by an increased lactate extraction in coronary sinus blood; therefore, once it is documented, it must be treated in order to avoid myocardial necrosis or ventricular arrhythmias. Three groups of drugs of drugs are used to counteract spontaneous or provoked spasm: alpha-blockers, especially phentolamine, nitrate derivatives, trinitroglycerine or isosorbide dinitrate, and calcium inhibitors nifedipine or diltiazem, which have a direct antispastic effect. The hemodynamic and pharmacological actions of these three groups of drugs depend on whether they are given orally, intravenously or by intracoronary injection. Twenty six coronary spasms were observed in 23 patients out of a total of 780 coronary angiographies (3,3 per cent) performed between June 1980 and June 1981: 12 spasms were spontaneous (1,5 per cent), 6 provoked by the catheter (0,8 per cent) and 8 by methylergometrine. There were no complications. Five coronary spasms were also observed during 70 coronary angioplasties (7,1 per cent). The spasm was relieved in all cases by intravenous injection of 1,5 to 3 mg of trinitrin (Lenitral). Calcium inhibitors, especially nifedipine, have been used successfully by Hugenholtz and Bertrand who consider that nifedipine has a slower action and the coronary dilatation obtained is never as great with the nitrate derivatives. Trinitrin remains the treatment of choice for the rapid relief of provoked spasm.

Calcium↗
PubMed1982

Surgery for cardiac complications caused by endocardial mural fibrin deposits in a hypereosinophilic syndrome.

A 31-year-old man presented with rapid onset of intractable congestive heart failure during the course of chemotherapy for eosinophilic leukemia. Patients with a hypereosinophilic syndrome usually die from complications of eosinophilic infiltration and fibrosis in target organs. The resulting cardiac lesions are a cause of death among these patients. Surgical intervention enabled our patient to survive the immediate medical crisis and has prolonged his life.

Adult↗
PubMed1982

Characterization of the pancreatic polypeptide response to hypoglycemia in man.

The human pancreatic polypeptide (hPP) responses to insulin injection (0.05-0.1 U/kg, i.v.) and to endogenous insulin release as provoked by i.v. tolbutamide (1 g) and oral glucose administration (1.75 g/kg) have been examined. The injection of insulin or tolbutamide was followed by a marked elevation of circulating hPP which was abolished by preventing the hypoglycemic effect of these substances by intravenous glucose infusion. Atropine pre-treatment (1 mg, i.v.) also blocked the hPP responses to insulin- or tolbutamide-induced hypoglycemia. Approximately three hours after glucose ingestion, coinciding with the hypoglycemic phase of the test, there was a clear-cut increase in circulating hPP. This hPP response was blunted by impeding the blood sugar fall to sub-baseline values-by means of a glucose infusion-as well as by prior atropinization. It is concluded that: 1) The hPP secretagogue activity of both, insulin and tolbutamide is mediated by their hypoglycemic effect. 2) The elevation of circulating hPP, which occurs during the late hypoglycemic phase of an oral glucose test, is also dependent upon the blood sugar decline to sub-baseline values. 3) Under the above conditions, the hPP response to hypoglycemia can be blocked by atropine, thus indicating that it is due to activation of the cholinergic system and not to the direct effect of glucose lack at the level of the hPP-cell.

Adult↗
PubMed1982

Lack of effect of bovine pancreatic polypeptide on glucose production by isolated rat hepatocytes.

We have examined the possible influence of bovine pancreatic polypeptide (bPP) on glycogenolysis and gluconeogenesis in hepatocytes isolated from fed rats. The activity of glycogen phosphorylase a and pyruvate kinase, enzymes implicated in the hormonal regulation of these pathways, was also measured. Glycogenolysis was estimated by glucose release into the medium and gluconeogenesis by (U-14C) pyruvate incorporation into glucose. Addition of bPP to the incubation medium did not modify endogenous glucose production or glycogen phosphorylase a activity, either under basal conditions or on stimulation by glucagon (3 x 10(-10) M) or phenylephrine (10(-5) M). bPP also failed to alter both the incorporation rate of (U-14 C) pyruvate into glucose and pyruvate kinase activity, under basal conditions as well as in the presence of glucagon. Furthermore, time-course experiments revealed no effect of bPP on glycogen phosphorylase a or pyruvate kinase activities. These data indicate that pancreatic polypeptide is not implicated in the control of glucose production by isolated liver cells from fed rats.

Animals↗