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Biomedical subjects

M Marre

Publications and source records attributed to M Marre.

At least 127 records · Page 7Linked to original sources
PubMed1986

[Relation between urinary albumin excretion and retinopathy in insulin-dependent diabetics].

To study the relationship between retinal and renal microangiopathy, the albumin excretion rate (AER) was measured by radioimmunoassay in 111 insulin-dependent diabetics and compared to their stages of retinopathy, as assessed by ophthalmoscopic examination and fluorescein angiography. The prevalence of pathological AER differed from that of diabetic retinopathy. The stage of retinopathy was related to the duration of diabetes (r = 0.59; P = 0.001), which was not the case for AER (r = 0.06; ns). Half of patients with proliferative retinopathy (11/22) had a normal AER, while 12% of those without retinopathy had a pathological AER (microalbuminuria). No relationship was found between glycaemic control and AER. The highest prevalence of hypertension was found in patients with macroalbuminuria (greater than 500 mg/24 h) and/or severe retinopathy. The mean AER was higher in hypertensive diabetics than in non-hypertensive diabetics (P less than 0.005). These results suggest that the risk of retinopathy is dissociated from the risk of glomerulopathy in diabetics, and that hypertension associates with diabetes mellitus in a greater risk of pathological AER.

Adolescent↗
PubMed1986

[Reduction of urinary kallikrein in hypertensive diabetics].

Renal Kallikrein, an enzyme of the distal tubule acting through kinin liberation, may participate to the control of renal circulation and blood pressure. To study if an impairment of its secretion may exist in diabetics, a cross-sectional study was carried out on 40 non-hypertensive and 29 hypertensive diabetics, compared to 30-age related controls. Urinary Kallikrein Activity (UKA) was measured by its kininogenase activity with and without trypsin preincubation. Compared to UKA in controls (86 +/- 9 micrograms lysyl-bradykinin [LBK] produced per minute of incubation), UKA was significantly reduced either in non-hypertensive diabetics (59 +/- 8 micrograms LBK. min.-1; p less than 0.05) and in hypertensive diabetics (26 +/- 6 micrograms LBK. min.-1; p less than 0.001). The ratio of total/active urinary kallikrein was similar in diabetics and in controls. The decline of UKA in diabetics was related to the duration of their disease (r = -0.38; p less than 0.05) and to their stage of retinopathy (r = -0.46; p less than 0.001). UKA values were proportional to creatinine clearance in diabetics (r = 0.58; p less than 0.001). The lowest UKA values were found in patients with a high urinary excretion of albumin (above 500 mg/day): 8 +/- 2 micrograms LBK. min-1 (p less than 0.001) and beta-2-microglobulin (above 382 micrograms/day): 12 +/- 4 micrograms LBK. min-1 (p less than 0.001). These findings support that an impaired secretion of renal kallikrein in diabetics can be related to the duration of diabetes and to the severity of microangiopathy.

Adult↗
PubMed1985

[Treatment of arterial hypertension in diabetics. Contribution of converting enzyme inhibitors].

The treatment of arterial hypertension in diabetic patients still raises numerous problems. In this type of patients, the most commonly prescribed drugs (beta-blockers, diuretics, antihypertensive agents acting on the central nervous system) have troublesome and potentially detrimental effects (e.g. effects on lipids). The new categories of antihypertensive drugs recently introduced (angiotensin-converting enzyme inhibitors, calcium antagonists) are likely to be most useful in these patients. In an open trial in non-insulin-dependent diabetics with arterial hypertension followed-up for 1 year, enalapril administered alone has proved effective and devoid of clinical and biochemical side-effects. If these results are confirmed, angiotensin-converting enzyme inhibitors will rank high as first-choice treatment of arterial hypertension in diabetics.

Adrenergic beta-Antagonists↗
PubMed1985

Survival and rehabilitation after total pancreatectomy. A follow-up of 36 patients.

Thirty-six totally depancreatectomized patients were followed up for 4-124 months. Pancreatectomy had been performed because of fulminant pancreatitis (in 10), chronic hyperalgic otherwise untractable pancreatitis (in 7), exocrine carcinoma of the pancreas (in 16), cystadenocarcinoma of the pancreas (in 2) and insulinoma (in 1). The longest survival duration was in chronic pancreatitis patients: 57 +/- 17 months. A normal socio-professional reinsertion was obtained in 16 patients, mainly those with non-malignant pancreotopathies. At the end of the survey, ten of the carcinoma patients had died, versus none in the other groups. Diabetes mellitus was characterized by the absence of ketonuria, and the frequent occurrence of hypoglycemia (in 15 patients) and infection (in 6). Malabsorption caused osteomalacia in one patient.

Acute Disease↗
PubMed1985

[Calcium antagonists and glycoregulation: dissociated effects of nicardipine on vascular tonus and insulin secretion].

Insulin release is coupled with a calcium entry into the pancreatic B cells. The use of calcium-antagonists may eventually alter glucose homeostasis. To evaluate this possibility, nicardipine action was tested both in vitro and in vivo: 1. on insulin release and vascular resistances from isolated perfused rat pancreases; 2. on 7 hypertensive patients with an established glucose intolerance, during two oral glucose tolerance tests (OGTT) performed successively under placebo and nicardipine (90 mg daily) at a two-week interval. In vitro, the basal insulin release from isolated perfused rat pancreases (86 +/- 15 ng.min-1; n = 27; M +/- SE) was inhibited according to the nicardipine dose by the 5 th min. of infusion: 7.2 +/- 1.5 p.100 of the initial output at 10(-4) M (n = 6; p less than %.001); 33.4 +/- 2.7 p.100 at 10(-6) M (n = 6; p less than 0.001); 87.5 +/- 14.8 p.100 at 10(-8) M (n = 6; ns). The pancreatic vascular resistances declined significantly for the 3 doses, but no dose-response could be registered. In vivo, the mean arterial blood pressure was significantly reduced by nicardipine from 114 +/- 3 mmHg to 95 +/- 3 mmHg (p less than 0.001) without any significant alteration of either glucose tolerance (glycaemias at the 120 th min of OGTT: 9.2 +/- 1.1 mmol.l-1 vs 8.9 +/- 1.2 mmol.-1) or insulin peak: 70 +/- 20 micrograms U.ml-1 vs 67 +/- 22 microU.ml-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

[Prevalence of antinuclear antibodies in hypertensive diabetics treated with acebutolol].

Acebutolol may induce the development of antinuclear antibodies and, exceptionally, of a lupus-like syndrome. The purpose of this study was to evaluate the prevalence of antinuclear antibodies in hypertensive diabetics under long-term treatment with acebutolol. Seventy-eight normal subjects, 75 diabetics under antidiabetic therapy only, and 75 hypertensive diabetics who received acebutolol in mean doses of 478 +/- 242 mg/day for at least one year were investigated. The 3 groups were comparable with regard to age and sex. Antinuclear antibodies were detected in 18.6% of diabetics under acebutolol, as against 3.8% and 1.3% respectively of subjects in the other groups (p less than 0.01). There was no correlation between the levels of antinuclear antibodies and the dosage or duration of acebutolol treatment. None of the sera tested contained antinative DNA antibodies, and none of the hypertensive diabetics exhibited signs of lupus-like syndrome.

Acebutolol↗
PubMed1983

Regulation of kallikrein and renin release by the isolated perfused rat kidney.

Rat kidneys perfused in vitro released kallikrein in urine, and renin and kallikrein in the perfusate. The kallikrein was characterized by its kininogenase activity and released bradykinin from bovine and dog substrates. Inactive trypsin activatable kallikrein was present in both perfusate and urine. Kallikrein secretion in urine was influenced by changes in perfusion pressure (PP). Raising the PP strikingly increased urinary kallikrein and lowering PP reduced it. Urinary water and electrolyte output were augmented to the same extent by furosemide and mannitol administration as by raising the PP, but neither drug affected kallikrein. Isoproterenol stimulated the release of renin but not kallikrein. Stopping the oxygen supply to the perfusate suppressed kallikrein secretion in urine and renin release in the perfusate. The kidneys released ten times less kallikrein in the perfusate than in urine, and perfusate kallikrein was not influenced by changes in PP. It is concluded that in this model, changes in PP and/or renal blood flow and/or oxygen supply regulate kallikrein secretion in urine, but that this secretion is unaffected by changes in urinary output. We also conclude that kallikrein release in urine and renin release in perfusate are regulated simultaneously by renal hemodynamic changes but are not affected concomitant by beta-adrenergic stimulation or changes in distal urine composition.

Animals↗
PubMed1983

The nervous control of rat glucagon secretion in vivo.

In order to study the efferent pathways of the nervous regulation of rat A and B cells, portal blood samples were obtained in vivo without interruption of the blood flow. Glucagon, insulin and catecholamines were determined and hepatic blood flow (EHBF) was estimated by a Brome-Sulfone-Phtaleine extraction method. Carotid blood pressure was monitored and a normal volaemia was maintained. Stimulation of the right vagus nerve increased EHBF and the releases of glucagon and insulin. Stimulation of splanchnic nerve increased the glucagon and catecholamine secretions and decreased that of insulin. Acute hypovolaemia as induced by blood withdrawal, caused hormonal consequences similar to those of splanchnic stimulation. It is suggested that the nervous control of pancreatic islets plays an important role in the rat species. Assessment of the haemodynamic status is critical for the valid interpretation of pancreatic hormone concentrations in experimental conditions. A sympathetic stimulation can account for the high glucagon and relatively low insulin secretions which characterize the hormonal pattern of stress.

Animals↗
PubMed1983

Reciprocal gastropancreatic modulations for the release of somatostatin-like immunoreactivity, glucagon, and insulin in the rat.

In order to assess the interrelationships between stomach and pancreas regarding the secretions of somatostatin-like immunoreactivity (SLI), glucagon (IRG), and insulin (IRI), concentrations of the three hormones were assayed in portal plasma and portal blood flow was measured in enterectomized rats before and after the selective removal of stomach or pancreas. Portal plasma SLI, IRG, and IRI concentrations were significantly increased by i.v. arginine in control rats (pancreas + stomach present). After gastrectomy, SLI, IRG, and IRI concentrations were, respectively, 52 +/- 13% (N = 15; P less than 0.005), 234 +/- 40% (P less than 0.001), and 119 +/- 15% (NS) of the pregastrectomy values. A decreased SLI secretion, an increased IRG release, and an unmodified basal IRI release were estimated by portal flow measurement. The A- and B-cell responses to arginine in the gastrectomized rats were significantly higher than in the control rats, while the D-cell response was no longer detectable. After pancreatectomy, by contrast, SLI concentrations were 360 +/- 75% of the prepancreatectomy values (N = 12; P less than 0.001). This reflected an actual increment of SLI release, taking into account the concomitant measurement of portal blood flow. The concentrations of IRG declined by 51 +/- 5% (P less than 0.001) and IRI was no longer measurable. A- and B-cell responses to arginine also were no longer detectable. These results suggest that in these experimental conditions (1) the stomach restrained pancreatic A- and B-cell responses to arginine, perhaps through the SLI released from the stomach and (2) the pancreas restrained gastric SLI secretion, perhaps through insulin.

Animals↗
PubMed1982

The brain-islet axis: the nervous control of the endocrine pancreas.

The central nervous system exerts a control on the endocrine pancreas and can modulate the basic feed-back loop linking the concentration of the main energy substrates in blood with islet cell functions. Thus, the elementary glucose-insulin system can be modulated under physiological conditions by both the long-recognized entero-insular axis and by a brain-islet axis, particularly when insulin release occurs in anticipation of meals. Experimental stimulation or section of afferent nerves to the pancreas have demonstrated the existence of this nervous control. Changes in islet cell secretion during stress illustrate this influence under clinical conditions. A variety of experimental data suggest intervention of the brain-islet axis under the physiological circumstances: 1) Manipulation of certain hypothalamic centres followed by modification of feeding behaviour and of islet secretion. 2) Input to the brain is both humoral (carried by arterial carotid blood or the cerebrospinal fluid) and nervous, of sensory and visceral origins. Changes in these afferent pathways may influence islet secretion via the efferent pathways of the vagus and splanchnic nerves. 3) Besides acetylcholine and catecholamines, peptide neurotransmitters are likely to be involved in the transmission of these nervous inputs to islet cells. 4) Furthermore, hypothalamic factor (s) may also modify the endocrine pancreatic secretions.

Adrenergic Fibers↗
PubMed1982

The nervous control of rat somatostatin, glucagon and insulin secretions.

Somatostatin-like-immunoreactivity (SLI), immunoreactive insulin (IRI), glucagon (IRG) and catecholamine concentrations were measured in rat portal plasma during electrical stimulation of the vagus and splanchnic nerves, and during experimentally-induced hypovolaemia and hypoxaemia. Blood pressure, arterial gases and pH were monitored and hepatic blood flow was estimated (EHBF). Stimulation of the vagus nerves induced an increase in IRG and IRI concentrations, but had different influences on SLI level according to the concomitant experimental conditions. Stimulation of the left splanchnic nerve induced a sharp rise in SLI, IRG and catecholamine concentrations, whereas IRI level decreased hypovolaemia and hypoxaemia. Phentolamine treatment augmented the basal IRI, IRG and SLI concentrations. It did not suppress the hypovolaemia-induced rise of IRG and SLI concentrations, but unmasked a strong IRI release. By contrast, propranolol and atropine reduced significantly the A and D cell responses to acute hypovolaemia. These results are consistent with a profound influence of pancreatic nerves on A, B and D cell functions, which should be taken into account for interpretation of results during in vivo experiments.

Animals↗
PubMed1982

Diuretic and natriuretic effects of nifedipine on isolated perfused rat kidneys.

The effects of nifedipine, a vasodilating drug which acts through calcium antagonism, were studied in vitro using isolated perfused rat kidneys. Most of the nifedipine was neither metabolized nor excreted by this preparation. Four doses were tested: 50, 250, 500 and 750 nM. The two higher concentrations enhanced urine flow and sodium (UNaV) and potassium excretion. Tubular reabsorption of sodium was reduced compared to untreated control kidneys. The glomerular filtration rate was not modified but the filtration fraction decreased. The magnitude of urine volume, UNaV, urinary potassium excretion and filtration fraction changes were related to the dose of nifedipine. The decrement of total renal resistance and the increment of UNaV were correlated for 500 and 750 nM nifedipine (n = 13; r = -0.77; P less than .001), suggesting that it acted by dilating the renal vascular bed. Nifedipine at 250, 500 and 750 nM significantly increased the renin secretion rate compared to that of untreated control kidneys. When renin secretion was enhanced by 50 nM isoproterenol, this stimulatory effect was enhanced in kidneys concomitantly treated with 500 and 750 nM nifedipine. Dihydralazine, another vasodilating drug, was tested at a comparable molar dose (500 nM) and induced similar changes in urine volume, UNaV, urinary potassium excretion and Na reabsorption. The variations in total renal resistance and UNaV were also inversely correlated (n = 8; r = -0.68; P less than .05). Dihydralazine did not modify renin secretion rate significantly. These results suggest that: 1) both nifedipine and dihydralazine increase diuresis, natriuresis and kaliuresis in the isolated perfused rat kidney and 2) nifedipine enhances basal renin release from the juxta-glomerular cells and potentiates renin release caused by beta receptor stimulation.

Animals↗