PubMed Health⌕ Search

Biomedical subjects

Y Minaire

Publications and source records attributed to Y Minaire.

At least 19 recordsLinked to original sources

Postdelivery anal function in primiparous females: ultrasound and manometric study.

PURPOSE: A study was performed to evaluate the early morphologic and functional consequences of vaginal delivery on the anal sphincter in primiparous females. METHODS: Among a cohort of 197 primiparous females who agreed to participate in a clinical evaluation of fecal incontinence and in a transanal ultrasound examination 12 weeks after delivery, 52 also underwent anal manometry using a radial six-port catheter, of whom 10 were asymptomatic and had a normal sphincter at ultrasound and the remaining 42 had clinical signs of anal incontinence or ultrasonographic defects of the anal sphincter or both. Anal sphincter pressures and asymmetry index were analyzed at rest and during voluntary squeeze. Manometric and ultrasound results were compared, together with clinical symptoms. RESULTS: Fourteen patients with clinical signs of anal incontinence had lower resting and squeeze anal pressures than continent patients (P < 0.05), but similar anal asymmetry indexes. Patients with incontinence and an anal defect had the lowest resting and squeeze anal pressures (P < 0.05). Forceps assistance to delivery was not associated with a higher frequency of anal sphincter lesions. Resting and squeeze anal pressures were lower in the forceps group (P < 0.005), but anal asymmetry indexes were similar. Finally, manometric results were identical in the presence or absence of anal sphincter endosonographic defects. CONCLUSIONS: Anal sphincter defects are frequent after the first vaginal delivery, but are not always associated with functional or clinical abnormalities. Resting and squeeze anal pressures were significantly decreased in patients with incontinence and an anal defect and after forceps-assisted deliveries. Anal asymmetry index was not found useful in this population of young primiparous females.

Adult↗

[13C]-Galactose breath test: correlation with liver fibrosis in chronic hepatitis C.

BACKGROUND: The galactose elimination capacity test is a quantitative liver function test that has been shown to be a potential surrogate marker for death in advanced chronic liver diseases. However, this test lacks sensitivity in early liver disease. The goal of this study was to evaluate a [13C]-galactose breath test (GBT) in a population of patients with chronic hepatitis C. DESIGN: The GBT was performed in 10 control subjects and 50 patients with chronic hepatitis C; the results were compared with the METAVIR pathological scoring of liver biopsy specimens and with standard biochemical liver function tests. RESULTS: In 10 patients, oral vs. intravenous administration of galactose yielded similar results for the GBT (3.01% +/- 0.12% dose h-1 for oral galactose vs. 2.98 +/- 0.21 for intravenous). The GBT was then performed orally in the remaining 40 patients and 10 control subjects. A significant difference was observed between control subjects and patients (4.51% +/- 0.18% vs. 2.97% +/- 0.14% dose h-1, P < 0.0001). A significant difference for GBT results was observed between each fibrosis stage, but not with regard to the activity score. CONCLUSIONS: The GBT results are dependent on the severity of liver fibrosis in chronic hepatitis C. Further studies are needed to evaluate the usefulness of the GBT for the follow-up of chronic hepatitis C.

Administration, Oral↗

Effects of ethanol and diabetes on galactose oxidative metabolism and elimination in rats.

Blood galactose clearance after an intravenous galactose load has been widely used for years as an index of liver function. We developed a noninvasive [13C]galactose breath test, which explores galactose oxidative metabolism; this test is well correlated with liver fibrosis in patients with chronic viral hepatitis. The goal of this study was to evaluate the influence of nonhepatic factors such as diabetes and ethanol on whole-body galactose clearance (measured as the serum galactose elimination capacity test) and oxidative metabolism (measured as the [13C]galactose-induced breath 13CO2 production) in rats. Acute ethanol administration induced a significant decrease of galactose clearance and 13CO2 production. There was a significant correlation between the amount of ethanol given and the inhibition of galactose metabolism (R2 = 0.72, p < 0.0001). In streptozotocin-induced diabetic rats, the [13C]galactose-induced breath 13CO2 production was significantly reduced (p < 0.0001) and normalized by insulin treatment. However, diabetes did not decrease whole-body galactose clearance, indicating an isotopic dilution of [13C]glucose produced from [13C]galactose metabolism into the enlarged glucose pool. These results must be taken into account when using the [13C]galactose breath test as a quantitative liver function test.

Animals↗

Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion.

BACKGROUND: Quantification of regional myocardial function is a major unresolved issue in cardiology. We evaluated the accuracy of pulsed Doppler tissue imaging (DTI), a new echocardiographic technique, to quantify regional myocardial dysfunction induced by acute ischemia and reperfusion. METHODS AND RESULTS: In nine open-chest anesthetized pigs, various degrees of regional wall motion abnormalities were induced by graded reduction of left anterior descending coronary artery (LAD) blood flow. Pulsed Doppler tissue imaging was performed from an epicardial apical four-chamber view with the sample placed within the middle part of the septal wall. Peak septal velocities were calculated during systole, isovolumic relaxation, and early and late diastole. Regional myocardial blood flow and systolic and diastolic dysfunctions were assessed by radioactive microspheres and ultrasonic crystals, respectively. Ischemia resulted in a significant rapid reduction of systolic velocities and an early decrease in the ratio of early to late diastolic velocities. Both changes were detected by pulsed DTI within 5 seconds of coronary artery occlusion. The decrease in systolic velocity significantly correlated with both systolic shortening (r=.90, P<.0001) and regional myocardial blood flow (r=.96, P<.0001) during reduction of LAD blood flow. CONCLUSIONS: These results suggest that DTI may be a promising new tool for the quantification of ischemia-induced regional myocardial dysfunction.

Animals↗

Stretch-induced protection shares a common mechanism with ischemic preconditioning in rabbit heart.

We sought to determine whether stretch-induced preconditioning may be related to activation of adenosine receptors, ATP-sensitive K+ (K+ATP) channels, and/or protein kinase C (PKC) in the rabbit heart. Anesthetized rabbits underwent 30 min of coronary artery occlusion followed by 3 h of reperfusion. Ischemic preconditioning was induced by one episode of 5 min of ischemia followed by 5 min of reperfusion, and stretch preconditioning was induced by a transient volume overload. The abilities of gadolinium (Gd3+), a blocker of stretch-activated channels, glibenclamide (Glib), a blocker of K+ATP channels, 8-(p-sulfophenyl)-theophylline (8-SPT), a blocker of adenosine receptors, and polymyxin B (PMXB), an antagonist of PKC, to prevent the infarct size-limiting effect of stretch-induced preconditioning were evaluated. Because the infarct size-reducing effect of stretch occurred in the absence of ischemia and was prevented by previous administration of Gd3+, Glib, 8-SPT, and PMXB, we propose that activation of mechanosensitive ion channels protects the rabbit heart from subsequent sustained ischemic insult, likely through a mechanism that involves downstream activation of PKC, adenosine receptors, and/or K+ATP channels.

Animals↗

Short-term cold-exposure does not improve insulin sensitivity in rats.

Effects of noradrenergic activation induced by short-term cold-exposure (7 days at 4 degrees C) on whole-body glucose utilization and tissue glucose uptake were investigated in rats. Measurements were realized on anesthetized normothermic animals at four different levels of insulinemia, within physiological range, allowing calculation of insulin sensitivity and responsiveness. Whole-body glucose utilization increased as a logarithmic function of insulinemias, and was always higher in cold-exposed than in control rats. However, neither insulin sensitivity nor responsiveness, literally, appeared different between the two groups. In the diaphragm, the only studied working muscle, glucose uptake was largely higher than in restin muscles. At basal insulin concentration, glucose uptake was higher in cold-exposed than in control rats and increased in the two groups with insulinemia. Among resting muscles, glucose uptake was increased by previous cold exposure in gastrocnemius, soleus, and tibialis. However, insulin sensitivity and responsiveness were found augmented only in the two former. In interscapular brown adipose tissue, glucose uptake was largely higher in cold-exposed than in control rats, but no difference could be evidenced in insulin sensitivity or responsiveness. In white adipose tissues, glucose uptake increased with insulinemia. Insulin responsiveness and sensitivity were higher only in the retroperitoneal depot.

Adipose Tissue↗

13C-urea breath test for Helicobacter pylori: cut-off point determination by cluster analysis.

1. This study was performed on a large set of 13C-urea breath test results to determine the optimal cut-off point of the test for the diagnosis of Helicobacter pylori (Hp) infection. 2. The following steps were applied to three sets of urea breath test results obtained in three groups of subjects (696 adults before anti-Hp treatment, 1056 adults after anti-Hp treatment and 173 children under 17 years of age): (1) demonstrate the distribution of urea breath test results as a mix of two normal populations (Hp negative and Hp positive) by logarithmic transformation of the results in each group of subjects; (2) apply statistical cluster analysis to determine the separation point between Hp-negative and -positive populations; (3) calculate the mean and SD of each population, and use these parameters in the equation of the normal distribution to establish the frequency curves of Hp-negative and -positive populations; and (4) determine the cut-off point of the urea breath test as the intersection of the two curves, and the risks of error related to it. 3. The optimal cut-off point was found at +3.00 delta/1000, with a risk of false-negative or -positive response of the urea breath test of less than 3%. From this, a cut-off point of +3.00 delta/1000 for the 13C-urea breath test is recommended, with an indetermined zone between +2.5 and +3.5 delta/1000 to account for the spontaneous variation of 13CO2 in breath and the limits of GC-isotope ratio-MS analytical precision.

Adolescent↗

Beneficial actions of preconditioning and stretch on postischemic contractile function of isolated working rat heart: effects of staurosporine.

Preconditioning is commonly induced by a brief ischemic insult; myocardial stretch can trigger this protection by an unknown mechanism. Myocardial stretch preconditions the in vivo canine heart; however, the existence of a stretch-induced protection in the rat heart remains unknown. The purpose of this study was to test this myocardial protection induced, in isolated working rat heart, by global ischemia and stretch initiated by a transient increase in the left ventricle (LV). Isolated rat hearts underwent 30 min of global ischemia followed by 30 min of reperfusion. Before this, hearts received a 15-min period of either no intervention (control; C), 5 min of global ischemia + 10 min of reperfusion (preconditioning; PC) or 5 min of stretch + 10 min with no intervention (stretch; S). Stretch was induced by a transient increase in LV preload from 5 to 20 cm H2O. LV work started under a afterload of 80 cm H2O. Control, PC, and S hearts received either no drug (untreated) or staurosporine (50 nM), a protein kinase C inhibitor, before the "preconditioning" period. Creatine kinase (CK) release, ventricular fibrillation during reperfusion, and postischemic recovery of contractile function (aortic flow) were the end points of the study. In the S group, the abrupt increase in preload resulted in a significant increase of aortic flow (42 +/- 2 to 47 +/- 2 ml/min; p < 0.05). During the 30-min reperfusion period, control hearts displayed a poor recovery of contractile functions (8 +/- 3 ml/min, 30 min after reflow, versus 40 +/- 2 ml/min at baseline; p < 0.05). Both untreated PC and S groups exhibited a significant reduction in CK release, incidence of ventricular fibrillation (55% of control hearts developed persistent VF vs. 6% in both the PC and S groups), and postischemic dysfunction during reperfusion (p < 0.05 vs. control). Staurosporine prevented these beneficial effects in PC and S groups. Our study suggests that myocardial protection can be induced by stretch in the isolated working rat heart, likely through activation of protein kinase C. In conclusion, our results show that ischemic preconditioning and stretch had comparable favorable effect on functional recovery after a sustained ischemic insult in the isolated rat heart.

Animals↗

Ventricular fibrillation in preconditioned pig hearts: role of K+ATP channels.

ATP-dependent potassium (K+ATP) channels play a role in the infarct size-limiting effect of preconditioning in pigs. We previously demonstrated that preconditioning shortens monophasic action potential duration (MAPD) and accelerates the time to ventricular fibrillation (VF) during a prolonged ischemia in pigs. We sought to determine whether the mechanism of the reduced time to VF in preconditioned pigs is a consequence of K+ATP, channel activation. Pigs underwent 40 min of coronary occlusion and 2 h of reperfusion. Before this, animals received either no intervention (control), 10 min of ischemia and 10 min of reperfusion (preconditioned), or an intravenous infusion of nicorandil, a K+ATP channel opener. Additional control, preconditioned, and nicorandil-treated pigs were pretreated by glibenclamide, an antagonist of K+ATP channels. Because 1) the K+ATP channel activator nicorandil did not produce shorter time to VF, 2) the K+ATP channel inhibitor glibenclamide did not block the acceleration of VF by preconditioning, and 3) there was no relationship between time to VF and infarct size or MAPD, the major conclusion is that reduced time to VF in preconditioned animals is not a consequence of K+ATP channel activation.

Action Potentials↗

Continuous monitoring of 13C-aminopyrine metabolism in rats: effects of cold exposure and noradrenaline.

A system was developed to allow constant monitoring of hepatic cytochrome P450 activity in awake and unrestrained rats. A continuous 13C-aminopyrine perfusion was performed, and breath samples obtained for endogenous CO2 production and 13C measurements, to calculate 13C O2 production due to aminopyrine demthylation. Increasing doses of 13C-aminopyrine produced a hyperbolic increase of expired 13CO2, compatible with an in vivo measurement of enzymatic activity. Acute-cold exposure of the rats during 13C-aminopyrine perfusion produced a two-fold increase of endogenous CO2 production, together with a 27% increased 13C-aminopyrine metabolism (p<0.05 vs basal conditions). In contrast, noradrenaline (20 microg/kg BW/min), despite a similar effect on energy expenditure, did not significantly change 13C-aminopyrine metabolism. Acute-cold exposure is known to stimulate both adrenal catecholamine secretion and the sympathetic nervous system. The observed difference in 13C-aminopyrine demthylation during cold exposure and nonadrenaline perfusion, therefore, could be due to a more specific effect of adrenal catecholamines on liver aminopyrine metabolism. These results suggest the possibility of prolonged in vivo monitoring of liver metabolism pathways such as aminopyrine demethylation, thus allowing the study of drug acute interactions with cytochrome P450 system.

Aminopyrine↗

Carbon tetrachloride-induced cirrhosis in rats: influence of the acute effects of the toxin on glucose metabolism.

In animal models, conflicting results on the effect of cirrhosis on glucose metabolism have been reported. The use of various toxins as well as differences in experimental protocols may be responsible for these controversial data. However, differences may be also be explained by the fact that glucose metabolism has been evaluated following different time intervals after cessation of the toxic injury. Therefore, we have performed intravenous glucose tolerance tests, euglycemic hyperinsulinemic clamps (at 2,6, and 30 mU/kg/min insulin infusion rates), and determination of peripheral tissue glucose metabolic index (by [3H]2-deoxy-glucose injection) in rats treated for 10 weeks with carbon tetrachloride, either 3 days (acute group) or 2 weeks (delayed group) after the last CCl4 dose was administered. Cirrhosis was confirmed by liver histological analysis, and by a 22% (P <.05) decrease in 13C-aminopyrine demethylation. In the acute group, whole-body glucose disposal was decreased at the highest insulin infusion rate only (19.7 +/- 1.2 vs. 23.4 +/- 1.2 mg/kg/min in controls, P <.05). In contrast, results of the delayed group were not different from controls at any insulin infusion rate. Peripheral tissue glucose metabolic index was significantly decreased in all muscles tested in the acute group compared with controls. A significant decrease of glucose utilization was found in some but not all muscles in the delayed group but was less pronounced than in the acute group. In conclusion, this study showed than insulin sensitivity in cirrhotic rats is time-dependent with regard to the last CCl4 administration. These results must be taken into account when using this experimental model of liver cirrhosis.

Animals↗

Demonstration of in vivo metabolic effects of 3,5-di-iodothyronine.

The objective of the present study was to test in vivo the metabolic effects of 3,5-di-iodothyronine (3,5-T2) in unanesthetized and unrestrained male Sprague-Dawley rats. Amino acid and lipid metabolisms were investigated by breath tests using as tracers the 13C-carboxyl-labeled molecules of leucine, alpha-ketoisocaproic acid (KIC) and octanoic acid, in four different groups of rats: hypothyroid animals (receiving propylthiouracil (PTU) and iopanoic acid), hypothyroid animals treated with either a daily i.p. injection of 3,5-T2 (25 micrograms/100 g body weight), or tri-iodothyronine (T3) (1 microgram/100 g body weight), and control euthyroid animals receiving equivalent volumes of the vehicle solutions. Energy expenditure was measured by continuous monitoring of O2 consumption and CO2 production in these different groups. Daily energy expenditure was decreased by 30% in PTU-treated rats. The chronic treatments with 3,5-T2 and T3 restored daily energy expenditure to the control level. 13CO2 recovered in breath following the i.v. injection of octanoic acid-[1-13C] was decreased in hypothyroid animals compared with control animals (P < 0.05) and restored to control values by T3 and 3,5-T2 treatments. The 13CO2 recovered in breath after i.v. injection of leucine-[1-13C] was increased in PTU-treated compared with control animals (P < 0.05). Chronic treatment with either 3,5-T2 or T3 restored 13CO2 to control values. Excretion of 13CO2 recovered in breath following the i.v. injection of KIC-[1-13C] was increased in PTU-treated compared with control animals. Chronic treatments with either 3,5-T2 or T3 did not restore KIC decarboxylation. These results suggest that 3,5-T2 exerts metabolic effects on energy expenditure, on both lipid beta-oxidation and leucine metabolism in hypothyroid rats. We conclude that 3,5-T2 is a metabolically active iodothyronine.

Amino Acids↗

In situ regulation of lipolysis by insulin and norepinephrine: a microdialysis study during euglycemic-hyperinsulinemic clamp.

Lipolytic responsiveness of subcutaneous and epididymal adipose tissue to norepinephrine (NE) was measured by microdialysis before and during a euglycemic-hyperinsulinemic clamp in male Sprague-Dawley rats (280 +/- 7g, n = 8). Microdialysis probes were perfused with standard Krebs-Ringer buffer without (basal condition [BC]) or with NE 10(-6) mol/L to determine basal and stimulated rates of lipolysis. The dialysate concentration of glycerol was measured (lipolytic index). NE infusion resulted in 3.0- and 4.2-fold increases in glycerol release in abdominal subcutaneous and epididymal adipose tissues, respectively. A euglycemic-hyperinsulinemic clamp at 6 mU/kg.min increased by ninefold the insulinemia (120 +/- 9 U/L). Hyperinsulinemia suppressed basal glycerol release by 57% and 42% in subcutaneous and epididymal adipose depots, respectively (BC + I). Lipolytic responses to NE infusion during a euglycemic-hyperinsulinemic clamp (NE + I) were reduced by 45% and 33% in subcutaneous and epididymal adipose tissues, respectively, as compared with BC. Under BC, the lipolytic response to NE was greater in epididymal than in subcutaneous adipose tissue. Physiological levels of insulin regulated basal lipolysis and counteracted adrenergic stimulation of lipolysis to a similar extent in both superficial (subcutaneous) and intraabdominal (epididymal) adipose tissue. Our findings show that lipolysis is more responsive to NE in epididymal than in subcutaneous adipose tissue. The antilipolytic effects of insulin are similar in both superficial and deep intraabdominal adipose tissues. Furthermore, physiological plasma insulin levels cannot fully antagonize the lipolytic effects of NE.

Adipose Tissue↗

Human hepatic macrovesicular steatosis: a noninvasive study of mitochondrial ketoisocaproic acid decarboxylation.

Differentiating between alcoholic and nonalcoholic hepatic steatosis is often a difficult clinical task. However, decreased fatty acid mitochondrial oxidation appears as the main factor for alcoholic steatosis, whereas nonalcoholic steatosis may be due to other causes. We studied mitochondrial function, based on a 13C-ketoisocaproic acid (13C-KIC) breath test, in nine alcoholic and 12 nonalcoholic steatosis patients and 10 healthy volunteers. Our results showed a 42% 13C-KIC decarboxylation decrease in alcoholic steatosis patients, but not in nonalcoholic steatosis patients. This noninvasive breath test appears helpful for the diagnostic work-up of hepatic steatosis.

Adult↗

Preconditioning reduces infarct size but accelerates time to ventricular fibrillation in ischemic pig heart.

Preconditioning protects the rat heart from ventricular arrhythmias. However, the mechanism of this beneficial effect and its existence in large animal models remain unknown. We submitted 49 pigs to 40 min of left anterior descending coronary occlusion and 2 h of reperfusion and assessed the incidence of ventricular fibrillation (VF) and time to VF. Monophasic action potential duration (MAPD) and ventricular fibrillation threshold (VFT) were measured throughout the experiment. Preconditioning significantly reduced infarct size but failed to reduce the incidence of VF either during the 40-min ischemic insult or the following reperfusion. Moreover, preconditioning accelerated the onset of VF during the prolonged ischemia; time to VF averaged 8 +/- 2 min in the preconditioned group vs. 18 +/- 2 min in the control group (P < 0.05). This premature peak of VF in preconditioned hearts was associated with a significant decrease of VFT and shortening of MAPD. This suggests that preconditioning does not limit the incidence of VF in the pig model. Rather, preconditioning decreases the time to VF in this species, likely through lowering of the VFT and shortening of the action potential duration.

Action Potentials↗

[Ischemic preconditioning: concept of endogenous myocardial protection].

Preconditioning is a temporary tolerance to ischaemia acquired by the myocardium after a short period of ischaemia. It results in the limitation of the infarct size induced by prolonged coronary occlusion. The mechanism of this cytoprotection remains poorly understood. The A1 adenosine receptors, the ATP-sensitive potassium channels and protein-kinase C seem to play prominent roles. The effects of preconditioning on the complications of ischaemia/reperfusion such as myocardial stunning, ventricular arrhythmias or decreased coronary reserve are not well known. Several studies suggest that the cytoprotection resulting from preconditioning could be applied to human myocardium and constitute a preventive anti-ischaemic therapy during coronary angioplasty, cardiac surgery or the conservation of transplant grafts.

Adaptation, Physiological↗

Mechanism of carbon tetrachloride autoprotection: an in vivo study based on 13C-aminopyrine and 13C-galactose breath tests.

This study was conducted to evaluate in vivo the hepatotoxic effects of CCl4 administration to rats using 13C breath tests: aminopyrine breath test (ABT) was used to monitor CCl4-induced cytochrome P450 inactivation, and galactose breath test (GBT) to quantitatively measure the CCl4-induced decrease of liver function. The ABT results showed profound aminopyrine demethylation inhibition lasting for three days and complete recovery at day 7, while GBT results were decreased only one day after CCl4. The protection induced by a first CCl4 dose against a second one paralleled cytochrome P450 inactivation: a second CCl4 dose given three days after the first one induced no GBT decrease and a mild increase of serum transaminase activities. On the other hand, the second dose administered 7 days after the first one produced a GBT decrease similar to the one observed after the first one. These results should be taken into consideration to determine the optimal CCl4 dosing schedule in the rat CCl4-induced cirrhosis model.

Alanine Transaminase↗

Short term effects of indomethacin on rat small intestinal permeability. Role of eicosanoids and platelet activating factor.

Short term effects of indomethacin on intestinal permeability were studied on a model of rat isolated vascularly perfused terminal ileum. The objectives of this study were (a) to assess the effects of indomethacin on intestinal permeability and histology; (b) to assess the effects of prostaglandins, leukotrienes, and platelet activating factor (PAF) on the same parameters; (c) to evaluate the role of these inflammation mediators on indomethacin induced permeability modifications. Intravascular administration of 1.25 and 2.5 mM indomethacin induced a significant increase of 51Cr-EDTA transfer rate. Histological analysis showed only mucosal oedema. Pretreatment with 16,16 dimethyl-prostaglandin E2 did not reverse these changes. Intravascular administration of PAF, leukotrienes B4 and D4 provoked a significant rise in 51Cr-EDTA transfer rate and intraluminal protein leakage, with an intense vascocongestion of the mucosal capillaries. These changes were completely prevented by perfusion of the respective specific antagonists (BN52021 for PAF, LY255,583 for leukotriene B4 and MK571 for leukotriene D4). None of these three antagonists, however, or MK886, a selective 5'-lipo-oxygenase inhibitor, could reverse the indomethacin induced permeability changes. Indomethacin induced increased intestinal permeability at these high concentrations does not seem to be a result of changed prostanoid or PAF metabolism. Alternative mechanisms of the initial damage of non-steroid anti-inflammatory drugs should be sought.

16,16-Dimethylprostaglandin E2↗