Publications by authors named "Gogny M"

Article Synopsis
  • The study examines how endothelial damage affects the reactivity of smooth muscle in bovine digital veins (BDVs) when exposed to 5-hydroxytryptamine (5-HT).
  • Immediate removal of the endothelium didn't show significant changes, but long-term deprivation led to increased smooth muscle reactivity, highlighting the role of endothelial-derived nitric oxide (NO) in vascular control.
  • Inhibitors targeting the RhoA/ROCK pathway and reactive oxygen species proved effective in reducing this hyper-reactivity, suggesting potential treatment avenues for chronic vascular issues like laminitis in animals.
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This work was designed to investigate (i) the effect of superoxide dismutase (SOD) inhibition on endothelial function and (ii) the free radical-induced endothelial dysfunction in equine digital veins (EDVs) and equine digital arteries (EDAs) isolated from healthy horses. EDV and EDA rings were suspended in a 5 ml organ bath containing Krebs solution. After a 60 min equilibration period, EDV and EDA rings were contracted with phenylephrine.

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Autoantibodies against β₁-adrenoceptors (β₁-ARs) have been detected in the serum of patients with various cardiac diseases; however, the pathological impact of these autoantibodies (β₁-AABs) has only been evaluated in cardiac tissue. The purpose of the present study was to evaluate whether β₁-AABs have deleterious effects on vascular reactivity in rats. An enzyme-linked immunosorbent assay was used to detect β₁-AABs in sera from immunized rats over a period of 1-3 months using the peptidic sequence of the second extracellular loop of human β₁-AR.

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In porcine coronary arteries (PCAs), celiprolol, a selective β(1)-adrenoceptors antagonist, induces vasodilatation by an endothelium- and nitric oxide (NO)-dependent pathway. However, the mechanisms of that vascular effect have not been precisely established. β(3)-Adrenoceptors have been shown to be involved in the relaxation per se of various vascular beds, including coronary vessels.

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We evaluated the vasorelaxant effect of propentofylline (PPF), a methylxanthine derivative, and its mechanism of action in equine digital veins (EDVs). Cumulative concentration-response curves to PPF (1 nM-300 µM) were recorded in phenylephrine-precontracted EDV rings under different experimental conditions. PPF-induced relaxation was partially inhibited by endothelium removal, but was unaltered by CGS-15943 (an adenosine receptor antagonist; 3 µM).

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Purpose: To evaluate the effect of active immunization with a peptide corresponding to the second extracellular loop of the human beta1-adrenoceptors (β(1)-AR) on the reactivity of Wistar rat isolated aorta.

Methods: Nine-week-old Wistar rats were actively immunized for 3months with a peptide corresponding to the second extracellular loop of the human β(1)-AR. Specific immunoglobulins G (IgG) were characterized by Elisa and the bicinchonic acid protein assay and their functionality were tested in isolated ventricular cardiomyocytes (IVC) from control rats.

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Circulating autoantibodies directed against the 2nd extracellular loop (EL-2) of β(1)-adrenoceptors (β(1)-AABs) have been detected in the serum of patients with various cardiovascular pathologies. β(1)-AABs induce agonistic, positive inotropic effects via β(1)-adrenoceptors (β(1)ARs). In the mammalian heart, β(1)-AR can exist in 2 distinct activated configurations (the so-called high- and low-affinity states).

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The direct vasodilatory action of pentoxifylline (1-(5-oxohexyl)-3,7-dimethylxanthine) and its signalling pathway was evaluated in equine digital veins. Cumulative concentration-response curves to pentoxifylline (1 nM to 300 μM) were recorded in phenylephrine-precontracted equine digital vein rings under different experimental conditions. Relaxation to pentoxifylline was partially inhibited by endothelium removal, but was unaltered by CGS-15943 (a non-xanthine adenosine receptor antagonist; 3 μM).

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The aim of this in vitro study was to compare the uterokinetic activity of oxytocin and dinoprost, the natural PGF2α, with or without aglepristone, in canine myometrial fibers. Thirty-three bitches were allocated into one of four groups, depending on their estrous stage and whether or not they had received a treatment with aglepristone (metestrus aglepristone, n = 5; metestrus without treatment, n = 9; anestrus aglepristone, n = 9; anestrus without treatment, n = 10). After hysterectomy, longitudinal and circular uterine strips were mounted in organ baths.

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We evaluated celiprolol-induced vasodilatation in aorta taken from 12-week-old spontaneously hypertensive rats (SHR) and the effect of AT(1) angiotensin II receptor antagonism on the vasodilatory action of celiprolol in Wistar Kyoto (WKY) rats and SHR. In WKY rats, the celiprolol-induced relaxation was greatly decreased in denuded aorta, and completely abolished in intact aorta by N(omega)-nitro-l-arginine methyl ester (l-NAME, 100 microM). In SHR, celiprolol-induced relaxation was reduced compared to WKY rats (E(max) (value obtained for the highest concentration, 300 microM)=39.

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Objective: To investigate the role of superoxide anions in the lipopolysaccharide (LPS)-induced impairment of beta-adrenoceptor-mediated equine digital vein (EDV) vasodilation.

Sample Population: EDVs isolated from forelimbs of 24 healthy adult horses.

Procedures: Endothelium-intact or endothelium-denuded EDV rings were incubated with or without LPS (10 microg/mL) of Escherichia coli (O55:B5) for 4 hours.

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Article Synopsis
  • The study explores improving analysis of cumulative concentration-response curves (CCRC) in drug effect research by using nonlinear mixed effects (nlme) models instead of traditional methods.
  • The analysis focused on data from experiments involving beta-adrenoceptor-induced relaxation in rat aorta, demonstrating that nlme models provide more accurate results compared to classical methods.
  • The findings suggest nlme models can effectively identify significant differences in pharmacological parameters even with smaller sample sizes, making them promising for future pharmacological research.
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Objectives: This study in swine assessed BIS stability in response to decreases and increases in cardiac output under two propofol/remifentanil dosage combinations, both producing the same depth of surgical anaesthesia.

Methods: Eight anaesthetized-paralyzed ventilated adult swine were studied using a random-order cross-over design. Four received a P low/R high combination (P, 8.

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CGP12177 is a non-conventional partial agonist, known to have cardiostimulating and vasorelaxant properties related to its agonist action on the low affinity state of the beta(1)-adrenoceptor (beta(1LA)-adrenoceptor). In normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), CGP12177-induced vasorelaxant effects were analysed in hindquarter vessels to assess modifications in hind limb vascular resistance, and in femoral artery rings. The global haemodynamic effects induced by CGP12177 were also investigated using telemetry in conscious animals.

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The aim of the study was to investigate the renal function in clinically normal dogs receiving meloxicam and pimobendan alone or in combination. Ten adult female beagle dogs were administered the treatment for 7 days in a randomized crossover trial (control/meloxicam/pimobendan/meloxicam and pimobendan). Renal function was assessed by blood urea, creatinine, sodium, potassium and chloride concentrations and by glomerular filtration rate, measured by means of renal scintigraphy [renal uptake of (99m)Tc-diethylenetriaminepentacetic acid (DTPA)] and plasma clearance of (99m)Tc-DTPA.

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Objective: To investigate renal function in clinically normal dogs when awake and during anesthesia with medetomidine; xylazine, ketamine, and halothane (XKH) combination; or propofol.

Animals: 10 adult female Beagles.

Procedures: At intervals of 15 days, dogs were administered medetomidine (0.

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The objective of this study was to investigate renal function in clinically normal dogs receiving tepoxalin, a nonsteroidal inflammatory drug, either in association with or without an angiotensin-converting enzyme inhibitor (ACEI). Ten adult female Beagle dogs were used in the three phases of the study. The dogs were administered the drugs once daily for 7 days (experiment 1: placebo/tepoxalin/tepoxalin and benazepril; experiment 2: enalapril/tepoxalin and enalapril) or for 28 days (experiment 3: tepoxalin and benazepril together).

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Low-affinity state beta1-adrenoceptor (beta1-AR) was functionally expressed in some blood vessels and was different from beta1, beta2 and beta3-AR. In rat aorta, low-affinity state beta1-AR activation produced an endothelium-independent relaxation which was impaired in spontaneously hypertensive rats (SHRs). In the present work, we investigated whether renin-angiotensin system was involved in this alteration by evaluating the effects of enalapril, an angiotensin converting enzyme (ACE) inhibitor or losartan, an AT1 angiotensin receptor antagonist.

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Although the impairment of beta-adrenoceptor (beta-AR)-induced vascular relaxation to isoprenaline has been extensively described, discrepancy persisted in the literature. In this work, we investigated beta-AR-induced relaxation in spontaneously hypertensive and normotensive rats aorta. We attempted to determine beta-AR subtypes involved in order to understand the conflicting data regarding the beta-AR-induced vasodilation to isoprenaline.

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1 In hypertension, a decrease of the vascular beta-adrenergic relaxation has been described. However, the specific involvement of each beta-adrenoceptor (beta-AR) subtype, in particular the low-affinity state of beta1-AR, has not yet been evaluated. We investigated whether the low-affinity state of beta1-AR-induced relaxation was impaired in Spontaneously Hypertensive Rats (SHR).

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Objective: to assess the changes in local brain PO2, PCO2, pH (PO2br, PCO2br, pHbr) measured by a intraparenchymal probe (Neurotrend, Codeman) and compare them to simultaneous recording of cerebral PvO2 and blood flow (CBF).

Methods: Arterial, venous longitudinal sinus blood samples and CBF were analyzed in 8 adult anesthetized, ventilated goats. Three step increase of intracranial pressure (ICP) (16, 22, 29 mm Hg) were performed by inflation of an epidural balloon.

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The aims of this study was to characterize the functional response of atypical beta-adrenoceptors (beta-AR) in rat aorta and to investigate whether this relaxation was altered before and during the development of hypertension. Aortic rings from 4 or 12 weeks old Wistar Kyoto (WKY) rats or spontaneously hypertensive rats (SHR) were placed in organ baths and constricted with phenylephrine. Then, cumulative concentration-relaxation curves to the beta-AR agonists were constructed.

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Article Synopsis
  • The study investigates the functional expression of beta3-adrenoceptors (beta3-ARs) in equine digital veins (EDVs) and how their relaxation response is affected by endotoxin.
  • Samples were taken from the forelimbs of 30 horses, with EDVs being isolated and tested for relaxation responses using various beta3-AR agonists in controlled conditions.
  • Results indicated that while beta3-ARs promote relaxation in EDVs, their efficacy is reduced when exposed to endotoxin, suggesting that inflammatory responses may interfere with this mechanism, potentially due to changes in prostanoid production.
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The aim of this study was to investigate the involvement of beta 3-adrenoceptors (beta 3-AR) in hypertension. Aortic rings were isolated from 12 weeks old WKY (Wistar-Kyoto) and SHR (spontaneously hypertensive rat) rats. Rings were placed in organ baths and constricted with phenylephrine.

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