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Biomedical subjects

D Jacques

Publications and source records attributed to D Jacques.

At least 55 records · Page 3Linked to original sources
PubMed1995

Apparent affinity and potency of BIBP3226, a non-peptide neuropeptide Y receptor antagonist, on purported neuropeptide Y Y1, Y2 and Y3 receptors.

The newly developed, purported non-peptide neuropeptide Y Y1 receptor antagonist BIBP3226 was evaluated for its potential effect on the recently characterized Y3 receptor subtype and for its apparent affinity in rat and human brain membrane binding assays using highly selective neuropeptide Y Y1 and Y2 radioligands. BIBP3226 potently blocked (pA2 = 7.36) the contractile effect of neuropeptide Y in the rabbit saphenous vein, a Y1 receptor bioassay and demonstrated nM affinity for Y1/[125I][Leu31,Pro34]peptide YY binding sites. In contrast, it failed to antagonize the biological effects of neuropeptide Y in the rat vas deferens (Y2) and rat colon (Y3) and did not significantly competed for Y2/[125I]peptide YY-(3-36) binding sites in rat and human brain homogenates. Taken together, the results demonstrate further the high potency and selectivity of BIBP3226 for the neuropeptide Y Y1 receptor by establishing its lack of antagonist activity on the Y3 subtype.

Animals↗
PubMed1995

[Severe acute buflomedil poisoning].

The severity of the acute intoxication from buflomedil, a vasodilator with papaverinic and alpha-adrenolytic effects, remains generally underestimated. We report the case of a 18-year-old girl who ingested a high amount of buflomedil. Two hours later, she developed seizures and ventricular arrhythmias. On admission to the ICU, she was in circulatory arrest followed by deep coma with mydriasis (GCS = 3). Buflomedil blood concentration, 2 hours after admission, was 97.3 mg.L-1. Toxicological screening for other drugs was negative. Therapy included external chest compressions tracheal intubation, mechanical ventilation, epinephrine and gastric lavage. The haemodynamic status improved within the first 24 h, although she remained comatose until the fifth day. She was discharged the eight day after her admission. This observation demonstrates that the potential severity of buflomedil poisoning is mainly due to early cardiac complications. Treatment remains purely supportive.

Acute Disease↗
PubMed1995

[Radionuclide ejection fraction at rest and in exercise in chronic aortic insufficiency. Pre- and postoperative study in asymptomatic or paucisymptomatic patients].

Twenty patients (17 men and 3 women: average age 50 +/- 14 years) with asymptomatic or paucisymptomatic aortic regurgitation were studied to compare the values of radionuclide left ventricular ejection fraction (EF) at rest and on exercise before (1) and 6 +/- 1 months (2) and 5.7 +/- 1.1 years (3) after surgery. The resting EF was similar at all three examinations: 53 +/- 8 (1); 57 +/- 8 (2); 55 +/- 16 (3). However, it increased significantly on exercise from 40 +/- 10 (1) to 54 +/- 12 (2) (p < 0.001) and to 52 +/- 20 (3) (p = 0.036 versus 1). In the 7 patients with resting EF greater than 55 before surgery, there was no postoperative improvement: 61 +/- 6 (1); 61 +/- 5 (2); 65 +/- 9 (3). However, the exercise EF increased from 44 +/- 13 (1) to 55 +/- 17 (2) and 69 +/- 11 (3) (p = 0.004 vs 1). In 13 patients with resting EF < 55%, the value increased in the early postoperative phase but not later: resting: 49 +/- 5 (1); 55 +/- 8 (2) (p = 0.04); 49 +/- 17 (3) (NS vs 1); effort: 38 +/- 7 (1); 54 +/- 10 (2) (p < 0.001); 40 +/- 16 (3) (NS vs 1). Left ventricular systolic function only returns to normal and exercise after surgery in patients with resting preoperative EF > or = 55%, but nothing indicates that this normalisation is an absolute condition for a successful surgical result in aortic insufficiency in terms of survival and quality of life.

Adult↗
PubMed1994

[Towards a decrease of myocardial infarction in the Bas-Rhin region? Results of the 6 first years of the Strasbourg MONIC Register].

The Bas-Rhin MONICA Register shows trends in myocardial infarction and other acute ischemic events between 1984 and 1989. Coronary heart disease mortality decreased by 27% in men and 30% in women. Morbidity trends were less favourable. The annual event rate for total acute ischemic events remained stable. However, a decrease of 14% for myocardial infarction was seen in men, particularly in patients with a past history of coronary disease. Another positive point is that the 28-day mortality rate in recent infarctions decreased in men by 33% during the 5 year period.

Acute Disease↗
PubMed1993

Atrial natriuretic factor blocks the high-threshold Ca2+ current and increases K+ current in fetal single ventricular cells.

The effect of atriopeptin III (ANF) was studied on K+, Ca2+ and Na+ currents of single heart cells of 10-day-old chick embryos and 17- to 20-week old human fetuses. ANF III (2 x 10(-9) M) greatly decreased the basal and cAMP prestimulated high-threshold (IL) Ca2+ current without affecting the low-threshold Ca2+ current (IT) or the TTX-sensitive fast inward Na+ current. ANF III was also found to increase the delayed outward K+ currents (IK) in a dose-dependent fashion (10(-10) to 10(-7) M). The effects of ANF III on IK and IL were reversible upon washout of this hormone. Increasing intracellular guanosine 3',5'-cyclic monophosphate (cGMP) blocked IL but had no effect on IK. These results suggested that ANF regulated one type of Ca2+ current and the delayed outward K+ current in single heart cells. The effects of ANF on IL (but not on IK) could be due in part to the increased [cGMP]i levels or to an unknown signal transduction that is stimulated by this hormone.

Animals↗
PubMed1992

Apamin, a highly potent fetal L-type Ca2+ current blocker in single heart cells.

Apamin, a bee venom polypeptide, was reported to block the naturally occurring Ca2+ slow action potentials (APs) in cultured cell reaggregates from old chick hearts [Bkaily, G. et al. Am. J. Physiol. 248 (Heart Circ. Physiol. 17): H961-H965, 1985] as well as the tetrodotoxin (TTX)- and Mn(2+)-insensitive slow Na+ current in young embryonic chick heart cells (Bkaily, G. In Vitro Toxicology. Academic, In press; Bkaily et al. J. Mol. Cell. Cardiol. 23: 25-39, 1991). With the use of the whole cell voltage-clamp technique in single ventricular cells from 10-day-old chick embryos and 17- to 20-wk-old human fetuses, two types of Ca2+ currents (ICa), T and L, were found. These two types of slow inward current in both heart preparations were nearly similar in their voltage, kinetics, and pharmacology. Apamin, a slow Ca2+ action potential blocker in old embryonic chick heart, was found to block the L-type ICa (IL) in a dose-dependent manner without affecting the T-type ICa in both heart cell preparations. The blockade of the IL by apamin was completely reversible upon washout with apamin-free solution. Therefore, when compared with nifedipine or to PN 200-110, apamin seems to be a highly potent L-type Ca2+ channel blocker in heart cells.

Animals↗
PubMed1991

Apamin, a highly potent blocker of the TTX- and Mn2(+)-insensitive fast transient Na+ current in young embryonic heart.

The whole-cell current clamp and voltage clamp techniques were used to record the slow Na+ action potentials (APs) and the inward current in cultured single ventricular cells isolated from young (3 day-old) embryonic chicks. The slow Na+ APs had a +Vmax of 21.5 +/- 7.5 V/s (in 10 different single cells) and the macroscopic inward current responsible for the rising phase of these APs was a fast transient (ft) current. The ft inward current was sensitive to changes in [Na]o but not to changes in [Ca]o. This channel was found to be permeable to Li+ and Ba2+. Analysis of Na+ current decay suggests a second-order process of current decay. The slow Na+ APs and the ft inward current were insensitive to tetrodotoxin (TTX) and Mn2+. This current was also insensitive to the inorganic Ca2+ blockers, Ni2+, Cd2+ and La3+. At low concentration (10(-9)-10(-6) M) the organic Ca2+ blockers, (-)D888 and nifedipine had no effect on the TTX- and Mn2(+)-insensitive INa. However, at a high concentration (10(-5) M), the Ca2+ blockers, (-)D888 and nifedipine, completely blocked the slow Na+ APs and the TTX- and Mn2(+)-insensitive ft inward Na+ current responsible for the rising phase of the APs. High concentration of verapamil (10(-5) M) and D-600 (10(-5) M) had little depressant effects due to their frequency dependence. Apamin, a toxin in the bee venom, that was previously reported by our group to block the slow Ca2+ APs (Bkaily et al., 1985) and the slow Ca2+ current (Bkaily et al., 1988b), greatly decreased the TTX- and Mn2(+)-insensitive ft INa at 10(-10) M. Thus, the inward current responsible for the rising phase of the slow Na+ APs in 3 day-old embryonic chick heart shows fast transient activation and is TTX- and Mn2(+)-insensitive. This channel is highly sensitive to apamin and shares few characteristics with the Ca2+ channel and the TTX-sensitive fast Na+ channel.

Action Potentials↗
PubMed1990

A tetrodotoxin- and Mn2(+)-insensitive Na+ current in Duchenne muscular dystrophy.

Muscle myotube cultures were obtained from normal and Duchenne muscular dystrophy (DMD) biopsies by using an explant technique. The current-voltage (I/V) curve of the whole sodium (Na+) current (INa) in normal myotubes was similar to that obtained from DMD myotubes. However, the inactivation curve of the whole INa was different in normal myotubes when compared to that obtained from DMD myotubes. Addition of 10(-4) M tetrodotoxin (TTX, a fast INa blocker) decreased the whole INa in both preparations. The inorganic calcium (Ca2+) blocker manganese (Mn2+) completely blocked the remaining TTX-resistant INa of normal myotubes and decreased this current in DMD myotubes leaving behind a TTX- and Mn2(+)-insensitive INa that was insensitive to the Ca2+ blocker desmetoxyverapamil ((-)D888). The slow inward barium current (IBa) of both normal and DMD myotubes was blocked by Mn2+ and (-)D888. However the kinetics of the slow channel in normal myotubes was different from that of DMD myotubes. This study demonstrates the presence of a TTX- and Mn2(+)-insensitive INa in DMD myotubes. This channel may contribute to the increase of intracellular Na+ [( Na]i) in DMD and allow Ca2+ to enter the cells through the Na(+)-Ca2+ exchanger, thus contributing to calcium loading.

Adolescent↗
PubMed1989

Effect of computer-assisted insulin delivery on glycemic control of type I diabetic patients: a preliminary experience.

The aim of the study was to evaluate the effect of a computer-assisted insulin delivery on the glycemic control of type I unstable diabetic patients. 6 subjects, who already received 2-4 daily insulin injections, were treated with a pocket-size microprocessor device for periods lasting 2-14 months. The total daily insulin doses remained unchanged during the experimental period. However, the percentage of regular insulin decreased significantly from 63 +/- 3% to 47 +/- 7% (p less than 0.05). HbA1 levels decreased from 10.1 +/- 0.6% to 9.4 +/- 0.4% after 2 months computer (p less than 0.05). However, in the 2 patients who used the device for 11-14 months, the overall glycemic control was comparable during the basal and experimental periods. Hypoglycemic episodes were not increased.

Adult↗
PubMed1988

Angiotensin II increases Isi and blocks IK in single aortic cell of rabbit.

The whole-cell voltage clamp technique was used in order to study the effects of Angiotensin II (Ang II) on the slow inward current and the K+ outward current in single aortic cells of the rabbit. Angiotensin II (10(-8) M) increased the slow inward Ba ++ current, and the addition of an antagonist of Ang II, [( Leu8] Ang II, 10(-8)M) rapidly reversed the effect of Ang II on IBa. Angiotensin II (5 x 10(-8)M) greatly decreased K+ current and the Ang II antagonist reversed this effect. Thus, it is quite possible that the decrease of IK and the increase of Isi in aortic single cells by Ang II may explain a part of the vasoconstrictor effect of this hormone in vascular smooth muscle.

Angiotensin II↗
PubMed1988

Three types of slow inward currents as distinguished by melittin in 3-day-old embryonic heart.

Membrane slow inward currents of 3-day-old embryonic chick single heart cells were investigated using the whole-cell patch clamp technique. In a solution containing only Na+ ions and in the presence of tetrodotoxin and Mn2+, the inward current-voltage relationship presented two maxima, confirming the existence of two different voltage-dependent slow inward currents. The first type, a fast transient slow inward current (Isi (ft], was activated from a holding potential of -80 mV and showed fast activation and inactivation. This current was highly sensitive to melittin (10(-8) M) and insensitive to low concentrations of desmethoxyverapamil [-)D888, 10(-9)-10(-6) M). Depolarizing voltage steps from a holding a potential of -50 mV activated two components of the slow inward current, i.e., a slow and a sustained current (Isi(sts] that showed a slow inactivation followed by a slow inactivation and a sustained component. Melittin at a high concentration (10(-4)M) completely blocked the slow transient component (Isi(st] and left unblocked the sustained component (Isi(s]. Both components (Isi(st) and Isi(s] were blocked by verapamil (10(-5)M) and low concentrations of (-)D888 (10(-8)-10(-6)M).

Animals↗
PubMed1985

Optimization of gentamicin therapy in very low birth weight infants.

In order to optimize gentamicin (G) therapy we studied G pharmacokinetics in 48 preterm infants (gest. age 31.6 +/- 3.4, range 25-37 wk; birth weight 1.5 +/- 0.5 kg, range 0.7-2.5 kg). They received IV G twice daily (5.2 +/- 0.6 mg/kg/day). After at least 2 days of treatment trough and peak levels were measured for 2 successive doses. Trough levels were significantly higher in infants less than 1 kg receiving 5 mg/kg/day than in other infants (1-2.5 kg) who received the same dose (3.1 +/- 1.0 vs. 2.3 +/- 0.5 micrograms/ml; p less than 0.01). Mean G t 1/2 was significantly longer in infants under 1 kg than in those weighing 1-2.5 kg (7.9 +/- 1.9 and 6.5 +/- 1.6 hr, respectively; p less than 0.01). These differences could be attributed to lower G clearance in infants less than 1 kg (31 +/- 6 vs. 39 +/- 8 ml/kg/hr; p less than 0.005). There was no difference in G distribution volume between less than 1 kg and 1-2.5 kg infants (0.35 +/- 0.07 and 0.38 +/- 0.13 L/kg, respectively). A correlation was found between clearance and t 1/2 for the total group (r = 0.57, p less than 0.01). No correlation was detected between BUN and clearance or between gestational age and clearance. Our data suggest that G dose in infants less than 1 kg should be reduced to 3.5-4 mg/kg/day in order to avoid excessive levels associated with nephrotoxicity.

Birth Weight↗
PubMed1979

Intracellular calcium deposition in brain following electrical stimulation.

The effects of electrical stimulation of the cat cerebral cortex have been evaluated by light and electron microscopy following a wide variety of stimulation parameters (QD/ph of 10 - 300 muC/cm2/ph). Platinum or rhodium disc electrode arrays were bilaterally implanted subdurally on the parietal cortex and subjected to 36-hour stimulations (9 hrs./day for 4 days). Prominent among the degenerative changes shown by electron microscopy were dense crystalline inclusions that were identified as calcium hydroxyapatite (CHA) crystals by electron diffraction and energy dispersive X-ray analysis. The appearance of intracellular calcification generally paralleled the onset of other degenerative changes in stimulated tissue, including gliosis, mitochondrial swelling, lipid inclusions, degenerating cells, neuronal loss, and phagocytic activity. A preferential deposition of calcium was noted in mitochondria of several cell types and in postsynaptic dendrites. The mechanism of the apparently electroresponsive calcium deposition is obscure; however, a plausible explanation is that increased cyclic AMP levels, known to occur with electrical stimulation of nervous tissue, result in enhanced calcium plasmalemmal permeability.

Animals↗
PubMedDate not supplied

Macroscopic Ca2+ -Na+ and K+ currents in single heart and aortic cells.

The whole-cell voltage clamp technique was used to study the slow inward currents and K+ outward currents in single heart cells of embryonic chick and in rabbit aortic cells. In single heart cells of 3-day-old chick embryo three types of slow inward Na+ currents were found. The kinetics and the pharmacology of the slow INa were different from those of the slow ICa in older embryos. Two types of slow inward currents were found in aortic single cells of rabbit; angiotensin II increased the sustained type and d-cAMP and d-cGMP decreased the slow transient component. Two types of outward K+ currents were found in both aortic and heart cells. Single channel analysis demonstrated the presence of a high single K+ channel conductance in aortic cells. In cardiac and vascular smooth muscles, slow inward currents do share some pharmacological properties, although the regulation of these channels by cyclic nucleotides and several drugs seems to be different.

Angiotensin II↗
PubMedDate not supplied

Bay K 8644 induce enhancement of K+ current in both single heart cell and smooth muscle cell.

The effects of the Ca2+ agonist Bay K 8644 on outward potassium currents have been studied in single ventricular cells of chick embryo and aortic single cells of rabbit using the whole-cell patch clamp technique. Bay K 8644 was found to increase 1K in both heart and aortic single cells. This effect of Bay K 8644 on both muscle was reversed by Mn2+ and blocked by 20 mM TEA. The Bay K 8644 potassium I/V curve of single heart cell had a N shape, which is Ca2+ dependent. These data strongly suggest that Bay K 8644 increases a gK(Ca) in both aortic and heart muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗