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Biomedical subjects

A Jardel

Publications and source records attributed to A Jardel.

At least 19 recordsLinked to original sources

Prolonged aspirin inhibition of anodal vasodilation is not due to the trafficking delay of neural mediators.

We previously reported that forearm vasodilation to a delivered all-at-once over 5 min or a 1-min repeated monopolar anodal 0.10-mA current application is aspirin sensitive and that a single high-dose aspirin exerts a long-lived effect in the former case. We hypothesized that 1) in the latter case, the effect of aspirin would also be long lived and 2) the time required to resupply nerve endings with unblocked cyclooxygenase through axonal transport could explain this phenomenon. We studied the time course for the recovery of vasodilation to repeated current application after placebo or 1-g aspirin treatment. We then searched for a difference at a proximal vs. distal site in the recovery of the response. Aspirin abolished current-induced vasodilation at 2 h, 10 h, and 3 days, with a progressive recovery thereafter, but no difference between distal and proximal site was observed for the recovery of the response. This suggests that, although neural cyclooxygenase could participate in the response, the time course of aspirin inhibition of current-induced cutaneous vasodilation is not due to the time required through neural transport to resupply nerve endings with unblocked proteins.

Adult↗

Dynamics of local pressure-induced cutaneous vasodilation in the human hand.

We recently demonstrated that a pressure-induced vasodilation results from local nonnociceptive stimulation of the skin of the human hand. We aimed to test the hypothesis that this vasodilation was not a short-lived response to a single type of pressure strain, but could be a widely activated and prolonged protective cutaneous response. We studied the dynamics of pressure-induced vasodilation during various ramp changes in local externally applied pressure using laser Doppler flowmetry. Changes from an adjacent control probe were subtracted from pressure-induced local changes. Following an initial transient decrease, continuous 4.4, 5.6, and 11.1 Pa.s(-1) increases of pressure resulted in a secondary increase of blood flow whose amplitude was maximal for 11.1 Pa.s(-1) (22.9 +/- 12.6% above baseline) (mean +/- SEM). The increase in flow was not noted at 16.7 Pa.s(-1). If the 16.7 Pa.s(-1) ramp pressure increase was interrupted at min 2 or 4, a prolonged vasodilation response was found, but not if it was stopped at min 8. When the 16.7 Pa.s(-1) increasing pressure was returned to zero after 4 min of pressure increase (-8.1 +/- 8.9% before pressure removal), vasodilation occurred and reached a maximum of 26.0 +/- 9.6% at 7 min after removal of pressure (P < 0.05 from baseline). Pressure-induced vasodilation is a slow-responding and transient adaptive phenomenon, initiated by a wide range of pressure changes below the range of noxious stimulation. We propose that this response is a protective mechanism without which certain pressure-associated lesions may develop.

Adult↗

Bacterial dissemination and metabolic changes in rats induced by endotoxemia following intestinal E. coli overgrowth are reduced by ornithine alpha-ketoglutarate administration.

The efficacy of ornithine alpha-ketoglutarate (OKG) in preventing bacterial translocation and dissemination, metabolic disorders and changes in mucosal enzyme activities was assessed in a model of bacterial translocation in rats. Antibiotic decontamination was performed 4 d before intragastric inoculation with an Escherichia coli strain (10(10) bacteria/kg body). Two days later, the rats were given either a lipopolysaccharide (LPS) 0127:B8 or a saline injection and were deprived of food for 24 h. Enteral nutrition, [Osmolite, 880 kJ/(kg. d)] supplemented with either OKG (LPS + OKG) or glycine (Saline + Gly or LPS + Gly), was then given for 2 d. Urinary total nitrogen losses and 3-methylhistidine excretion were determined daily. On killing at d 3, bacterial translocation to the mesenteric lymph nodes (MLN) and dissemination to the spleen and liver were evaluated, jejunal mucosa enzyme activities were assayed and tissue free amino acids in muscles were measured. Endotoxin induced translocation from the gut lumen to the MLN in all groups, whereas dissemination occurred only in LPS-treated rats. OKG significantly reduced dissemination of the bacteria in the spleen. 3-Methylhistidine excretion was greater in the LPS + Gly group (+25%, P: < 0.05) than in either the LPS + OKG or Saline + Gly group. The group fed the OKG-enriched diet had higher muscular glutamine, ornithine and arginine concentrations than did the Gly-supplemented groups (P: < 0.05). Intestinal sucrase and aminopeptidase activities were higher in the LPS + OKG group than in the LPS + Gly group (-30%, P: < 0.05). OKG supplementation limits bacterial dissemination and metabolic changes after injury in rats and thus may be useful in the prevention of gut-derived sepsis in critically ill patients.

Animals↗

Estimation of intraoperative aortocoronary bypass saphenous vein graft circumference from its preoperative compliance.

The aim of this study was to determine if the intraoperative circumference of aortocoronary saphenous vein bypass grafts could be predicted from preoperative measurement with B-mode ultrasound sonography in 50 patients. The circumference of the saphenous vein was measured during stepwise increments of a thigh congestive cuff from 0 to 60 mmHg. The circumference of the corresponding segment of the coronary bypass vein graft was measured intraoperatively with callipers. The intraoperative circumference was higher (11.8+/-2.3 mm) than the preoperative circumference (10.2+/-2.4 mm, P=0.006) matched to its corresponding intraoperative mean arterial pressure (57+/-15 mmHg). The prediction of the intraoperative circumference by estimation from the preoperative pressure-circumference relationship fitted by a linear model (r = 0.412, P = 0.004) did not improve on the preoperative circumference matched by arterial pressure alone (r = 0.429, P = 0.003). The intraoperative circumference of the graft vein exceeded its preoperative circumference by 12%. Prediction of the intraoperative graft vein circumference is underestimated by a linear model of its preoperative compliance.

Aged↗

Cutaneous vasodilation induced by local warming, sodium nitroprusside, and bretylium iontophoresis on the hand.

Local warming alone induces a cutaneous vasodilation considered as maximal. The argument that local warming generates a maximum flow is being tested by vasodilation with alternate approaches to see if a greater vasodilation is possible: blockade of the release of transmitters from the adrenergic nerve endings with bretylium tosylate or direct pharmacological action on vascular smooth muscle using sodium nitroprusside. Nine healthy subjects participated in two experiments in which SkBF was measured simultaneously by laser Doppler flowmetry on the dorsal aspects of both hands. In the first protocol the vasodilator effects of 20 min of local warming at 44 degreesC were measured on one hand and the effects of iontophoresis of sodium nitroprusside on the other. The second protocol was like the first except that iontophoresis of bretylium tosylate instead of sodium nitroprusside was performed. Local warming induced an increase of SkBF from 17.6 +/- 4.4 to 140.2 +/- 33.2 AU (P < 0.01) while it rose from 16.7 +/- 4.0 to 114.7 +/- 11.0 AU (P < 0.001) during sodium nitroprusside iontophoresis. During the second protocol local warming induced an increase of SkBF from 14.9 +/- 2.1 to 117.7 +/- 25.4 AU (P < 0.01) while it rose from 19.6 +/- 2.6 to 120.5 +/- 11.3 AU (P < 0.001) during bretylium iontophoresis. However, in both experiments, the increase of SkBF attained during iontophoresis did not differ significantly from the increase achieved by local warming. We conclude that the effects of iontophoresis of sodium nitroprusside or of bretylium produce a cutaneous vasodilation as high as a local warming on the dorsal aspect of the hand.

Adult↗

Calf vein compliance increases following bed rest after aortocoronary bypass surgery.

Early post-operative ambulation (< 3 days) is expected to decrease the risk of venous thrombosis, whereas late ambulation (> 7 days) increases the risk of orthostatic hypotension. The effect of post-operative bed rest on calf vein compliance was studied before (D - 1) and 7 days (D + 7) after aortocoronary bypass surgery in 50 patients (41 men and nine women, 65 +/- SD 10 years). Calf vein compliance was measured by strain gauge plethysmography and stepwise increases in thigh congestive pressure from 20 to 60 mmHg. Calf compliance [median (25 percentile-75 percentile)] increased significantly by 48% from D - 1 to D + 7 [0.044 (0.039-0.051) vs. 0.065 (0.048-0.083) ml (100 ml mmHg)-1, P < 0.001]. This increase was reflected as increased calf volume for the 50 mmHg [D-1 2.10 (1.75-2.65) vs. D + 7 2.60 (1.70-3.00) ml 100 ml-1, P < 0.01] and 60 mmHg [D - 1 2.50 (2.10-2.95) vs. D + 7 3.20 (2.30-4.00) ml 100 ml-1, P < 0.001] occlusion pressure levels. The associated pathologies (diabetes and arterial hypertension) and NYHA grades had no significant influence on the increase in compliance. Among the vasoactive therapeutic regimens, calcium channel blockers contributed significantly to the increased calf compliance, but only on D-1. The increase in venous compliance following aortocoronary bypass surgery is multifactorial but should be considered for prophylactic management of these patients.

Aged↗

Enteral administration of ornithine alpha-ketoglutarate or arginine alpha-ketoglutarate: a comparative study of their effects on glutamine pools in burn-injured rats.

OBJECTIVES: Ornithine alpha-ketoglutarate has proved to be an efficient nutritional support in trauma situations, especially after burn injury. To determine whether the action of ornithine alpha-ketoglutarate is due to its alpha-ketoglutarate moiety (as a glutamine precursor), we studied the effects of alpha-ketoglutarate administered to rats as ornithine alpha-ketoglutarate, or in combination with arginine salt (arginine alpha-ketoglutarate), as the two closely related amino acids have similar metabolic behavior. DESIGN: Prospective, randomized trial. SETTING: Animal laboratory. SUBJECTS: Forty-six male Wistar rats, weighing approximately 90 g. INTERVENTIONS: Rats were burned over 20% of their body surface area, starved for 24 hrs, with water ad libitum, and then enterally refed for 48 hrs using Osmolite (210 kcal/kg/day, 1.2 g of nitrogen/kg/day), supplemented with one of the following: a) an amount of glycine isonitrogenous to ornithine alpha-ketoglutarate (group 1); b) 5 g of monohydrated ornithine alpha-ketoglutarate/kg/day (group 2); c) an amount of arginine alpha-ketoglutarate isonitrogenous to ornithine alpha-ketoglutarate (group 3); or d) an amount of arginine alpha-ketoglutarate isomolar to ornithine alpha-ketoglutarate (group 4). MEASUREMENTS AND MAIN RESULTS: We measured amino acid concentrations in plasma, muscle, and liver, and plasma urea concentration. At refeeding, ornithine alpha-ketoglutarate increased plasma glutamine concentration (p < .05 vs. the three other groups), and counteracted the increase in plasma phenylalanine concentration. In muscle, although the three alpha-ketoglutarate combinations induced similar increases in the glutamate pool, ornithine alpha-ketoglutarate induced the highest increase in glutamine (7.0 +/- 0.3 vs. 5.4 +/- 0.3 micromol/g in group 3, 6.3 +/- 0.3 in group 4, and 4.6 +/- 0.2 in group 1, p < .01 between group 2 and groups 3 or 1). Also, only ornithine alpha-ketoglutarate increased liver glutamine concentration. Finally, isomolar arginine alpha-ketoglutarate increased plasma urea concentration (+50% vs. the three other groups, p < .01). CONCLUSIONS: Our results demonstrate, for the first time, the following: a) the action of ornithine alpha-ketoglutarate as a glutamine precursor cannot solely be ascribed to alpha-ketoglutarate since arginine alpha-ketoglutarate combinations did not exhibit this effect to the same extent; and b) the action of ornithine alpha-ketoglutarate is not due to its nitrogen content since isonitrogenous arginine alpha-ketoglutarate did not reproduce the effects of ornithine alpha-ketoglutarate.

Amino Acids↗

Ornithine alpha-ketoglutarate counteracts thymus involution and glutamine depletion in endotoxemic rats.

This work studied the action of ornithine a-ketoglutarate (OKG) supplementation in an experimental model of endotoxemia in the rat. Male Wistar rats were injected intraperitoneally with lipopolysaccharide (LPS) from Escherichia coli (0127:B8). They were fasted for 24 h, then refed for 48 h with an enteral diet supplemented with either OKG (66 mg N x kg(-1) x d(-1)) or glycine, isonitrogenous to the OKG group. A control (sham) group was also studied. LPS treatment induced a decrease in thymus and muscle weights compared to controls, and a decrease in glutamine and arginine concentrations in the anterior tibialis muscle. Supplementation with OKG restored thymus weight and muscle arginine level and increased muscle glutamine concentration, when compared to controls. We conclude that OKG counteracts the thymic involution that occurs with endotoxemia, and restores the muscular content of glutamine and arginine, both of which are involved in the regulation of immune function.

Journal Article↗

High-performance liquid chromatographic assay for the simultaneous determination of ethyl clofibrate and clofibric acid in plasma. Evaluation of plasma stability of ethyl clofibrate polylactic nanocapsules in human and rat plasmas.

A rapid, sensitive, and selective HPLC assay was developed for the simultaneous determination of ethyl clofibrate and its major metabolite, clofibric acid, in plasma of humans and rats. The assay involves extraction of the compounds into chloroform-isoamyl alcohol (99:1, v/v) from plasma acidified with sulfuric acid. For human plasma, the overall recoveries of ethyl clofibrate and clofibric acid were 63 and 90%, respectively. The limits of detection of the assay for ethyl clofibrate and clofibric acid in human plasma were 1.1 and 1.5 micrograms/ml, respectively. Limits of quantitation of the assay for ethyl clofibrate and clofibric acid in human plasma were 3.6 and 4.9 micrograms/ml, respectively. The HPLC assay was used to monitor the plasma concentration-time profiles of ethyl clofibrate released from polylactic nanocapsules both in man and rat. The simultaneous determination of ethyl clofibrate and clofibric acid provided evidence that these colloidal systems are stable in human plasma whereas they are lysed in rat plasma.

Animals↗

[Vitamin D supplementation in institutionalized elderly. Effects of vitamin D3 (100,000 IU) orally administered every 3 months on serum levels of 25-hydroxyvitamin D].

A clinical trial carried out during the autumn/winter season in 46 institutionalized elderly subjects (35 women, 11 men) (group mean age = 83 +/- 2 years) revealed a severe deficiency in vitamin D in these subjects (25-hydroxyvitamin D level less than or equal to 3 ng/ml). After oral administration of 100,000 IU of vitamin D3, an increase in 25-hydroxyvitamin D levels above the 10 ng/ml threshold was observed and maintained for three months. A second dose, administered after 3 months, made it possible to sustain this level. No sign of toxicity was detected, notably no trace of hypercalcemia. In contrast, no change in the deficit (25-hydroxyvitamin D level less than or equal to 3 ng/ml) was seen in the placebo population. Three-monthly administration of the moderate dosage of 100,000 IU of vitamin D3 all year round would offer a simple, effective and risk-free system to counteract vitamin D deficiency in the elderly and of preventing the risk of osteomalacia, thus reducing the incidence of fractures.

Administration, Oral↗

Circadian variations and reference intervals for some enzymes in urine of healthy children.

Circadian variations of alanine aminopeptidase (EC 3.4.11.2), gamma-glutamyltransferase (EC 2.3.2.2), and N-acetyl-beta-glucosaminidase (EC 3.2.1.30) in urine were studied in 10 healthy children, ages six to 15 years. Urine specimens were collected during 24 h, grouped into four time intervals. Enzymes were measured spectrophotometrically, with automation. These enzymes all showed diurnal variation, with morning (8 a.m.-12 noon) excretion being highest. We also analyzed timed urinary specimens (8 a.m.-12 noon) from 136 healthy children, ages two to 11 years. Reference intervals are presented for these enzymes. High excretion of the three enzymes was observed in children two and three years old.

Acetylglucosaminidase↗

[Administration of a single dose of 100,000 U.I. of vitamin D3 in the pregnant woman in winter. The effect on blood calcium level of the newborn infant].

Serum levels of 25-hydroxyvitamin D [25-(OH)D], calcium, phosphate and alkaline phosphatase activity were measured between December and July in 110 pregnant women during the last trimester of pregnancy, and in their infants on the fifth day of life. This study showed a fall, during spring, below 6 ng/ml, of the maternal 25-(OH)D concentration at the time of delivery, and a fall of the 25-(OH)D and calcium concentrations in newborns. The existence of a positive correlation between calcium and 25-(OH)D levels in the newborns suggests that the low calcium concentrations found in the infants born in spring is related to a vitamin D deficiency of the infant and therefore of the mother. The administration of a single low dose of vitamin D3 (100,000 I.U.) on the sixth or seventh month of pregnancy allowed to prevent the seasonal fall in serum calcium and 25-(OH)D concentrations. This dosage appears therefore to be sufficient to reduce the risk of vitamin D deficiency of the newborn and the occurrence of neonatal hypocalcemia.

Adult↗

[Usual values of serum vitamin A using a modified fluorimetric method].

We report a fluorimetric technique for the determination of serum vitamin A. The critical study of this micromethod included trials of repeatability, inter-series reproducibility and an evaluation of its accuracy. It was compared with a method using high performance liquid chromatography followed by detection with UV spectrophotometry. Normal values were established for adults. The variations according to age were determined for children between the ages of 10 months and 15 years.

Adolescent↗

Action of enterally administered ornithine alpha-ketoglutarate on protein breakdown in skeletal muscle and liver of the burned rat.

Several studies concerning burn patients have shown that supplementation of enteral nutrition with ornithine alpha-ketoglutarate (OKG) favorably modifies protein metabolism. Therefore, the effect of OKG administration on muscular and hepatic protein catabolism was evaluated in burned rats. Four groups of six rats were used. Two groups were scalded by immersion of the dorsum in water at 90 degrees C for 10 seconds and then starved for 24 hours. Controlled enteral nutrition was then administered in three boluses daily (Osmolite, 210 kcal/kg/d, 1.2 g N/kg/d); one group was supplemented with OKG (5 g/kg/d, ie, 0.68 g N/kg/d), while the other group received an equivalent amount of nitrogen in the form of glycine. One group of healthy control rats received Osmolite supplemented with glycine and the last group was fed ad libitum. The animals were killed after 2 days of nutrition. Protein catabolism was assessed in vitro by measuring the amount of valine (liver catabolism) and phenylalanine (muscle catabolism) released into the incubation medium of isolated tissues. Tissular and serum glutamine were also assayed. Burn injury induced muscle hypercatabolism without affecting hepatic catabolism. The administration of OKG limited both muscle weight loss and muscle protein hypercatabolism and significantly improved the muscle glutamine pool. These results demonstrate the nitrogen-sparing effect of OKG in muscle in hypercatabolic states.

Animals↗

Ornithine alpha-ketoglutarate and glutamine supplementation during refeeding of food-deprived rats.

The aim of this study was to compare the efficiency of ornithine alpha-ketoglutarate (OKG) and glutamine supplementation in an experimental model of denutrition that provides well-characterized disturbances of amino acid patterns. Male Wistar rats (187 +/- 11 g; five in each group) were starved for 3 days and then refed for 7 days with an oral diet (192 kcal kg-1.day-1 and 2.25 g of nitrogen kg-1.day-1), supplemented with 0.19 g of nitrogen kg-1.day-1 in the form of OKG, glutamine, or casein (control group). Food deprivation induced a fall in most tissue amino acids, with the notable exception of muscle leucine and liver glutamate, which increased by 43% (p < .01), and 11% (p < .05), respectively. The main effect of OKG was seen in the viscera, with a normalization of most amino acid pools (including proline and branched-chain amino acids) in the small bowel and liver. The main effect of glutamine was observed in the muscle, with a normalization of the glutamine and leucine pools. We conclude that, in this model and with the doses used, OKG and glutamine act in different target tissues, ie, splanchnic areas and muscle, respectively.

Acid-Base Equilibrium↗

[Vitamins and aging].

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Age Factors↗