Biomedical subjects
Publications and source records attributed to O Mercier.
Emphysematous cholecystitis is a rare but real entity, which have to be recognized early in order to quickly start the best treatment. We report a case of acute emphysematous cholecystitis diagnosed with computed tomography. A successful outcome was obtained by antibiotherapy and cholecystectomy in emergency.
An interlaboratory study was carried out to determine the feasibility and reliability of a method using the hamster cheek pouch as a model for assessing the potential irritative properties of substances intended to be applied to the lips or other mucous membranes. The test substances were applied once daily to both pouches for 14 consecutive days. Local and general tolerances were appraised throughout the study. At the end of the study, histologic examination of the pouches and the main organs was performed. Results of the feasibility study, conducted on various types of commercial products, indicated that this model is suitable for preparations of various consistence and composition. Results of the reliability study, carried out on gel-type preparations containing various concentrations of a known irritant, sodium lauryl sulfate, indicated that the method elicits a dose-dependent reaction for this compound. This hamster cheek pouch method was reproducible for the various parameters under consideration: local tolerance, general tolerance, histologic examination. For all products, results were in good agreement among the various laboratories participating in the study. The French regulatory authorities of the Fraud Repression Department have accepted it as an official method for the evaluation of the potential irritative properties of cosmetics and hygiene products intended to be applied to the lips or other mucous membranes.
Acute PTH administration enhances final urine acidification in the rat. HCl was infused during 3 h in rats to determine the parathyroid and renal responses to acute metabolic acidosis. Serum immunoreactive PTH (iPTH) concentration significantly increased and nephrogenous adenosine 3H,5H-cyclic monophosphate tended to increase during HCl loading in intact and adrenalectomized (ADX) rats despite significant increments in plasma ionized calcium. Strong linear relationships existed between serum iPTH concentration and arterial bicarbonate or proton concentration (P less than 0.0001). Serum iPth concentration and NcAMP remained stable in intact time-control rats and decreased in CaCl2-infused, nonacidotic animals. Urinary acidification was markedly reduced in parathyroidectomized (PTX) as compared with intact rats during both basal and acidosis states; human PTH-(1-34) infusion in PTX rats restored in a dose-dependent manner the ability of the kidney to acidify the urine and excrete net acid. Acidosis-induced increase in urinary net acid excretion was observed in intact, PTX, and ADX, but not in ADX-thyroparathyroidectomized rats. We conclude that (a) acute metabolic acidosis enhances circulating PTH activity, and (b) PTH markedly contributes to the renal response against acute metabolic acidosis by enhancing urinary acidification.
Paired micropuncture experiments were carried out in somatostatin-infused volume-expanded rats to examine the effects of a glucagon infusion (0.05 ng.min-1.g body wt-1) on urinary acidification and tubular handling of bicarbonate. Whole kidney and single-nephron glomerular filtration rate were not affected by glucagon. In thyroparathyroidectomized (TPTX) rats, glucagon inhibited the reabsorption of total CO2 in Henle's loop. In intact animals, however, the latter effect was not observed. In the distal tubule accessible to micropuncture, net total CO2 absorption was observed during volume expansion plus somatostatin infusion, which reversed to net total CO2 secretion during glucagon infusion in Wistar rats; thus the late distal delivery of total CO2 increased almost 80%. Marked inhibition of urinary acidification occurred in all animals as evidenced by a rise in urine pH and bicarbonate excretion. Conversely, a somatostatin infusion, which decreased the plasma glucagon concentration, stimulated net total CO2 absorption along the distal tubule and augmented final urine acidification in Wistar rats. Finally, urine-minus-blood PCO2 during alkaline diuresis was significantly reduced by glucagon infusion in bicarbonate-loaded TPTX rats. We conclude that 1) glucagon inhibits bicarbonate absorption in superficial Henle's loop in TPTX but not in intact rats, and 2) glucagon stimulates bicarbonate secretion and/or inhibits proton secretion in the distal tubule and collecting ducts, which leads to reduced urinary acidification.
The effects on urinary acidification of an acute infusion of glucagon (GLU) were studied by paired experiments in plasma-replete rats whose endogenous GLU secretion was restrained by a 0.7 ng.min-1.g body wt-1 somatostatin infusion. GLU did not affect the glomerular filtration rate in any of the plasma-replete rats studied. In 10 thyroparathyroidectomized (TPTX) rats and five intact rats subjected to hypotonic volume expansion, a low-dose (0.02 ng.min-1.g body wt-1) GLU infusion that raised the plasma GLU concentration from 302 +/- 63 to 1,010 +/- 140 pg/ml significantly increased the urinary bicarbonate excretion and decreased the urinary net acid excretion; a high-dose (0.05 ng.min-1.g body wt-1) glucagon infusion in the intact rats, that increased the plasma GLU concentration to 1,609 +/- 307 pg/ml, further enhanced the urinary bicarbonate excretion rate. In intact plasma-replete rats that were not subjected to a hypotonic volume expansion, low- and high-dose GLU infusions failed to affect the urinary bicarbonate excretion rate. Finally, no change in urinary excretion rates was noted in TPTX volume-expanded time control rats. We conclude that 1) physiological increments in plasma GLU concentration decrease urinary acidification by affecting the tubular H+/bicarbonate transport; 2) the bicarbonaturic effect of GLU may be blunted by the renal effects of high circulating antidiuretic hormone levels, or may be facilitated in an undetermined manner by hypotonic volume expansion.
Paired micropuncture experiments were carried out in plasma-replete volume-expanded rats to examine the acute effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on urinary acidification and tubular handling of bicarbonate and chloride. No effect was detected on the fractional absorption of water, total CO2, and chloride at end-proximal and early distal sites of superficial nephrons in intact animals; dDAVP, however, inhibited the fractional absorption of total CO2 in Henle's loop while stimulating that of chloride in thyroparathyroidectomized (TPTX) somatostatin-infused rats. In the distal tubule accessible to micropuncture, net total CO2 secretion was observed during hypotonic volume expansion, which reversed to net total CO2 absorption during dDAVP infusion in intact Wistar rats. Marked stimulation of urinary acidification occurred in all animals as attested by a fall in urine pH and bicarbonate excretion. Net acid excretion almost doubled in intact rats. We conclude that (a) antidiuretic hormone (ADH) inhibits fractional bicarbonate absorption in the thick ascending limb while stimulating that of chloride at least in TPTX somatostatin-infused rats, and (b) ADH stimulates proton secretion (or inhibits bicarbonate secretion) in the distal tubule and cortical collecting ducts, which leads to enhanced urinary acidification.
In seeking a method for the routine observation of copulatory behaviour in rats we compared the use of a standard rectangular Makrolon cage, commonly used in toxicology studies, with a Plexiglas cylinder that provided 2.5 times more floor area. The cylinder resulted in a much higher incidence of copulation, either once or for multiple series, within 30 min. This was not affected by whether oestrus was natural or induced. Using the cylinder and 4 h observation periods, we found that the dark phase of a 12-12 h inverse light cycle resulted in many more copulations than occurred during the light phase of a natural cycle. The incidence increased from the first to the second to the last 4 h of the dark phase. We found that placing a virgin receptive female and a naive male together in a Plexiglas cylinder for 1 h towards the end of the dark phase is a useful tool in reproductive toxicology studies in which it is important to know the precise time of insemination.
Recollection micropuncture experiments were carried out in thyroparathyroidectomized volume-expanded rats to examine the effects of CaCl2 infusion on the renal and nephronal segmental handling of chloride and bicarbonate. In group 1A, a 0.23 mM increase in plasma calcium concentration [delta(Ca)P] reduced urinary total CO2 (tCO2) excretion from 401 +/- 90 to 166 +/- 43 nmol X min-1 X g kidney wt-1 (P less than 0.05), whereas tCO2 filtered load was slightly diminished from 34,086 +/- 3,627 to 28,904 +/- 2,496 nmol X min-1 X g kidney wt-1 (NS). In group 1B [delta(Ca)P, 0.73 mM], whole kidney filtered loads were significantly lowered, as was urinary tCO2 excretion; however, urinary excretion of sodium, chloride, and water remained constant. Calcium infusion inhibited the proximal reabsorption of chloride 25% and water 16%; however, calcium infusion caused the end-proximal tCO2 concentration to significantly decrease so that the absolute and fractional tCO2 reabsorption remained constant. In group 2 [delta(Ca)P, 0.43 mM], whole kidney filtered load was unchanged for chloride and water but decreased for bicarbonate; urinary tCO2 excretion was reduced, whereas chloride and water excretion increased. In this group, early distal micropunctures evidenced that superficial single-nephron filtered loads were significantly reduced during calcium infusion; early distal chloride delivery was enhanced from 348 +/- 32 to 441 +/- 36 pmol X min-1 X g kidney wt-1 (P less than 0.05), whereas tCO2 delivery decreased from 47 +/- 5 to 38 +/- 4 pmol X min-1 X g kidney wt-1 (P less than 0.05). In group 3 of time control animals, whole kidney and early distal data were unchanged during second period. In group 4, H+ secretion in the collecting duct, as assessed by analyzing the relationship between urine-minus-blood PCO2 and urinary bicarbonate concentration in maximally alkaline urine, was not modified during CaCl2 infusion [delta(Ca)P, 0.79 mM]. We conclude that increase in plasma calcium concentration inhibits proximal NaCl and water reabsorption, whereas it stimulates the bicarbonate transport relative to that of chloride, leading to an enhanced proximal and renal bicarbonate-to-chloride reabsorptive ratio that could generate metabolic alkalosis; and decreases urinary bicarbonate excretion by also lowering the bicarbonate filtered load.
Recollection micropuncture experiments were carried out in plasma-replete euvolemic thyroparathyroidectomized rats to examine the effects of a purified bovine parathyroid hormone (PTH) infusion on urinary acidification. After a 60-min equilibration period, PTH administration had the following effects: reabsorption in the proximal convoluted tubule was inhibited 13% for total CO2, 31% for chloride, and 28% for water; early distal delivery, however, remained unchanged for bicarbonate, chloride, and water principally as a result of stimulation of bicarbonate and chloride absorption in Henle's loop; the urinary bicarbonate and chloride excretion rates did not vary significantly, but the urinary pH decreased from 6.78 +/- 0.11 to 6.39 +/- 0.07 and titratable acid and ammonium excretion increased from 63 +/- 18 to 405 +/- 45 and from 422 +/- 30 to 647 +/- 44 nmol X min-1 X g kidney wt-1, respectively. In another group of rats, the bicarbonate urinary excretion rate increased more than twofold during the first 60 min of PTH infusion and then returned to control levels as was observed in the other groups; the transient increase in bicarbonaturia was attributable to a PTH-induced transient augmentation in glomerular filtration rate and bicarbonate filtered load. Finally, no change was noted in micropuncture or whole-kidney data in time-control rats. We conclude that PTH only transiently enhances the bicarbonate filtered load and urinary excretion rate during the first 60 min of administration secondary to an early hemodynamic action but that the steady effect is to stimulate urinary acidification and net acid excretion, which could generate metabolic alkalosis; and that the inhibition of the proximal bicarbonate and chloride reabsorption induced by PTH is counterbalanced by stimulation of reabsorption in Henle's loop.
Urine-minus-blood PCO2 (U - B PCO2) during alkaline diuresis (urinary pH greater than 7.8) was determined in paired experiments using bicarbonate-loaded rats to assess the effects of parathyroid hormone (PTH) and urinary phosphate concentration [( Pi]u) on collecting duct H+ secretion. U-B PCO2 was higher for any value of urinary bicarbonate concentration ([HCO3]u) in the presence of PTH [intact rats and thyroparathyroidectomized (TPTX) PTH-infused rats] than in its absence (calcium-infused intact rats and TPTX rats). However, when [Pi]u was maintained constant by prior phosphate infusion, PTH administration in TPTX rats failed to elevate U-B PCO2. When PTH was infused in TPTX rats to maintain constant the plasma PTH level, subsequent phosphate infusion increased [Pi]u and elevated U-B PCO2 for any value of [HCO3]u. Moreover, when the data were pooled, there was a positive linear relationship between U-B PCO2 factored for [HCO3]u and [Pi]u (P less than 0.001). In all experiments, other factors that may affect U-B PCO2, such as plasma acid-base status, urinary osmolality, and extracellular fluid volume, did not vary. We conclude that PTH stimulates collecting duct H+ secretion indirectly via the increase in [Pi]u.
Volume expansion inhibits the proximal reabsorption of water, bicarbonate, and chloride. The present work tested a hypothetical role of parathyroid hormone (PTH) in the expansion effect. We studied 19 Sprague-Dawley rats during a plasma-replete euvolemic state and following 10% body wt colloid-free expansion. In group I, six intact rats, volume expansion decreased plasma ionized calcium concentration ([Ca2+]P) from 2.28 +/- 0.06 to 2.11 +/- 0.04 meq/liter and increased nephrogenous cAMP (NcAMP) from 29 +/- 5 to 66 +/- 10 pmol X min-1 X g kidney wt-1. In group II, six acutely thyroparathyroidectomized (TPTX) rats, [Ca2+]P also fell from 2.18 +/- 0.08 to 1.80 +/- 0.08 meq/liter but NcAMP did not rise significantly (9 +/- 3 vs. 17 +/- 5 pmol X min-1 X g kidney wt-1). These data strongly suggest that stimulation of PTH activity occurred during expansion in intact animals. In group III, seven TPTX rats, volume expansion inhibited proximal reabsorption of total CO2 by 11%, of chloride by 24%, and of water by 19%. Volume expansion-induced reduction in bicarbonate, chloride, and water reabsorption was smaller in TPTX than in intact rats previously studied. We conclude that volume expansion inhibits proximal reabsorption in part by decreasing the active transcellular NaHCO3 and NaCl transport secondary to stimulation of PTH activity.
The hydrolyzate of Delonix Regia seed extract is fractionated sequentially on Dowex 50 X 8 resin and on QAE Sephadex A 25. Purification is completed by recrystallisation from ethyl alcohol. 3-hydroxyproline is destroyed by NO2H and by chloramine T, which prevents from using most of the colorimetric reactions in use for 4-hydroxyproline. For its characterization, 3-hydroxyproline may be clearly separated from 4-hydroxyproline by TLC chromatography and by high voltage paper electrophoresis.