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Biomedical subjects

F Martinez

Publications and source records attributed to F Martinez.

At least 163 records · Page 9Linked to original sources
PubMed1990

A role for adenosine calcium and ischemia in radiocontrast-induced intrarenal vasoconstriction.

These studies were designed to test the hypothesis that adenosine and calcium are important in mediating radiocontrast-media-associated reduction in renal blood flow (RBF) in the dog. Intravenous verapamil (V) and diltiazem (DTZ) infusion significantly attenuated the magnitude of the vasoconstrictor response observed after each intrarenal contrast media (CM) injection. (First injection: -47 +/- 8% control vs. -14 +/- 3% V, p less than 0.03; -38 +/- 4% control vs. -19 +/- 3% DTZ, p less than 0.02. Second injection: -33 +/- 6% control vs. -12 +/- 1% V, p less than 0.03; -32 +/- 5% control vs. -17 +/- 2% DTZ, p less than 0.03. Third injection: -32 +/- 6% control vs. -11 +/- 5% V, p less than 0.03; -38 +/- 5% control vs. -10 +/- 5% DTZ, p less than 0.02). Furthermore, V and DTZ almost completely abolished the increase in renal vascular resistance (RVR) induced by each CM administration. Theophylline also significantly attenuated the magnitude of the vasoconstrictor response observed after CM injection (first injection: -31 +/- 3% control vs. -12 +/- 3% theophylline, p less than 0.05; second injection: -26 +/- 3% control vs. -12 +/- 3% theophylline, p less than 0.03). Similarly, theophylline blunted the increase in RVR induced by CM injection. In addition, theophylline inhibited exogenous adenosine-induced decrease in RBF (-61 +/- 10% and -26 +/- 1% decrease in RBF without and with theophylline, respectively). In contrast, dipyridamole significantly enhanced the vasoconstriction induced by CM (first injection: 25 +/- 3% control vs. 49 +/- 4% dipyridamole; second injection: 31 +/- 3% control vs. 48 +/- 4% dipyridamole p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1990

Renal effects of radiocontrast agents in rats: a new model of acute renal failure.

The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosaminidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 +/- 0.1 to 0.8 +/- 0.1 and 1.0 +/- 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 +/- 18 to 48 +/- 20 and 8 +/- 4 mumol h-1/mmol creatinine at 24 and 48 h, respectively (p less than 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 +/- 0.1 to 0.4 +/- 0.1 and 0.8 +/- 0.1 ml/min at 24 and 48 h, respectively (p less than 0.01). Urinary NAG excretion increased also significantly from 43 +/- 9 to 352 +/- 79 and 64 +/- 23 mumol h-1/mmol creatinine at 24 and 48 h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1990

Renal and hemodialysis clearances of endogenous natriuretic peptide. A clinical and experimental study.

The purpose of the present study was to assess the plasma levels of atrial natriuretic peptide (ANP) in chronically uremic patients not submitted to dialysis and to determine the predialysis plasma concentration of ANP, the effect of ultrafiltration on plasma levels of ANP (hemodialysis, (HD), and the HD clearance of ANP in a population of adult patients treated with maintenance HD. The mean plasma ANP concentration (pg/ml) in HD was 370.2 +/- 35.5 pg/ml (mean +/- SEM) before HD and decreased to 165.3 +/- 15.2 after HD (p less than 0.01). Both values were significantly higher than in controls (28 +/- 2; n = 39). The changes in plasma ANP levels correlated inversely with those in plasma protein concentration (r = -0.53; p less than 0.03; y = 48.6 +/- 0.8 x). ANP clearance across the cuprophan membrane averaged 13 +/- 6.4 ml/mn. Resting plasma ANP values in the 16 uremic patients ranged between 16 and 277 pg/ml (124 +/- 11 pg/ml). These levels were significantly higher than those observed in controls (p less than 0.01). In these patients there was a highly significant correlation between serum creatinine and plasma ANP concentrations (p less than 0.01; r = 0.75; y = 0.2x + 3). Furthermore we report the results of the determination of the renal clearance of ANP in normal dogs. In all dogs a fall in plasma ANP concentration was recorded between the aorta (28.6 +/- 4.5 pg/ml) and the renal vein (14.2 +/- 2.7 pg/ml). The renal extraction ratio averaged 51.3 +/- 3.7%. Mean ANP renal clearance was 38.2 +/- 5.2 ml/mn.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Urate and p-aminohippurate transport in the brush border membrane of the pig kidney.

The transport of urate and p-aminohippurate (PAH) across the pig renal brush border membrane was investigated using membrane vesicles. Compared to a pH equilibrium condition (pHin = 7.4; pHout = 7.4), an outwardly directed OH- gradient (pHin = 7.4; pHout = 5.8) stimulated markedly both lactate and pyrazinoate uptake with overshoots exceeding 2 times that of the steady state. In contrast, neither OH-/urate nor OH-/PAH exchange could be demonstrated. An outwardly directed Cl- gradient (Cl-in = 100 mM; Cl-out = 16.7 mM) increased 2.6-fold 15-sec PAH uptake compared to Cl- equilibrium (Cl-in = Cl-out = 100 mM) but this stimulation was due solely to an effect of membrane potential. Creation of an electropositive intravesicular space, by imposing an inwardly directed K+ gradient (K+in = 0 mM; K+out = 100 mM) in the presence of valinomycin, was very effective to drive uphill PAH and urate accumulation compared to the control condition (no valinomycin). Four-second potential-stimulated PAH uptake was saturable (Km, 0.8 mM; Vmax, 1.7 nmol/mg of protein x 4 sec). Different organic anions cis-inhibited both 4-sec potential-stimulated PAH and urate uptakes in a similar fashion. PAH and urate, moreover, decreased each other's accumulation. In countertransport experiments, PAH and urate uptakes were not significantly stimulated by trans-unlabeled substrate. These results are consistent with the presence, in the pig renal brush border membrane, of a mediated secretory pathway common for urate and PAH, which could be facilitated by the potential difference existing in vivo across the luminal membrane of the proximal tubule.

Aminohippuric Acids↗
PubMed1989

Cyclosporin A versus methotrexate, followed by rescue with folinic acid as prophylaxis of acute graft-versus-host disease after bone marrow transplantation.

Fifty-seven patients undergoing bone marrow transplantation were randomly assigned to receive either cyclosporin A (CsA, n = 26) or methotrexate, followed by rescue with folinic acid (MTX + FA, n = 31) as prophylaxis for graft-versus-host disease (GVHD). All patients but one receiving CsA had evidence of sustained engraftment, and there was no difference between the two groups on the day in which marrow engraftment was documented. Oropharyngeal mucositis was of similar incidence and severity in the two groups. In contrast, patients receiving CsA showed higher renal and hepatic toxicity rates than those treated with MTX + FA. Severe-to-moderate acute GVHD (grades II-IV) was documented in 12 patients receiving CsA and in 12 treated with MTX + FA. The cumulative incidence of this complication was similar in both groups (46.1% and 38.7%). Similarly, there was no difference in the incidence of chronic GVHD. The leukemic relapse rates were also comparable, as well as the estimated probability of survival, which was 55% in patients treated with MTX + FA and 41% in those who were given CsA. We conclude that MTX + FA is as effective as CsA in the prevention of GVHD, with the additional advantage of reduced renal and hepatic toxicities.

Actuarial Analysis↗
PubMed1989

Foscarnet nephrotoxicity: mechanism, incidence and prevention.

Foscarnet is a pyrophosphate analogue that has been successfully used in severe cytomegalovirus (CMV) infections. Little is known of the incidence and mechanisms of foscarnet-induced nephrotoxicity as most data comes from recipients of renal allografts or from patients with severe underlying disease or with other nephrotoxic drugs. We have retrospectively analyzed the evolution of renal function after 56 courses of foscarnet. In addition, we have prospectively studied the protective effects of hydration on foscarnet nephrotoxicity (2.5 liters of saline/day during the night before the foscarnet therapy and throughout the course of treatment). Foscarnet-induced acute renal failure was defined as a rise in serum creatinine of at least 25% from the basal value. An increase in serum creatinine occurred in 37 cases out of the 56 courses of foscarnet (66%). The mean serum creatinine prior to foscarnet was 80.5 +/- 3.3 mumol/l and the mean increase was 190 +/- 28.3 mumol/l (range 80-1,000). Peak serum creatinine was higher than 200 and 300 mumol/l in 16 and 13 patients, respectively. Kidney obtained at autopsy from a 30-year-old male with AIDS, CMV pneumonitis and acute renal failure secondary to foscarnet administration showed an extensive tubular necrosis. In the group which was prospectively hydrated only 1 patient had an acute renal failure. The mean serum creatinine at the peak (96 +/- 4 mumol/l) and at the end of the treatment (83 +/- 4 mumol/l) was significantly lower (p less than 0.05) than in non hydrated patients. In conclusion, foscarnet is a highly nephrotoxic drug which induces acute tubular necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1989

The effects of selected drugs, including chlorpromazine and non-steroidal anti-inflammatory agents, on polyclonal IgG synthesis and interleukin 1 production by human peripheral blood mononuclear cells in vitro.

We tested a range of drugs for their effects on in vitro polyclonal IgG synthesis by human peripheral blood mononuclear cells (PBMC) stimulated with the lectin pokeweed mitogen (PWM). The test drugs were selected on the basis of reported disruptive effects on immune function in vivo. IgG production between day 4 and days 7 or 8 of culture was measured by biotin-streptavidin sandwich ELISA. The anti-psychotic agent chlorpromazine (0.55-1.7 microM) enhanced IgG synthesis to approximately double control levels. In contrast, the non-steroidal anti-inflammatory drugs (NSAIDs) indomethacin, piroxicam, ibuprofen and aspirin inhibited IgG synthesis by up to 50%, with a rank order of potency that reflects their activity as inhibitors of cyclo-oxygenase. Phenytoin, procainamide, propylthiouracil, methimazole, D-penicillamine and D-penicillamine-L-cysteine all failed to modulate IgG synthesis at non-toxic concentrations. The potentiation and inhibition of IgG synthesis by chlorpromazine and indomethacin, respectively, was observed only when the drug was present during the first 24 h of culture. Neither chlorpromazine nor indomethacin, at non-toxic concentrations, affected PHA- and PWM-stimulated proliferation of PBMC. In addition, chlorpromazine, indomethacin and piroxicam, at concentrations which produced maximal modulation of IgG synthesis, and D-penicillamine and D-penicillamine-L-cysteine at 10 microM failed to influence production of interleukin-1-like activity. We conclude that chlorpromazine and NSAIDs, although they exert opposite effects on IgG synthesis, act at an early stage of B cell differentiation that appears to be independent of interleukin 1 synthesis and early proliferative events.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1988

Renal function and blood pressure in patients treated with cyclosporin A for uveitis.

Renal function has been evaluated in 21 patients treated with cyclosporin A (CyA) for 9 months for idiopathic uveitis. Serum creatinine, which was 82 mumol.l-1 before treatment, was significantly elevated after 1 month (111 mumol.l-1). After 9 months of treatment, and despite a decrease in CyA dosage, the mean plasma creatinine remained elevated at 132 mumol.l-1. Hypertension developed in 6 patients, five of them being concomitantly treated with corticosteroids. In 8 patients serum creatinine 3 months after CyA had been stopped had decreased from 148 to 93 mumol.l-1. Two of those patients remained hypertensive 3 months after CyA treatment had ceased. In patients with idiopathic uveitis CyA induces a reversible increase in serum creatinine. However the reversibility of such a biochemical marker does not preclude a histopathological lesion. Chronic renal damage may be responsible for the persistence of hypertension after cessation of CyA treatment.

Adult↗
PubMed1988

[Functional renal effects of cyclosporin. Physiopathological mechanisms].

Animals and humans undergoing a treatment with cyclosporin (CsA) show a reversible increase in renal vascular resistance and decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. In animals potential mechanisms for CsA induced renal functional impairment are an increase in urinary thromboxane A2 excretion, plasma renin activity and renal sympathetic nervous system activity and an enhancement of vasopressin stimulated Ca++ mobilisation and cell contraction in vascular smooth muscle cells. In human, the problem is far less clear. CsA induces an inhibition in PRA and urinary prostaglandins excretion. Furthermore CsA does not modify urinary and plasma levels of catecholamines. Whatever the mechanism underlying the vasoconstriction induced by CsA, the inhibition of PGI2 synthesis and angiotensin II formation may participate in the decrease in renal blood flow and glomerular filtration rate which is observed in patients receiving CsA.

Animals↗
PubMed1987

Contributions of in vitro fertilization to knowledge of the reproductive endocrinology of the menstrual cycle.

The administration of ovarian stimulants to endocrine-normal women in IVF programmes gives the clinical endocrinologist an opportunity to modify natural folliculogenesis. Use of antioestrogens and/or gonadotrophins at the correct time has demonstrated that follicular atresia can be prevented and that multiple pregnancy-potent haploid ova can be obtained. Scrutiny of spontaneous menstrual cycles in patients who show unsatisfactory IVF responses has identified two new syndromes, premature follicle selection and occult ovarian failure, in these patients. The incidence of these disorders in fertile women is still unclear. Early results suggest that endocrine manipulations may overcome premature follicle selection and induce codominant folliculogenesis. Inhibin is a recently characterized ovarian protein which is increased in peripheral blood during IVF treatment. Results from IVF cycles suggest that plasma inhibin may be a new index of follicular function. Other potential indices of ovarian function, such as the luteal protein relaxin, may also develop from the application of basic research to IVF and advance knowledge of the human ovarian and menstrual cycles.

Estradiol↗