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A Iaina

Publications and source records attributed to A Iaina.

157 records · Page 9Linked to original sources
PubMedDate not supplied

Paramagnetic enhanced proton magnetic resonance measurement in rats: correlates with renal function.

Renal cortical, medullar and papillary T1 and T2 relaxation times were measured in rats with normal (n = 13) and impaired renal function (n = 11) with a Bruker Multispec, 20 MHz at 37 degrees C. In one group of seven rats, decreased renal function was obtained by 50% glycerol solution administration (10 ml/kg-body weight) 24 hours before the experiment, while in another group of four rats the renal function was decreased, by ureteral ligation for 72 hours. Immediately after the excision of one kidney, Gadolinium-DTPA (70 mumole/kg body weight) was injected intravenously. The second kidney was excised 5 min later. From the T1 and T2 relaxation times measured in the cortex, medulla, and papilla, their respective ratios before and after GdDTPA administration were calculated and correlated with GFR determined by creatinine clearance (Ccr range was between 0 and 850 microliters/min/g kidney weight). For T1: the ratios in the cortex, medulla, and papilla the correlation coefficients were r = 0.81 (p less than 0.001), r = 0.85 (p less than 0.001), and r = 0.87 (p less than 0.0001), respectively. The respective correlation coefficient r values for T2 were r = 0.38 (NS), r = 0.76 (p less than 0.001), and r = 0.73 (p less than 0.001). The present study indicates that a combination of MR measurements, with and without GdDTPA paramagnetic enhancement, can offer a new possibility for obtaining information on renal function and suggest the possibility of concomitant anatomo functional magnetic resonance imaging.

Animals↗
PubMedDate not supplied

Effects of an acute dose of L-arginine during coronary angiography in patients with chronic renal failure: a randomized, parallel, double-blind clinical trial.

BACKGROUND: Contrast media (CM) are nephrotoxic and might further worsen renal function in patients with chronic renal failure. L-Arginine, the substrate of nitric oxide, protects kidney function and may improve endothelial function in patients with coronary artery disease. HYPOTHESIS: Acute administration of L-arginine in a subset of patients with combined coronary artery disease and impaired kidney function during coronary angiography might prevent superimposed acute renal failure. METHODS: A double-blind study of patients with mild/moderate chronic renal failure (Cr >1.7 mg/dl) undergoing coronary angiography (meglumine ioxaglate) was conducted. Patients received either L-arginine (300 mg/kg) or placebo and were followed for 48 h. Cardiac hemodynamic parameters, renal function and nitric oxide production were sequentially recorded. RESULTS--PRIMARY AND SECONDARY: Both groups experienced a decrease of creatinine clearance 48 h following the procedure (p < 0.05). Creatinine levels slightly increased following the administration of L-arginine (p < 0.05) but not in the placebo treated group. No changes of systemic and cardiac pressures, total peripheral resistance or cardiac output were recorded within and between the treatment and placebo groups. CONCLUSION: CM injection causes an impairment of renal function. Addition of intravenous L-arginine during cardiac catheterizations in patients with chronic renal failure does not prevent CM-induced nephrotoxicity and does not affect endothelial dysfunction in the particular population studied by the authors, i.e. patients with coronary artery disease (CAD) of various degrees, or suspicion of CAD and chronic mild renal failure.

Acute Kidney Injury↗
PubMedDate not supplied

Renal proton magnetic resonance in experimental acute renal failure in rats.

Cortical, medullary and papillary T1 and T2 water proton relaxation times were measured at 37 degrees C, 20 MHz. The measurements were made using kidneys from rats affected by many forms of experimental acute renal failure (ARF), namely acute hemorrhagic hypovolemia, angiotensin II administration, antidiuretic hormone (ADH) administration, glycerol, and other nephrotoxins (gentamicin, cisplatinum, cyclosporine), renal artery occlusion for different periods of time, and ureteral ligation. From the T1 and PW (percent tissue water content) the bound water (FB) and HF (percent water bound/g solid) were calculated according to a fast proton diffusion model. In most experimental models studied, the experiments were repeated following paramagnetic enhancement with GdDTPA administration (70 mmol/kg BW). By profiling the deviations from normal, it was possible to differentiate the ischemic (shortened T1, prolonged T2), obstructive (very high T1 and T2 in both cortex and medulla) and nephrotoxic (prolonged T2) forms of ARF. Significant changes in free/bound water compartments occurred, though their biological significance is unknown. T1 and T2 ratios before and after paramagnetic enhancement correlated well with estimates of glomerular filtration rate. In the first minutes following acute hemorrhagic hypovolemia, the intrarenal water distribution remained unchanged. After GdDTPA significant water proton T1 and T2 changes characterized the immediate posthemorrhagic state similar to the effect of ADH.

Acute Kidney Injury↗
PubMedDate not supplied

Congenital Leber amaurosis, keratoconus, and mental retardation in familial juvenile nephronophtisis.

Two siblings suffering from congenital Leber amaurosis were found to be affected also by juvenile nephronophtisis. Keratoconus in one child and mental retardation in the other developed during their later growth. An extensive laboratory study showed normal results but revealed an impaired urinary concentrating ability. The hereditary pattern operating in this complex disease was found to be consistent with an autosomal recessive trait.

Adolescent↗
PubMedDate not supplied

The outcome of non-selective vs selective nitric oxide synthase inhibition in lipopolysaccharide treated rats.

UNLABELLED: Nitric oxide (NO), generated by inducible nitric oxide synthase (NOS) following lipopolysaccharide (LPS) administration, produces renal failure through autoinhibition of glomerular endothelial NOS activity. Preadministration of selective iNOS inhibitors abolishes this effect. Although nonselective NOS inhibitors further decrease GFR, current clinical trials investigate the effect of nonselective NOS inhibition in septic patients. The goals of our study were to determine whether treatment with selective NOS inhibitors can reverse the decrease in GFR in LPS treated rats with already established renal failure and to define the outcome of LPS treated rats following nonselective NOS inhibition. Four hours following the administration of LPS (4 mg/kg), we measured creatinine clearance (CrCl) before and after the administration of either L-NIL (selective iNOS inhibitor, 3 mg every 20 minutes) or saline. Selective iNOS inhibition attenuated the decrease in blood pressure [ CONTROLS: 105 +/- 6 to 98 +/- 5, LPS: 92 +/- 5* to 83 +/- 4*, LPS + L-NIL: 88 +/- 6* to 94 +/- 6 mm Hg; *p < 0.05, vs controls (n = 6)], and reversed the decrease in GFR after LPS [ CONTROLS: 2.21 +/- 0.13 to 2.07 +/- 0.11, LPS: 0.82 +/- 0.18* to 0.66 +/- 0.22*, LPS + L-NIL: 0.76 +/- 0.15* to 1.86 +/- 0.15 ml/min; *p < 0.05 vs controls (n = 6)]. We next studied the effect of complete non-selective NOS inhibition (L-NAME 200 mg, 2 hours after LPS) on LPS treated rats. All (6/6) animals treated with both LPS and L-NAME died within 2 hours following LPS, while rats treated with either LPS, L-NAME, or LPS + L-NIL survived. Histologic studies performed in all experimental groups were unremarkable. Overnight mortality was studied using smaller doses of L-NAME. All LPS + L-NAME (10/10) and 1/10 LPS treated rats died. L-NAME, control, and LPS + L-NIL animals survived. The characteristic histologic findings in LPS + L-NAME rats were diffuse ischemic changes, most importantly acute myocardial infarction. IN CONCLUSION: Selective iN-OS inhibition might prove to have clinical application as it prevents the decrease in GFR following LPS, even after renal failure is established. Treatment with a non selective NOS inhibitor in septic patients should be reconsidered.

Analysis of Variance↗
PubMedDate not supplied

Beta-adrenergic receptors in the urinary bladder of adult and developing rats.

Specific beta-adrenergic receptors were demonstrated in the urinary bladder of adult and developing rats, by direct tissue binding with LD [125I]-cyanopindolol (CYP). The maximum number of binding sites (Bmax) was 167 +/- 25 fmol/mg membrane protein and the dissociation constant (KD) equalled 61 +/- 33 pM. The Hill slopes of the LD [125I]-CYP binding showed a single class of noncooperative receptor sites. The rank order of potency of agonist competition for LD [125I]-CYP binding suggests that the receptors are mostly of the beta 2 subtype. Beta-adrenergic receptor density was approximately half in the first 10 days of life (Bmax 63 to 77 fmol/mg protein) compared with the older age-groups studied (Bmax 91 to 167 fmol/ng protein). On the 1st day after delivery, the calculated beta-adrenergic receptor number/bladder was 9.4, and it increased significantly with age to 2,496 in the adult rat. This is a 250-fold increase in the number of receptors/bladder, while only a 20-fold increase in membrane protein and a five- to sixfold increase in the bladder weight was observed. Thus, an age-dependent increase of beta-adrenergic receptors on the cell membrane surface area occurred in the developing urinary bladder of the rat.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Renal proton magnetic resonance and bound and free water distribution in the normal, angiotensin II-and ADH-infused rats, before and after Gd DTPA paramagnetic enhancement.

Female Charles River rats, 250-300 g, were used in all experiments. The rats were divided into the following experimental groups. Group A: Normal rats were injected with 1 ml saline intravenously. Exactly after 8 min the kidneys were excised as rapidly as possible. The papilla was dissected and cortical and medullary slices were prepared. Immediately following the excision T1 and T2 were measured with a Bruker PC-20 Minispec spectrometer operating at 20 MHz at 37 + 1 degree C. Water content (PW) of the samples was calculated as a percentage tissue weight, after 24 h drying to constant weight. The fraction bound (FB = % water bound) and hydration fraction (% water bound/g solid) were computed from T1 relaxation time, and the PW, according to a fast proton diffusion model. Group B: As group A but 3 min after the saline administration bolus of 1 ml solution of Gd DTPA. 70 mumol/kg body weight, was given intravenously. Group C: As group A but instead of saline the rats were given a solution of ADH (5 mU/kg body weight i.v.). Group D: As group C plus Gd DTPA as in group B. Group E: As group A but instead of saline the rats were given a solution of angiotensin II (Ag II) (5 micrograms/kg body weight). Group F: As group E plus Gd DTPA as in group B. In groups B-F the magnetic resonance and water distribution were determined and calculated as in group A. In the normal rats there is a prolongation of T1, T2 and an increased total water content from the cortex to the papilla.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗