Search PubMed⌕ Search

Biomedical subjects

A Iaina

Publications and source records attributed to A Iaina.

At least 91 records · Page 5Linked to original sources
PubMed1988

Erythrocyte glutathione peroxidase activity in asthmatic children.

Erythrocyte glutathione peroxidase (GPX) levels were determined in 56 asthmatic children. Lowest levels were found during acute asthmatic attack (13.53 +/- 2.94 IU) which were significantly less than controls (20.4 +/- 5.44 IU) (P less than .001). Post-attack levels 1 week later rose significantly (16.77 +/- 2.63 IU), but were still less than normal values (P = .001). GPX levels (16.96 +/- 3.28 IU) were less than controls (P less than .03) even in patients with mild symptomatology. Asymptomatic patients receiving theophylline had normal levels. Low GPX activity in asthmatic patients may play a role in the pathogenesis of the disease.

Asthma↗
PubMed1987

Proton magnetic resonance in experimental acute and chronic renal failure in rats.

Kidney cortical and medullary "spin-lattice" (T1) and "spin-spin" (T2) relaxation times were measured by spectroscopy in several types of experimental renal failure in rats. The T1 and the measured tissue water content were used to calculate the fraction bound (FB) and hydration fraction (HF) according to a fast proton diffusion model. The present study demonstrated the possibility to differentiate between normal and pathological renal tissue resulting from renal artery clamping (RAC), renal pedicle clamping (RPC) with or without reflow, glycerol-induced acute renal failure with or without previous dehydration, and chronic hypertensive renal failure induced by 5/6 nephrectomy and saline loading, with low (6%) or normal (21%) protein diet. Shortened T1 and prolonged T2 found in both cortex and medulla of the glycerol-induced ARF in dehydrated rats seem to represent a MR ischemic pattern. The prolongation of T1 and T2 and the increase in water content in the other groups seem to relate to different amounts of tubular obstruction and renal congestion. In summary, characteristic MR properties of different types of renal failure may provide etiological and pathogenetic diagnostic possibilities.

Acute Kidney Injury↗
PubMed1987

Relationship between plasma renin activity and distal nephron sodium delivery and reabsorption in man.

The relationship between plasma renin activity and distal tubular sodium delivery and reabsorption was examined in man. Distal sodium delivery and reabsorption were measured during hypotonic volume expansion by the free water clearance method, or during hydropenia or isotonic volume expansion by the lithium clearance method. The maximal water diuresis method and the lithium clearance method both showed a negative correlation between plasma renin activity and distal sodium delivery and reabsorption. Only with the lithium clearance method, however, was it possible to measure plasma renin activity, distal sodium delivery and reabsorption in hydropenia without disturbances of water and electrolyte balance and plasma renin activity level. In hydropenia the plasma renin activity was higher and the fractional distal sodium delivery and reabsorption lower than during volume expansion. Our results support the idea that sodium chloride reabsorption at the macula densa region is negatively correlated to the plasma renin activity in man.

Absorption↗
PubMed1987

Improved renal function following acute peritoneal dialysis in patients with intractable congestive heart failure.

Nine patients, six men and three women, 40 to 73 years of age, were included in the study. All of the patients had severe heart failure refractory to aggressive therapy including digitalis, diuretics, and vasodilators. Eight patients underwent one treatment of peritoneal dialysis while the remaining patient received two dialyses. The urine output was measured by an indwelling catheter; glomerular filtration rate (GFR) was determined by creatinine and inulin clearance, and renal blood flow (RBF) was determined by sodium paraamino hippurate (PAH) clearance. Following one peritoneal dialysis, the mean fluid loss/patient was 3,995 ml (range 3,200 to 5,100 ml). Dialysis was generally well tolerated. One patient, who had underlying hepatic cirrhosis and underwent two dialyses, developed hepatic failure and died 10 days after the second dialysis. At postmortem, peritonitis was discovered. All of the patients showed a marked subjective and objective clinical improvement. The mean plasma urea decreased from 154 to 71 mg/dl (P less than 0.005), and mean plasma creatinine decreased from 1.83 to 1.13 mg/dl (P less than 0.005). Blood pH was 7.30 before dialysis and increased to 7.37 (P less than 0.0125) after treatment. Mean urine output predialysis was 955 ml and increased to 1,472 ml post dialysis (P less than 0.0005). Creatinine clearance increased from 35 to 73 ml/min (P less than 0.0005). The mean inulin clearance increased from 33 ml/min predialysis to 69 ml/min post dialysis (P less than 0.0005), and mean PAH clearance increased from 96.7 to 362.5 ml/min (P less than 0.0005). Acute peritoneal dialysis is a safe and effective means for removing large quantities of excess fluid from patients with intractable heart failure.

Adult↗
PubMed1986

Proton MR study of different types of experimental acute renal failure in rats.

Kidney cortical and medullary spin-lattice (T1) and spin-spin (T2) relaxation times were measured in several types of experimental acute renal failure in rats with a Bruker PC "Multispec." Gentamicin ARF was obtained after one i.p. injection of 100mg Gentamicin/kg BW/day for 8 days. Glycerol ARF: 24 hours after one i.m. injection of 10 ml 50% Glycerol/kg BW. Obstruction ARF: 3 days after complete ureteral ligation. Renal tissue total water content, hydration fraction, fraction bound, blood urea and creatinine were measured at the end of the experiments. Shortened T1 and prolonged T2 were found in both cortex and medulla in the Glycerol ARF group. Gentamicin renal toxicity and the non-functioning kidney with ureteral obstruction are characterized by significant prolongation of T1 and T2 in cortex, while the medullary T1 and T2 were prolonged only in obstruction ARF. The highest T1 and T2 were found in the obstructed non-functioning kidney. The total water content decreased in the Glycerol ARF, increased in the obstruction and remain unchanged in Gentamicin ARF. The hydration fraction and the fraction bound changed significantly in the opposite direction with the total water content. Different profiles of renal cortical and medullary magnetic resonance properties found in several models of experimental ARF in rats indicate that MR properties may provide etiopathogenetic diagnostic possibilities.

Acute Kidney Injury↗
PubMed1986

Hemodynamic effects of nifedipine in hypertension in the presence of elevated angiotensin-II and beta-adrenergic blockade.

The hemodynamic effects of the slow release form of a calcium channel blocker, nifedipine retard, in essential hypertension patients after angiotensin II (AII) infusion were studied using nuclear ventriculography. Sublingual nifedipine lowered blood pressure that had been acutely raised by an infusion of AII to its baseline level. When used for 4 weeks, nifedipine retard maintained its blood-pressure-lowering effects without a change in heart rate, both when used alone and when used in addition to beta-adrenergic blockers. In the patients with untreated essential hypertension, nifedipine counteracted the lowering effect of AII on left ventricular ejection fraction (LVEF), which was 67.5 +/- 8.9% at recumbency, 61.2 +/- 6.6% (+/- SD) during AII infusion, and 72.1 +/- 7.5% 30 minutes after sublingual nifedipine. These acute effects seem to result from a marked reduction in total peripheral resistance (TPR) and are accompanied by a rise in cardiac index (CI). The TPR, in dynes/sec/cm-5, was 1376.9 +/- 275.8 at recumbency, 2000.7 +/- 358 during AII infusion, and 1228.6 +/- 289 30 minutes after sublingual nifedipine. The corresponding figures for CI in liters/M2 BSA, were 4.02 +/- 0.77, 3.03 +/- 0.64, and 4.32 +/- 0.79. In patients receiving beta-blocker therapy (propranolol or atenolol) with inadequate control of blood pressure, similar results were obtained in LVEF (69.7 +/- 8.87% at recumbency, 63.7 +/- 11.9% during AII infusion, and 72.2 +/- 6.05% 30 minutes after sublingual nifedipine). The initial TPR was much higher than that of untreated essential hypertensive patients. Nevertheless, the increase obtained during AII infusion was counteracted by sublingual nifedipine. CI was decreased by AII.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Calcium entry-blockade with verapamil in cyclosporine A plus ischemia induced acute renal failure in rats.

The possible alleviating effect of verapamil, a calcium entry blocker, on the resulting renal damage from the combination of a short episode of ischemia and CyA was studied in rats. Immediately after right nephrectomy the rats were divided into five experimental groups. Group 1: left renal pedicle clamping for 20 minutes. Group 2: as group 1 plus CyA 60 mg/kg bw i.p. Group 3: CyA as in group 2 but sham operated. Group 4: as group 2 plus verapamil 10 mg% in the drinking water. Group 5: as group 3 plus verapamil given as in group 4. The experiments lasted 4 days. By analysis of variance: CyA + ischemia (group 2) showed lower creatinine clearance (p less than 0.001), higher blood urea (p less than 0.01), fractional excretion of sodium (p less than 0.05) and fractional excretion of potassium (p less than 0.01) and fractional excretion of negative free water clearance (p less than 0.001) compared to ischemia alone (group 1). The CyA + ischemia rats treated with verapamil had higher creatinine clearance (p less than 0.05), lower blood urea (p less than 0.01), fractional excretion of sodium (p less than 0.001), fractional excretion of potassium (p less than 0.001) and fractional excretion of negative free water clearance (p less than 0.05) compared with the untreated verapamil CyA + ischemia group. The CyA + sham operated verapamil treated group had similar creatinine clearance with the corresponding verapamil untreated group. The CyA + ischemia group had the higher mean daily body weight reduction compared with all other groups. Histology showed more vacuolization of tubular epithelial cells in the CyA + ischemia than in ischemia alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1985

Beta-adrenergic receptors on polymorphonuclear cell membranes in essential hypertension.

Beta adrenergic receptor binding sites were determined and characterized by specific binding of (+/-)[125I] iodocyanopindolol to membranes obtained from circulating polymorphonuclear leukocytes. No difference was found in the number of receptor sites and in their dissociation constants (Kd) between patients with untreated essential hypertension (EH), EH treated with drugs other than beta blockers, and in normotensive controls. The group with EH receiving treatment with beta blockers had a significantly higher receptor density and Kd as compared with all the other groups (p less than 0.05). It is concluded that the beta-adrenergic system of patients with essential hypertension at the receptor level is not different from normotensive subjects and responds to beta blockers by up-regulation.

Adult↗
PubMed1985

Anorexia nervosa, laxative abuse, hypopotassemia and distal renal tubular acidosis.

A case of anorexia nervosa in a 28-year-old woman with laxative abuse, hypopotassemia and severe metabolic acidosis, is described. The diagnosis of classical renal tubular acidosis, Type I, was confirmed by our inability to decrease urinary pH beyond 5.5 and to increase ammonia excretion during an ammonium chloride loading test. A bicarbonate loading test and normal plasma aldosterone with high renin activity excluded proximal renal tubular acidosis, hyporeninemic-hypoaldosteronemic renal tubular acidosis and Bartter's syndrome. The inability to increase ammonium excretion during severe metabolic acidosis following ammonium chloride loading did not favor the possibility of a transient physiological adaptation of ammoniagenesis at the tubular cell level, related to potassium depletion. Although mental disorder, laxative abuse, abstinence from food intake and severe potassium depletion intermingled in a vicious cycle, we assume that one of the following possibilities may explain the clinical presentation in our patient: either two separated and unrelated disorders, or laxative abuse as the cause of renal tubular acidification impairment.

Acidosis, Renal Tubular↗
PubMed1985

Cyclosporine and short ischaemia: a new model of experimental acute renal failure in rats.

To determine whether a mild episode of ischaemia may be a factor in the production of cyclosporine (Cys) toxicity, right nephrectomy was performed in three groups of Charles River rats: I. Ischaemia (left renal pedicle clamping) for 20 minutes, without treatment; II. Ischaemia of 20 minutes, followed by IP Cys 60 mg/kg BW/day; III. Sham (no ischaemia) followed by Cys as in Group II. The rats were sacrificed after four days. Cys plus ischaemia produced a lower creatinine clearance (136 +/- 15 microliter/min/100g BW, p less than 0.001) and a higher FENa per cent (0.94 +/- 0.14, p less than 0.05), FEK (1.07 +/- 0.02, p less than 0.01) compared with ischaemia alone creatinine clearance 261 +/- 39, FENa per cent 0.61 +/- 0.08, FEK 0.54 +/- 0.08, FEH2O -0.04 +/- 0.005. Histology showed more vacuolisation of tubular epithelial cells in the Cys plus ischaemia group than in the ischaemia alone group.

Acute Kidney Injury↗
PubMed1984

Receptor-cyclase coupling protein in erythrocytes of patients with essential hypertension.

In order to define the alteration of the function of the adrenergic system in hypertension, we studied directly the receptor-cyclase coupling protein (N protein), which is one of the components of the enzyme adenylate cyclase. N protein was determined in erythrocyte membranes of patients with essential hypertension and normal subjects, with a complementation assay in vitro. Fifteen normal subjects and 18 patients with essential hypertension (eight untreated and ten treated with beta-adrenoreceptor blocking drugs alone or in combination with other antihypertensive drugs), and two patients with pseudohypoparathyroidism type Ia (known to have deficient N protein activity), were studied. Erythrocyte N protein activities in the various groups expressed as percentages of the means +/- SD of normals were: normal subjects 100 + 13.7, untreated hypertensive 108.9 +/- 20.4, treated hypertensive 104.3 +/- 11.3 and pseudohypoparathyroidism type Ia 43%. The difference between N protein activity in the hypertensive patients and normals was not statistically significant. We suggest that the molecular basis for the altered sympathetic responsiveness in essential hypertension may reside in other components of the cyclic AMP protein kinase effector system.

Adolescent↗
PubMed1984

Attenuation of injury due to unilateral renal ischemia: delayed effects of contralateral nephrectomy.

The functional abnormalities associated with unilateral postischemic acute renal failure in the rat, as produced by 60 min of complete renal artery occlusion, are influenced by the presence or absence of the contralateral kidney. When the contralateral kidney is removed prior to the ischemia, reflow of blood to the postischemic kidney is more complete. To determine whether this maneuver influenced the ultimate severity of the injury and, if so, to investigate the mechanism by which this occurred, studies were performed conjointly at Tel-Hashomer, Israel, and Chapel Hill, N.C., in uninephrectomized (UNx) and sham-operated (Sh) rats. At Tel-Hashomer, V from UNx rats was nearly double that found in Sh rats at 1 to 3, 3 to 5, and 24 hr after ischemia. By 24 hr, CCr was substantially greater in UNx rats and was similar to that from the nonischemic kidney of Sh rats. Differences in tubular function were also noted. In UNx rats, FENa at 24 hr was significantly less and TCH2O was significantly greater than the corresponding values determined in Sh rats. At Chapel Hill, by 24 hr, RBF and PGCe in UNx rats were significantly greater than the corresponding values in Sh rats, although both were less than values obtained in nonischemic kidneys. In UNx rats, RT and RPG were considerably less than the corresponding values in Sh rats and similar to the values obtained in nonischemic kidneys. Microscopic examination at 24 hr revealed widespread tubular epithelial cell necrosis in Sh rats. In contrast, tubular epithelial cell structures were preserved in UNx rats. These data indicate that substantive differences exist in the response to temporary unilateral renal ischemia, which depend in part on the absence of the contralateral kidney and which result in less severe reduction in RBF and CCr and the preservation of tubular epithelial structure and function.

Acute Kidney Injury↗
PubMed1984

Calcium-entry blockade and pressor effect of angiotensin II in normal and nephrectomized rats.

The pressor effect of intravascular boli of 1.5 micrograms/kg angiotensin II was studied in untreated and in verapamil-pretreated intact rats and in rats 24 h after bilateral nephrectomy. An initial i.v. dose of 250 micrograms/kg verapamil was followed by a continuous infusion of 7 micrograms/min per kg. This resulted, within 2 min, in an average decrease in mean arterial pressure of 19 +/- 3 (SE) mm Hg and 18 +/- 3 (SE) mm Hg in intact and bilaterally nephrectomized rats, respectively. This continuous dose of verapamil did not significantly prevent the pressor effect of angiotensin II. When the continuous infusion of verapamil was increased to 50 micrograms/min per kg, the rise in blood pressure following angiotensin II administration was significantly lower than in the untreated rats: 21 +/- 2 (SE) mm Hg in intact rats, compared with 39 +/- 3 (SE) mm Hg (P less than 0.001) in the untreated animals and 31 +/- 3 (SE) mm Hg in rats in the renoprival state, compared with 47 +/- 6 (SE) mm Hg (P less than 0.01) in the corresponding untreated group. The present study suggests that verapamil can be used as a calcium blocker to reduce blood pressure associated with, or caused by, an increased renin-angiotensin system activity.

Angiotensin II↗