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Biomedical subjects

A Hishida

Publications and source records attributed to A Hishida.

At least 163 records · Page 9Linked to original sources

The effect of saline loading on uranium-induced acute renal failure in rats.

Studies were performed to examine the effect of saline loading on uranium-induced acute renal failure (ARF) in rats. Forty-eight hours after the i.v. injection of uranyl acetate (UA, 5 mg/kg), inulin clearance rate (Cin) decreased to approximately 43% of the control value in water drinking rats (P less than 0.005). Animals receiving continuous isotonic saline infusion following UA showed higher urine flow and Cin (60% of control, P less than 0.01), and lessened intratubular cast formation when compared with water-drinking ARF rats. A short-term saline infusion following UA did not attenuate the decline in Cin (43% of control). An inverse relationship was found between Cin and the number of casts (r = -0.75, P less than 0.01). Multiple regression analysis showed that standardized partial regression coefficient is statistically significant between Cin and cast formation (-0.69, P less than 0.05), but not between Cin and tubular necrosis (-0.07, P greater than 0.05). Renin depletion caused by DOCA plus saline drinking did not attenuate the decline in Cin in ARF (47% of control). No significant difference was found in urinary uranium excretion between water-drinking and saline-infused ARF rats. The findings suggest that continuous saline infusion following UA attenuates the decline in Cin in ARF rats; and that this beneficial effect of saline loading is associated with lessened cast formation rather than with suppressed renin-angiotensin activity or enhanced urinary-uranium excretion.

Acute Kidney Injury↗

Direct vasodilatory action of atrial natriuretic factor on canine glomerular afferent arterioles.

Studies were performed to examine whether atrial natriuretic peptide (ANP) has a direct action on glomerular afferent arterioles, and if so, whether the action is mediated by guanosine 5'-cyclic monophosphate (cGMP). A single superficial afferent arteriole was dissected from the canine kidney and perfused with the single glomerular perfusion technique described by Osgood et al. [Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13): F349-F354, 1983]. Norepinephrine (NE, 1 x 10(-6) M) significantly increased arteriolar resistance, calculated from the perfusion rate and arteriolar pressure. Synthetic human ANP (hANP) provoked afferent arteriolar dilation and attenuated the NE-induced increase in arteriolar resistance with 1 x 10(-10) to 1 x 10(-6) M concentrations. This vasodilatory effect was significantly potentiated by 2-o-propoxyphenyl-8-azapurin-6-one (M&B 22,948, 4 x 10(-12) M), a cGMP phosphodiesterase inhibitor, probably due to a sequential interaction of synergistic drugs. Also, the 1 x 10(-4) M concentration of 8-bromoguanosine 5'-cyclic monophosphate or dibutyryl guanosine, 5'-cyclic monophosphate (DBcGMP) lessened NE-induced arteriolar constriction, but DBcAMP did not. We conclude from these observations that ANP has a direct vasodilatory action on canine glomerular afferent arterioles, and that this ANP-induced vasodilation is mediated by enhanced cGMP synthesis.

Animals↗

Glomerular refractoriness to contractile stimuli in rabbits recovering from ischemic acute renal failure.

The present work was performed on uninephrectomized rabbits recovering from ischemic acute renal failure (ARF) in an attempt to elucidate whether or not intraglomerular events are a determinant factor in the development of resistance to ARF. 14 days after a 2-hour clamping of the renal artery (the recovery phase), the animals did not show resistance to an additional ischemia. On the other hand, glomeruli derived from normal kidneys displayed a contractile response to angiotensin II, arginine vasopressin or norepinephrine in Eagle's minimum essential medium, whereas glomeruli from rabbits recovering from ischemic ARF were refractory to the vasoconstrictor agents. The findings suggest that glomerular refractoriness to contractile stimuli does not provide resistance to an additional renal ischemia in the ischemic model of ARF.

Acute Kidney Injury↗

Water intoxication due to excessive water intake: observation of initiation stage.

A patient who had experienced water intoxication despite normal renal function and normal urinary diluting ability was observed during the initiation stage of hyponatremia. Upon the excessive water intake (10 to 15 L) for several days, he developed moderate hyponatremia (121 mEq/L) and headache, an early symptom frequently seen in water intoxication. During this period, his urine was maximally dilute (50 to 60 mOsm/kg H2O), and his urinary sodium excretion increased. This report suggests that 10 to 15 L of water intake for several days can cause water intoxication in subjects with normal urinary diluting ability and that the increase in sodium excretion is prerequisite for the high urine flow rate.

Adult↗

Intramesangial passage of mononuclear phagocytes in murine lupus glomerulonephritis.

By repeated biopsies, time-sequential changes of the injected colloidal carbon distribution were investigated in glomeruli of NZB/W F1 mice. The intraglomerular shift of the carbon, evaluated by counting the particles at several time intervals after carbon injection, demonstrated the movement of the carbon from the glomerular capillaries to the extraglomerular areas. Electron-microscopic examination disclosed that most of the increased cells of the glomeruli were mononuclear phagocytes rich in ingested carbon particles and that extracellular carbon was scarcely present. This strongly suggested that the carbon particles observed at the light-microscopic level reflected those ingested by the phagocytes. The mesangial cells per se scarcely ingested carbon particles. Instead, mononuclear cells, extending their cytoplasmic protrusions toward the dense (immune complex) deposits, were frequently noticed. It is concluded that the mononuclear phagocyte is a principal component of the hypercellular glomeruli, presumably contributing to the scavenging of the mesangium, and also that there is a pathway in the mesangium for these cells to shift from the capillary to the extraglomerular area by way of the vascular pole and lacis area.

Animals↗

Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF.

Glomerular responses to angiotensin II (AII), arginine vasopressin (AVP), and norepinephrine (NE) were estimated in rabbits recovering from uranium-mediated nephropathy or ischemic acute renal failure (ARF) to examine roles of intraglomerular events in resistance to ARF. Uranyl acetate (UA, 0.8 mg/kg) produced ARF in some animals but did not in others. Rabbits recovering from UA-induced ARF were highly resistant to a rechallenge with a larger dose of the agent (2 mg/kg). Their glomeruli did not respond to AII, AVP and NE in vitro. In animals having not experienced ARF following the initial insult, however, resistance to the rechallenge was lower than in animals recovering from ARF, and the glomerular response to contractile stimuli was well sustained. A two hour clamping of the renal artery induced ARF in uninephrectomized rabbits. These animals were not resistant to an additional ischemia in the recovery phase, despite inhibited glomerular contractile responses to AII. These data indicate a nonspecific inhibition of glomerular responses to contractile stimuli in the recovery phase of ARF. It is unlikely, however, that resistance to ARF can be attributed to the loss of the glomerular contractile response.

Acute Kidney Injury↗

Reticuloendothelial system and glomerular deposition of heat-aggregated human IgG.

The influence of functional impairment of reticuloendothelial system on glomerular deposition of heat aggregated human IgG (HAIgG) was studied. I-125 HAIgG was injected to mice treated either with dextran-containing 0.9% saline or with the saline alone. The HAIgG clearance rate from the blood decreased in the dextran-treated mice. The chronologically measured HAIgG contents in the liver, spleen and glomeruli increased in the dextran-treated animals. Immunofluorescent technique also demonstrated an increase in HAIgG and host C3 in the glomeruli. The glomerular hypercellularity was not demonstrated morphologically. Assuming that the function of the hepatic Kupffer cells principally affect the clearance rate of the foreign macromolecules from the blood, it is likely that the dextran administration impaired the function of these cells to digest the phagocytosed HAIgG, and that consequently the injected HAIgG stayed longer in the blood. Thus, increased supply of the HAIgG from the blood and/or the dextran-induced reduction of digesting function of the mesangial cell per se might have led to the accumulation of glomerular HAIgG. We suggest, therefore, that even small amount of immune complex may induce immune complex-mediated glomerular lesion, when associated with long lasting functional impairment of the Kupffer cells.

Animals↗

Influence of alternate-day prednisolone administration on urinary electrolyte excretion.

The administration of 30 mg of prednisolone on an alternate-day schedule produced an increase in sodium and potassium excretion, followed by a compensatory decline on the succeeding nontreatment day. Water and electrolyte excretion in patients receiving a daily steroid treatment was intermediate between that on the treatment and nontreatment days in the patients on an alternate-day schedule. Fractional sodium and potassium excretion was significantly lower on the nontreatment days as compared to the treatment days. Body weight loss, elevated serum albumin, slightly reduced serum potassium and significantly decreased cortisol concentrations were found in the morning on the nontreatment days, while serum sodium and plasma aldosterone concentrations, and the creatinine clearance rate did not change significantly. Replacement of steroid-induced body fluid loss lessened a decline in water and electrolyte excretion on the nontreatment days. Reduced water and electrolyte excretion on the nontreatment days might have been associated with decreased extracellular fluid volume, suppressed cortisol secretion, or both.

Adult↗

Glomerular alterations in uranyl acetate-induced acute renal failure in rabbits.

The study was performed to elucidate the progression and regression of superficial and inner glomerular alterations in uranyl acetate-induced renal failure in rabbits. Fifteen hours after the drug injection, creatinine clearance (CCr) decreased to 55% of controls with slightly elevated plasma creatinine concentration (initiation stage). After 5 days, urine flow and CCr decreased to approximately zero, with severe azotemia (maintenance stage). Scanning electron microscopic observations in these stages revealed a flattening and spreading of podocyte cell bodies associated with loss of epithelial foot processes, and reduction in the density of endothelial fenestrae. These changes were more advanced in the maintenance stage. Glomerular and fenestral diameters did not significantly change in the initiation stage but increased in the maintenance stage. There was no significant difference in these morphologic alterations, however, between the superficial and inner glomeruli. Glomerular alterations reverted to normal within 14 days, with good recovery of glomerular function. The findings show no significant difference in the progression or regression of the glomerular changes between the superficial and deep cortex. These morphologic changes may play a role in the reduction of CCr observed in this model.

Acute Kidney Injury↗

Ischemic acute renal failure in the rat: protective effect of uninephrectomy.

Experiments were performed to investigate the effect 2-wk prior nephrectomy has on the recovery from a 40-min renal artery occlusion. Two groups were initially examined. Group 1 animals underwent sham nephrectomy and group 2 animals right nephrectomy 14 days prior to a 40-min left renal artery clamp. The percent recovery of inulin clearance in group 2 (33 +/- 6%) was not significantly different from that in the group 1 (36 +/- 8%) when measured 3 h after reflow. At 24 and 48 h of reflow, however, group 2 animals had a significantly higher percent recovery of inulin clearance (24 h: 31 +/- 5%; 48 h: 50 +/- 11%) than group 1 animals (24 h: 1 +/- 1%; 48 h: 8 +/- 4%). Similarly the histology was better preserved at 24 and 48 h in group 2. To further investigate this enhanced recovery, three additional groups were studied. Group 3 underwent right nephrectomy at the time of renal artery occlusion. Group 4 had right uretero-venostomies created immediately prior to the ischemic insult, and group 5 had their aortas rather than left renal arteries clamped. Each group shared with group 2, ischemia to all functioning excretory tissue. The percent recovery of inulin clearance in group 3 (48 +/- 9%), group 4 (54 +/- 5%), and group 5 (42 +/- 6%) were each significantly (P less than 0.005) higher than in group 1 (8 +/- 4%) when measured at 48 h. We conclude that the protection offered by uninephrectomy is not a consequence of hypertrophy but that alterations in the environment which follow ischemia to all functioning excretory renal tissue are responsible for the enhanced recovery seen.

Acute Kidney Injury↗

Renal handling of salt and water in the early stage of obstructive jaundice in rabbits.

Renal handling of salt and water in the early stage of obstructive jaundice was studied in rabbits 10 days after the ligation of the common bile duct (BDL). Sham-operated (SO) animals served as controls. No sodium retention was found in BDL rabbits, despite reduced renal perfusion and elevated plasma aldosterone level. A redistribution of intrarenal blood flow was not found. The filtration fraction did not change. A saline load resulted in decreases in arterial hematocrit and total serum proteins, and increases in urine output, urinary sodium excretion and osmolal clearance. Blood pressure, glomerular filtration rate (GFR), RPF, the filtration fraction and the intrarenal flow distribution were not significantly affected by the saline load. No significant difference was found in the natriuretic response to the saline load between the BDL and SO groups. After 60 h of water deprivation, there was no significant difference in urine-to-plasma osmolality ratios or renal tissue fluid osmolality between the BDL and SO animals. The findings indicate that renal handling of salt and water was well maintained in the early phase of obstructive jaundice in rabbits. The data also suggest the critical role of the redistribution of intrarenal blood flow rather than of GFR or aldosterone in determining sodium retention in obstructive jaundice.

Aldosterone↗

Diurnal variation of urinary potassium excretion in chronic renal insufficiency.

Diurnal variation of urinary potassium excretion was examined on 10 adult patients with chronic renal insufficiency and 24 control subjects without cardiorenal functional disturbances. The daily cycle of potassium excretion, similar to that in controls, was present but less obvious in chronic renal insufficiency. In the controls, urinary potassium excretion reached a peak in the early morning (5.30 to 7.30) with a minimum in the night (21.00 to 5.30). The morning rise in potassium excretion was associated with increases in urinary sodium excretion, arterial blood pH, and plasma potassium and aldosterone concentrations. Creatinine clearance rate did not change significantly. In renal insufficiency, plasma potassium level and potassium excretion increased in the morning as compared with the night, whereas sodium excretion, the creatinine clearance rate, arterial blood pH and plasma aldosterone concentration did not change. 9 alpha-Fluorohydrocortisone gave rise to markedly enhanced potassium excretion. The findings suggest that the blunted cycle of potassium excretion in renal insufficiency is due, in part, to suppressed diurnal variations of sodium delivery to the distal tubule, acid-base balance and/or aldosterone secretion.

Adult↗