Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the calcium blocker S-(+)-methyl 4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitro-phenyl)thieno[2,3-b]pyridine- 5-carboxylate (S-312-d) on ischemic acute renal failure (ARF) was studied in rats. Ischemic ARF was induced by temporary (30-60 min) clamping of the left kidney 2 weeks after contralateral right nephrectomy. Plasma creatinine, creatinine clearance, urinary osmolality and fractional excretion of sodium were used to test the effectiveness of the drug. S-312-d (0.01-0.1 mg/kg b.wt. i.v.) administration before ischemia offered dose-dependent protection against the functional impairment induced by ischemia. This effect was accompanied by an increase in the survival rate of ischemic rats. S-312-d given after ischemia was not effective. The renal cortical edema induced by ischemia was significantly reduced by pretreatment with S-312-d. The increase in renal tissue calcium content observed after ischemia was also suppressed by S-312-d. Comparison with other established calcium blockers indicated S-312-d to be a good candidate for protection against ischemic ARF. These findings indicate that S-312-d may be clinically useful against renal ischemia.
 ...
PMID:Protective effect of a novel calcium blocker, S-312-d, on ischemic acute renal failure in rat. 224 38

The ability of the Ca entry blocker nitrendipine to improve postischemic renal function was studied in nine groups (n = 70) of rats. After anesthesia, nitrendipine was administered for 15 min through the femoral vein. The dose administered depended on the group. Group 1 (n = 7), the control, received only 0.9% NaCl, group 2 (n = 12) 0.25 mg/kg; group 3 (n = 10) 0.50 mg/kg; group 4 (n = 8) 0.75 mg/kg; group 5 (n = 6) 1.00 mg/kg; group 6 (n = 7) 1.50 mg/kg; group 7 (n = 7) 2.00 mg/kg; group 8 (n = 6) 2.50 mg/kg; and group 9 (n = 7) 3.00 mg/kg. After the administration of nitrendipine, the kidneys were rendered ischemic for one hour by cross-clamping the renal vessels. Comparison of 24-h creatinine clearances for 72 h after reversal of ischemia demonstrated that nitrendipine was capable of providing a degree of protection against renal ischemia and the protective effect was dose dependent (p less than .05).
 ...
PMID:Effect of calcium entry blocker nitrendipine on renal function after renal vascular occlusion. 224 16

The effects of two different H2-receptor antagonists, cimetidine and famotidine, on the acute renal failure induced by 20 min of renal artery occlusion and gentamicin (240mg/kg BW, s. c., for 3 days) were investigated in Sprague-Dawley rats. The animals were treated with either cimetidine (80 or 160 mg/kg BW) or famotidine (4 or 8 mg/kg BW) mixed in the drinking water for 7 days. The low dose of cimetidine and famotidine did not alter the renal function in the absence of renal trauma. However, the high dose of cimetidine or famotidine decreased the GFR by 32% and 22%, whereas RPFR increased by 46% and 62%, and % FENa by 92% and 558%, respectively. The data for the renal function obtained 24 hrs after 20 min of renal ischemia demonstrated a decrease of 54% in GFR, a decrease of 47% in RPFR and an increase of 370% in %FENa over the non-ischemic control values (p less than 0.05). Cimetidine (80 mg/kg BW) or famotidine (4 mg/kg BW) did not modify the recovery of renal function following the ischemic insult, showing 55% and 539% decreases in GFR, 74% and 101% increases in RPFR, and 393% and 461% increases in %FENa over the non-ischemic control rats, respectively. Famotidine reduced the decrease in RPFR significantly during the recovery period following ischemia. In the gentamicin study, gentamicin treatment was found to lower the renal function significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Do the H2-receptor antagonists, cimetidine and famotidine, modify the degree of renal recovery following renal insult? 225 Apr 7

The effect of 48 hours of hypothermic renal ischemia utilizing Euro-Collins flush and short term reperfusion on renal prostaglandin synthesis was studied in dogs. Hypothermic ischemia followed by 60 minutes of reperfusion in-vivo resulted in significant elevations in renal Thromboxane B2 (TXB2) production in the outer cortex, inner cortex, and medulla, relative to non-ischemic kidneys. Prostaglandin E2 (PGE2) and 6-keto Prostaglandin F1 alpha (6-K PGF1 alpha) production were not significantly affected by ischemia and reperfusion. Enhanced TXB2 production was not seen with ischemia alone (without reperfusion) or with reperfusion with O2 saturated buffer, indicating a blood born source or stimuli. Early postreperfusion renal blood flow after hypothermic ischemia followed a biphasic pattern; blood flow increased for the first 10 minutes of reperfusion to achieve normal values, and then steadily declined over the next 20 minutes. This pattern was not altered by the cyclooxygenase inhibitors Idomethacin (5 mg/kg, P.O.) or Mefenamic acid (10 mg/kg, I.V.). Administration of the TXA2 synthesis inhibitor CGS-12970 (3 mg/kg, I.V.) or the TXA2/endoperoxide receptor antagonist SQ-29548 (80 micrograms/min, I.A.) significantly increased renal blood flow during reperfusion but neither agent altered the basic time dependent pattern observed in the control group. These data indicate that 48 hours of hypothermic renal ischemia results in dramatic changes in intrarenal TXA2 synthesis at the time of reperfusion. Enhanced TXA2 production is not dependent on reoxygenation per se, but rather requires reperfusion with blood suggesting a circulatory source.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Prostanoids and hypothermic renal preservation injury. 228 Nov 20

Several functional parameters were applied in an experimental model of ischemia to test the ability to localize the distribution of tubular lesions. Canine kidneys were perfused with protective solutions and rendered ischemic for definite periods. Renal function was determined during a subsequent 3-h reperfusion. The pattern and the extent of renal injury were influenced by varying the duration of ischemia and by modifying the protective solution used. The results suggest that by employing an appropriate selection of parameters it is possible to allocate renal injury to definite sections of the tubules. According to such an evaluation, under protection with HTK-solution, the proximal tubule limits the tolerance of renal ischemia. The thick ascending limb shows some vulnerability that is aggravated by disadvantageous modifications of the protective solution and that may become more pronounced in the course of reperfusion. In contrast, more distal parts of the nephron retain a remarkable reserve transport capacity after a tolerable level of ischemia.
 ...
PMID:Postischemic diagnostic localization of tubular lesions. 231 10

Oxygen metabolites formed during reperfusion of ischemic kidneys prevent recovery of renal function after short periods of renal ischemia. Xanthine oxidase has been proposed as a source of toxic oxygen metabolites during reperfusion of ischemic kidneys. To determine whether the enzyme is converted from the non-oxygen metabolite-producing dehydrogenase (type D) to the oxygen metabolite-producing oxidase (type O), we measured type D and type O (total, reversible, and irreversible) xanthine oxidase in renal cortical homogenates after 30 min of ischemia in vivo and 60 min of reperfusion by the isolated perfused kidney technique. Total enzyme activity (type D plus type O) was not altered by ischemia or reperfusion. Compared with nonischemic conditions, ischemia increased total type O (53 +/- 5 vs. 21 +/- 3%, P less than 0.01) and reversible type O (15.4 +/- 1.5 vs. 2.1 +/- 1.4 U/g) xanthine oxidase activities. Reperfusion further increased total type O (82 +/- 3%) and reversible type O (27.7 +/- 3.3 U/g, both P less than 0.01 vs. nonischemic perfusions) xanthine oxidase activities. To determine the physiological role of xanthine oxidase in renal ischemia, we depleted rats of xanthine oxidase by feeding tungsten. After 4 wk of tungsten, renal xanthine oxidase levels were reduced by greater than 90% and renal function was markedly improved during reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Role of xanthine oxidase in ischemia/reperfusion injury. 231 73

In order to assess the potential nephrotoxicity of antibiotics, effects of these agents on rat kidney lysosomal membrane were investigated in various conditions. Antibiotics were given to Wistar rats for 5 successive days. After nephrectomy rat lysosomes were separated and their membrane stability was examined by measuring the activities of acid-phosphatase. In addition, after separation of lysosomes from normal untreated Wistar rats, antibiotics were added in the incubation system to assess the in vitro effect of antibiotics. Effects of renal ischemia and the lysosomal membrane stabilizer (cortisol) were also examined. Aminoglycosides antibiotics (streptomycin, kanamycin, gentamycin), doxytetracycline, chloramphenicol, and cephems (cephalothin, cephaloridine, ceftezol, latamoxef) were used for this purpose. It was clearly pointed out that aminoglycosides interfered with the lysosomal stability in vivo and in vitro. After a 60 minutes ischemia of the rat kidneys by clamping the renal arteries, effects of antibiotics on administration of 5 successive days on rat lysosomal stability were investigated. It was demonstrated that aminoglycosides also made the lysosomal membrane more unstable. Effects of the lysosomal stabilizer, cortisol, on rat kidney lysosomes were examined. Use of cortisol simultaneously with an antibiotic was more effective than that before and after it.
 ...
PMID:[Basic study of nephrotoxicity of antibiotics. II. Studies of the effect of antibiotics on lysosomal stability in rat kidneys]. 232 26

The influence of neutrophils on peritubular capillary permeability and intravascular red blood cell (RBC) aggregation after renal ischemia was studied in anesthetized Sprague-Dawley rats. Intraperitoneal administration of antineutrophil serum (ANS) reduced the number of neutrophils in the blood to 3% of normal. The control group received an equal volume of inactive serum. Renal macromolecular capillary permeability was studied from 1) extravasation of albumin and 2) plasma to lymph transport of plasma proteins and of neutral and negatively charged lactate dehydrogenase (LDH). The net driving force (NDF) for fluid transfer over the peritubular capillary membrane was determined by the micropuncture technique. The intrarenal distributions of neutrophils and RBC were measured by a histochemical method and 51Cr-labeled RBC, respectively. Under preischemic control conditions neither macromolecular permeability nor renal clearance of inulin was affected by ANS. However, the steep increase in the macromolecular transport from plasma to lymph resulting from 45 min of ischemia and reperfusion was blunted by ANS, and preischemic control values were restored after 1 h of recirculation. In the control group the mass transport of plasma proteins increased twofold and that of both neutral and negatively charged LDH fourfold. NDF was equal in the two groups. In the ANS-treated animals the intrarenal neutrophil content was only 2% of the control. Neutrophils were found mainly in the cortex, whereas RBC aggregation was observed only in the renal medulla. It is concluded that neutrophils mediate postischemic capillary leakage. It is suggested that this leakage underlies RBC aggregation and incomplete return of blood flow in the renal medulla after ischemia.
 ...
PMID:Peritubular capillary permeability and intravascular RBC aggregation after ischemia: effects of neutrophils. 233 Sep 69

Acute cyclosporin A (CysA) nephrotoxicity has been attributed to intrarenal vasoconstriction. It has been previously demonstrated that CysA decreases whole kidney and cortical blood flow. The effect of CysA on medullary blood flow has not been adequately studied, despite the high susceptibility of structures in the renal medulla to ischemia and the common use of CysA after the kidney is subjected to transient ischemia. To determine its effects on medullary blood flow in the normal and postischemic kidney, CysA was administered acutely in anesthetized Munich-Wistar rats at doses ranging from 4 to 20 mg/kg. Total renal blood flow (TRBF) and glomerular filtration rate (GFR) were determined in normal kidneys (group 1) by standard clearance techniques before and after infusion of CysA. In animals subjected to 40-min unilateral renal ischemia (group 2) TRBF was measured with an electromagnetic flowmeter. Vasa recta blood flow was determined in both groups by fluorescence videomicroscopy. In group 1, infusion with 20 mg/kg CysA, but not with 4 or 8 mg/kg, increased renal vascular resistance (RVR) and decreased TRBF. GFR was not affected and filtration fraction increased. Vasa recta blood flow was not significantly altered. In group 2, 20 mg/kg CysA increased RVR and decreased TRBF. Vasa recta blood flow decreased significantly in the descending but not in the ascending vasa recta. These results suggest that, in the normal kidney, vasa recta blood flow in the renal medulla is not affected by acute administration of CysA, whereas in the postischemic kidney, CysA decreases blood flow preferentially in the descending vasa recta, in proportion to the decline in TRBF.
 ...
PMID:Acute effect of cyclosporin on inner medullary blood flow in normal and postischemic rat kidney. 233 45

Although it was initially performed in 1935, aortic fenestration has been infrequently employed and reported in recent years. We have continued to use fenestration for descending aortic dissection with complicating organ ischemia (lower-extremity ischemia, renal ischemia, and paraplegia). Our technique involves complete transection of the infrarenal abdominal aorta, removal of a generous intimal flap proximally, and reconstitution of layers distally. We report our experience with 12 patients, all of whom survived the operative procedure. Nine patients were discharged from the hospital, and with a mean follow-up of 6.8 years, 7 are still alive. Fenestration immediately restored organ perfusion in all but 1 of the patients, and no patient died of late rupture. We recommend fenestration for descending aortic dissection in patients presenting with organ ischemia. Fenestration is not recommended for acute dissection with rupture or for chronic enlarging dissection.
 ...
PMID:Fenestration revisited. A safe and effective procedure for descending aortic dissection. 234 78


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>