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)

Receptors for thiazide diuretic drugs in the rat renal cortex have recently been identified through the binding of [3H]metolazone, a potent diuretic with a thiazide-like mechanism of action. The present studies describe the rapid and reversible alterations that occur in thiazide receptors following acute renal ischemia in the rat. The apparent density of thiazide receptors in kidney membranes as measured by the binding of [3H]metolazone was reduced by 90% following 10 min of renal ischemia produced by clamping the renal pedicle. With release of the clamp and subsequent reperfusion for 10 min, thiazide receptor density returned to within 40% of control levels. Ischemia did not alter apparent affinity of receptors for [3H]-metolazone. Sections prepared from renal cortex and incubated in oxygenated media in vitro displayed similar rapid changes in thiazide receptors. Hypoxia of 10- to 30-min duration produced by incubating sections in vitro in nitrogen-saturated media caused a significant decrease in [3H]metolazone binding that was reversible with return to oxygenated media. Similar decreases were obtained in oxygenated sections that were incubated with mitochondrial inhibitors, dinitrophenol and rotenone, but not in sections incubated with ouabain. These results indicate that renal thiazide receptors undergo a rapid and reversible form of regulation and that controlling mechanisms are dependent on metabolic energy.
 ...
PMID:Reversible downregulation of thiazide diuretic receptors by acute renal ischemia. 291 65

Cerebral angiography is used to diagnose brain death of cadaver kidney donors. Clinical and animal data suggest that angiographic contrast media may potentiate the noxious effect of renal ischemia. In order to find out if cerebral angiography of cadaveric kidney donors prior to nephrectomy interferes with function or survival of the renal grafts, two groups of cadaveric donors were compared. One group had been exposed to contrast medium from cerebral angiography in median 18 hours before nephrectomy and the other had not. There was no difference in graft survival and function between the two groups. In a previous investigation angiography was performed two hours before explantation and in that investigation there was a shorter graft survival in the angiography group than in a control group. A delay of 12 hours is suggested between cerebral angiography and explanation, to decrease the combined harmful effects of contrast media and ischemia on renal grafts.
 ...
PMID:Does cerebral angiography of cadaveric kidney donors interfere with graft function? 295 62

Because of its ability to increase glomerular filtration, antagonize the actions of vasoconstrictors, and produce vasodilation, alpha human atrial natriuretic peptide (alpha-hANP) was evaluated for its potentially beneficial effects in experimental ischemic renal failure induced by 45-60 min of renal artery occlusion in bilaterally or unilaterally renally intact Sprague-Dawley rats. After ischemia, a 4-h intrarenal infusion of alpha-hANP restored 14C-inulin clearances in bilaterally and unilaterally intact animals from 0.05 +/- 0.006 and 0.05 +/- 0.01 ml/min per 100 g to 0.314 +/- 0.04 and 0.25 +/- 0.01 ml/min per 100 g, respectively (P less than 0.001, n = 8), compared with normal values of 0.49 +/- 0.023 ml/min per 100 g. Histologically, there was a progressive decrease in medullary hyperemia and prevention of intratubular cell shedding and granulocyte margination as a result of the 4-h alpha-hANP infusion such that after 24 and 48 h the histological appearance of the tissue was essentially normal. The results show that a 4-h intrarenal infusion of alpha-hANP after renal ischemia can preserve glomerular filtration rate and reduce renal tissue damage.
 ...
PMID:Atrial natriuretic peptide protects against acute ischemic renal failure in the rat. 296 Jun 93

Visceral ischemia secondary to increased intraabdominal pressure (IAP) following closure of abdominal wall defects presents a serious postoperative problem. Currently, the method of closure and postoperative management are determined by clinical impressions rather than measurement of IAP. In this study various methods of indirectly measuring IAP were compared in 17 rabbits in which IAP was sequentially increased with an intraabdominal balloon. Vesical and inferior vena caval (IVC) pressures were found to have good statistical correlation with IAP. Other methods tested were gastric, rectal, superior vena caval, femoral and brachial artery, and rectus compartment pressures. All were found to be poor indicators of actual IAP. In nine of the rabbits, radiolabeled microspheres were used to assess cardiac output and visceral blood flow. Renal blood flow was very sensitive to increased IAP with dramatic impairment at IAP above 10 to 15 mmHg. Small intestinal flow was less sensitive and did not become significantly diminished until IAP exceeded 25 to 30 mmHg. Our studies suggest that vesical and IVC pressure monitoring should be used to evaluate IAP in the clinical setting. If IAP is in excess of 10 to 15 mmHg surgical intervention is indicated to prevent the development of renal ischemia.
 ...
PMID:The relative merits of various methods of indirect measurement of intraabdominal pressure as a guide to closure of abdominal wall defects. 296 19

Toxic O2 metabolites have been postulated to contribute to renal ischemia-reperfusion injury, but their biochemical assessment and contribution as a function of the duration of ischemia is unclear. To address this issue we measured renal function and renal cortical glutathione levels following 20, 30, or 45 min of ischemia in situ and then 60 min of reperfusion by the isolated kidney technique. Increasing durations of ischemia were associated with progressive decreases in perfusion flow rate, glomerular filtration rate, tubular Na reabsorption, and renal cortical glutathione following reperfusion. However, reperfusion following simultaneous addition of the permeable O2 metabolite scavenger dimethylthiourea (DMTU; but not urea) prevented glutathione consumption and attenuated reperfusion-induced injury after 20 and 30 min of ischemia. In contrast, reperfusion with DMTU prevented glutathione consumption but did not improve renal function after 45 min of ischemia. Similarly, reperfusion with dimethyl sulfoxide also attenuated renal injury after 20 and 30 min, but not after 45 min of ischemia. Thus reperfusion of kidneys made ischemic for 20 or 30 min is associated with decreases in tissue glutathione and renal function that were both inhibitable by addition of O2 metabolite scavengers during reperfusion. In contrast, addition of O2 metabolite scavengers during reperfusion of kidneys previously made ischemic for 45 min prevented decreases in glutathione but did not improve renal function. We conclude that O2 metabolites formed during reperfusion contribute to functional impairment in kidneys made ischemic for short durations up to 30 min) but that after prolonged ischemia (greater than 30 min) injury is primarily mediated by non-O2 metabolite-dependent cellular events.
 ...
PMID:O2 metabolites cause reperfusion injury after short but not prolonged renal ischemia. 311 59

To determine whether iron participates in free radical-mediated postischemic renal injury and lipid peroxidation, we examined the effects of removal of endogenous iron or provision of exogenous iron following renal ischemia, as well as the effects of renal ischemia and reperfusion on renal venous and urinary "free" iron. Rats underwent 60 minutes of renal ischemia and were studied after either 24 hours (inulin clearance) or 15 minutes (renal malondialdehyde content) of reperfusion. Infusion of the iron chelator deferoxamine (200 mg/kg/hr) during the first 60 minutes of reperfusion resulted in a marked improvement in renal function (inulin clearance: 879 +/- 154 vs. 314 +/- 74 microliter/min; P less than 0.025) and a reduction in lipid peroxidation (renal malondialdehyde: 0.449 +/- 0.06 vs. 0.698 +/- 0.08 mmol/mg prot; P less than 0.05) compared to control animals. Infusion of 50 mg/kg/hr deferoxamine also protected renal function after ischemia (inulin clearance: 624 +/- 116 vs. 285 +/- 90 microliter/min; P less than 0.05) and resulted in less histologic injury. Iron-saturated deferoxamine had no protective effect. Conversely, infusion of the iron complex EDTA-FeCl3 during reperfusion exacerbated postischemic renal dysfunction and lipid peroxidation. Following renal ischemia there was no detectable increase in "free" iron in arterial or renal venous plasma. However, urinary "free" iron increased 10- to 20-fold following reperfusion. Iron chelators which underwent filtration and gained access to this free iron in the urine (free deferoxamine or inulin-conjugated deferoxamine) provided protection, whereas a chelator confined to the vascular space (dextran-conjugated deferoxamine) did not.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Role of iron in postischemic renal injury in the rat. 314 49

Nineteen mongrel dogs had 30 minutes of thoracic aortic occlusion to determine the effects that blockade of the renin-angiotensin system may have on preserving spinal cord blood flow and function during a period of temporary spinal cord ischemia. Cross-clamping of the thoracic aorta causes renal ischemia and activates the renin-angiotensin system with resulting increased production of angiotensin II. Angiotensin II is a potent peripheral constrictor and elevated levels may constrict collateral spinal cord circulation. At the time of aortic cross-clamping, 10 dogs received 100 mg/kg of MK422 (intravenous enalapril maleate), a converting enzyme inhibitor, and nine animals served as controls. The blockade of the renin-angiotensin system had no preserving effects on spinal cord flow as measured by microspheres and on spinal cord function as graded with the Tarlov scale. However, the paraplegic animals all had significantly increased lower thoracic and lumbar spinal cord flows 30 minutes after clamp release when compared with those animals that remained neurologically intact. In conclusion, marked hyperemia occurring after a period of hypoperfusion may lead to spinal cord edema and compartment syndrome with resulting paraplegia.
 ...
PMID:The effect of hyperemia on spinal cord function after temporary thoracic aortic occlusion. 317 89

The increase in free fatty acids in the ischemic tissue is a consistent observation and these free fatty acids are considered to play a role in the cellular toxicity. To elucidate the cause of higher levels of free fatty acids in ischemic tissue, we examined the catabolism of fatty acids. The beta-oxidation of lignoceric (24:0), palmitic (16:0) and octanoic (8:0) acids and the peroxidation of fatty acids were measured at different times of renal ischemia in whole kidney homogenate. The enzymatic activities for the oxidation of fatty acids decreased with the increase in ischemia time. However, the lipid peroxide levels increased 2.5-fold of control with ischemic injury. Sixty min of ischemia reduced the rate of oxidation of octanoic, palmitic and lignoceric acids by 57, 59 and 69%, respectively. Almost similar loss of fatty acid oxidation activity was observed in the peroxisomes and mitochondria. These data suggest that loss of mitochondrial and peroxisomal fatty acid beta-oxidation enzyme activities from ischemic injury may be one of the factors responsible for the higher levels of free fatty acids.
 ...
PMID:Fatty acid metabolism in renal ischemia. 318 24

Renal ischemia and reperfusion have been shown to be associated with an enhanced renal lipid peroxidation. Because glutathione (GSH) serves to protect cells from oxidative stress, the role of GSH in renal ischemia was investigated. The content of renal GSH in the rat declined to 40% of control values during 35 min of renal artery occlusion. Renal GSH levels only partially recovered after 120 min of blood reflow. To assess the significance of this effect, renal GSH levels were altered before occlusion of the renal artery. Rats were treated with either buthionine sulfoximine (BSO) or glutathione monoethylester (GSH-ester) to lower or elevate, respectively, renal GSH levels. The ischemia-induced changes in renal ATP, ADP, and AMP after 35 min of ischemia and 90 min of blood reflow were not affected by prior alteration of renal GSH levels. The ischemia-induced decrease in the respiratory control of isolated cortex mitochondria was also unaffected. In control animals, ischemia of 35 min increased urine flow rate 3.2-fold and decreased GFR to 29% of normal values during the reflow period. Similar changes occurred in kidneys with a depleted GSH level. In kidneys with an elevated GSH, however, both urine flow rate and GFR were decreased to values 50 and 3% of normal, respectively. Morphological analysis demonstrated that ischemia produced an enhanced degree of damage with an increase in cast formation in kidneys pretreated with GSH-ester; however, the ester also produced morphological changes in nonischemic kidneys. The severity of ischemic damage was similar in kidneys with a lower GSH content when compared with controls. We conclude that renal GSH is depleted by ischemia but depletion of renal GSH with BSO before ischemia has no effect on ischemic-induced damage to the kidney. However, ischemic-induced renal dysfunction is enhanced when GSH is elevated with glutathione monoethylester before ischemia.
 ...
PMID:Effect of an altered glutathione content on renal ischemic injury. 318 64

Placental ischemia is one of the etiological factors of pregnancy induced hypertension (PIH), however, the pathogenesis of placental and renal ischemia has not been clarified. The purposes of this investigation are (1) to clarify the fetomaternal hemodynamic changes in PIH and the influence of maternal postural change on fetomaternal hemodynamics, measured by thermodilution method, impedance cardiography and pulsed doppler method during pregnancy, (2) to provide to relationship between intrauterine resting tonus and maternal hemodynamics, that is, blood pressure, placental and renal blood flow measured by electromagnetic flowmeter and thermocouple method, and renal nerve activity, and (3) to study the influence of placental ischemia on vascular sensitivity to angiotensin II measured by Magnus method in animal experiment. (1) The increase in C.O and blood volume were recognized from the beginning of pregnancy to 24 GW, and subsequently, the decreasing tendency were found from about 32 GW to the onset of labor. However this decreasing tendency were subsided in the lateral position. These circulatory changes were observed in both normotensive and PIH cases, and especially, the decrease in C.O and blood volume in late pregnancy were more remarkable in PIH than that in normotensive pregnancy. From the results of Starling curve, left ventricular work was more hyperdynamic status in PIH than that in normotensive pregnancy, these results show that there are a compensatory mechanism against high vascular resistance in PIH. A/B (S/D) ratio in uterine artery, umbilical artery and fetal aorta were lowered in II-nd and III-rd trimester and more decreased in the lateral position from the supine position, on the other hand these ratio in PIH were elevated respectively. These results show that there are the aortocaval compression by the heavy tensive uterus and subsequent sluice flow mechanism in fetoplacental circulation in the supine position in late pregnancy. (2) These vascular compression were recognized very often in PIH accompanying with increasing in uterine resting tonus. It was recognized in pregnant rabbit that an increase in uterine resting tonus in the ovarian side caused an increasing blood pressure, a decrease in renal and placental blood flow and an increase in renal sympathetic nerve activity (RSNA). After resection of the suspensory ligament of ovarii, an increase in resting tonus in the ovarian side did not only cause an increase in RSNA, but also a decrease in renal blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Clinical and experimental studies on the pathogenesis in pregnancy induced hypertension]. 325 61


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