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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the PGs operate mainly in the renal medulla the demonstration of PG biosynthesis in the renal cortex has provided a biochemical basis for a direct relationship between the PGs and the renin-angiotensin system. The formation of PGs is influenced by circulating levels of A I probably by indirect mechanisms. That the release of renin at least under certain experimental conditions is dependent on the PG system is suggested by the following findings: 1. C20:4 increases PRA in the rabbit and rat. 2. Indomethacin decreases PRA in the rabbit. 3. C20:4 stimulates renin release from slices of rabbit kidney cortex. 4. Reduced renal perfusion pressure and ischemia are accompanied by release of both PGs and renin. 5. The release of PG and renin following renal ischemia is blocked by treatment with indomethacin. The actions of the renin-angiotensin system and the renal PGs are, as far as we know them, antagonistic to each other. PGEs are vasodilator, increase renal blood flow, inhibit adrenergic neurotransmission, and cause excretion of electrolytes and water. Conversely, A II is vasoconstrictor, decreases renal blood flow, stimulates adrenergic neurotransmission, and conserves water and electrolytes. Thus, the interaction between the renal PGs and renin seems to be one in which the two hormonal systems stimulate each other's formation or release, but opposes each other's actions. Further studies are necessary to reconcile this apparent contradiction.
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PMID:Interactions between the renal prostaglandins and the renin--angiotensin system. 79 Sep 16

The effect of meclofenamate and indomethacin on renal blood flow and renal vascular resistance was determined under basal experimental conditions and during renal ischemia in pentobarbital-anesthetized dogs. Renal blood flow was measured with an electromagnetic flowmeter and renal arterial pressure was recorded from a catheter in the renal artery. Intra-arterial infusion of indomethacin or meclofenamate in concentrations of 4 and 4 to 8 mu-g/ml, respectively, did not cause any significant change in renal blood flow or renal vascular resistance under basal conditions. During the period of ischemia (50% reduction in renal blood flow), 4 mu-g/ml of either prostaglandin synthetase inhibitor caused a marked increase in renal vascular resistance. Prostaglandin E in the renal venous blood was decreased at the time renal vascular resistance was increased by meclofenamate. The renal vasoconstrictor response to angiotensin II injected intravenously was potentiated by both inhibitors under basal as well as ischemic conditions, which also suggested that prostaglandin synthesis was inhibited. The angiotensin antagonist 1-sar-8-ala-angiotensin II was infused intra-arterially in concentrations of 20 and 40 mmu-g/ml during renal ischemia. Subsequent administration of meclofenamate increased renal vascular resistance only slightly. The results of these experiments indicated that renal prostaglandins have more influence on renal blood flow during renal ischemia than under basal conditions, and that the renin-angiotensin system may be involved in activating synthesis and release of prostaglandins during ischemia.
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PMID:Influence of the renin-angiotensin system on the effect of prostaglandin synthesis inhibitors in the renal vasculature. 80 74

The effect of nearly total renal ischemia during a two hour period on glomerular filtration and urine composition was studied in relation to tubular permeability and tubular obstruction, two mechanisms that could explain renal insuficiency after iscehmia. Studies on creatinine clearance, micropuncture and microinjection of 14C-inulin into the proximal tubules by means of a hydraulic system were performed before and after the period of ischemia. Thirty minutes after the withdrawal of arterial obstruction, the animals exhibited a maintained diuresis, 50 per cent reduction in glomerular filtration in the superficial nephrons and in the total kidney, a reduction in the proximal fractional absorption of water, and also an increase in the urinary elimination of sodium. The glomerular filtrate of cortical nephorns obtained by micropuncture in anterior areas of the proximal tubules did not differ significantly from the one obtained by micropuncture in more distal areas. The inulin injected into the proximal tubules of a kidney was entirely eliminated by it.
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PMID:[Tubular permeability maintained in post-ischemic acute renal failure (author's transl)]. 85 78

The half-life of circulating renin was studied in normal rats and in rats with a single kidney that was ischemic. The resulting disappearance curve represented the sum of two exponentials. The average half-life of the fast component was 11.5 minutes for normal rats, 11 minutes for rats with mild renal ischemia, and 8 minutes for rats with severe renal ischemia. The mean half-life of the slow component was 67 minutes in normality, 84 minutes in mild ischemia, and 121 minutes in severe ischemia. Also, the calculated proportion of the slower component was different for each group--60.3% in normality, 68.2% in mild ischemia, and 82.2% in severe iischemia. The results suggest that more than one kind of renin may be produced and released by the kidney, and also that renal ischemia may modify the normal metabolism of renin.
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PMID:Half-life of circulating renin under different experimental conditions. 87 63

The influence of temporary ischemia followed by recirculation on the ultrastructure of glomerular capillaries and some portions of the nephron was studied in 20 albino rats which were subjected to compression of the vascular bundle of the left kidney for 30 min., 1, 2 and 3 hours followed by recovery of the blood stream in the ischemic organ for 3 hours (with a simultaneous nephrectomy of the right kidney). The electron microscopic analysis has established that the amount of micropinocytic vesicles become markedly increased within 3 hours following 30-min. ischemia of the kidney with the recovery of blood circulation in the cytoplasm of endotheliocytes of glomerular blood capillaries. With increased terms of the left kidney ischemia (1, 2, 3 hs) the ultrastructural changes in endotheliocytes increased. There appeared microclasmatosis of the internal plasmalemma of endotheliocytes, the flattened peripheral part of the cytoplasm underwent considerable destruction. Swelling of microvilli of the brush border and vacuolization of the cytoplasm were observed in nephrocytes of the proximal part of the nephron in short-term ischemia (30 min) followed by the recovery of circulation for 3 hours. Longer periods of ischemia (1, 2, 3 hs) casued destruction of the brush border. There appeared secondary lysosomes, in mitochondria there occurred discomplexation and lysis of cristae.
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PMID:[Effect of temporary ischemia with subsequent recirculation on the ultrastructure of glomerular capillaries and nephrons]. 98 9

A new technique for in vivo renal perfusion is described which eliminates the need for autotransplantation. In short term ischemia studies using three solutions, Sacks' solution was found to provide the optimal renal ischemia protection.
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PMID:A technique for isolated in vivo renal perfusion. 99 69

Reaction constants of renin in juxtaglomerular apparatus and plasma renin activity after renal ischemia and hemorrhage. During and after total renal ischemia and acute hemorrhage, renin activity in plasma (PRA) and microdissected juxtaglomerular apparatus (JGA) of rabbits were investigated. In controls, the apparent Michaelis-Mentoen constant (MMC) of semipurified standard renin of rabbits was 1025 plus or minus 223 SD ng/ml. Plasma renin of normal rabbits showed similar values: 1062 plus or minus 138 SD ng/ml. Intrarenal JGA renin, however, showed a great scatter of MMC (920 to 4760 ng/ml) and a significantly higher mean value of 2572 plus or minus 1156 SD ng/ml (pis less than 0.001). After complete renal ischemia by clamping both renal arteries for a 90-min period, the following results wereobtained: 1) Sixty min after the beginning of ischemia, PRA decreased from 20.9 plus or minus 9.8 SD to 7.6 plus or minus 5.2 SD ng/ml-hr (P is less than 0.05) and increased to 103, 68 and 42 ng/ml-hr 10, 30 and 90 min after removal of the clamps, respectively (P is less than 0.05).
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PMID:Reaction constants of renin in juxtaglomerular apparatus and plasma renin activity after renal ischemia and hemorrhage. 113 98

Radioimmunoassay was used to study the effects of renal ischemia on the distribution of PGE-like material between renal venous plasma and urine in anesthetized dogs. Renal venous and urinary concentrations of these substances were equal during control, ischemia and recovery periods. This relationship obtained despite significant increases in the concentration of PGE of both compartments during the ischemic insult. The renal secretion rates of PGE, calculated as the product of renal plasma flow and renal venous concentrations, was reduced during ischemia while urinary excretion, was unchanged. The evidence suggests that the increased PGE concentrations observed in both compartments during renal ischemia are primarily due to a dilutional factor rather than an increased synthesis. Furthermore, the data suggest that the net secretion of renal PG's per unit time may, in fact, be reduced during renal ischemia.
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PMID:Partition of PGE between renal venous plasma and urine during renal ischemia. 116 85

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 mug/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6-7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65-70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50-70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90-130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (delta GFR - 120-160%) than the contralateral control (deltaGFR = 30-40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.
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PMID:The effect of glucagon on glomerular filtration rate in dogs during reduction of renal blood flow. 117 90

During the acute renal ischemia (lasting up to 24 hrs) in rabbits the serotonin level displayed similar changes in the ischemic and contralateral kidney. In the tissues under study serotonin decreased during the first fifteen minutes of ischemia; then a tendency to increase with a maximal rise in the ischemic kidney after a 60-min ischemia was seen; as to the contralateral kidney--the maximal rise occurred after a 3 hr ischemia. At the further stages of ischemia serotonin content fell again, particularly in the ischemic kidney. The blood serotonin level increased somewhat during the 60-min ischemia. An increase in the 5-hydroxyindolacetate concentration in the urine coincided with the period of decrease of the tissue serotonin content.
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PMID:[Serotonin and 5-hydroxyindolacetate during acute renal ischemia]. 122 75


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