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

We examined in anesthetized dogs the effects of left (L) intrarenal artery infusion of angiotensin II (AII) on renal hemodynamics, urinary concentration and Na excretion, and papillary plasma flow (PPF) (measured by the albumin accumulation technique) in both kidneys. Following AII infusion (0.5 ng/kg/min) into the L renal artery, urinary Na excretion decreased and osmolality increased slightly ipsilaterally, whereas Na excretion did not change significantly and osmolality decreased in the right (R) kidney. PPF was significantly lower in the L compared to the R kidney. When saline loading was superimposed on L intrarenal AII infusion, there was a blunted natriuretic response ipsilaterally with a significantly smaller decrease in urine osmolality compared with the R kidney. PPF increased significantly in the R, but not in the L kidney. Finally, AII blockade with saralasin prior to AII infusion and saline loading prevented the differences between the two kidneys, including PPF. In all groups GFR and renal blood flow did not differ between the two kidneys before or after AII. These data suggest that AII regulates regional blood flow in the medulla, and that the exogenously administered AII induces papillary ischemia, which serves to preserve medullary hypertonicity, preventing an increase in PPF during saline loading, and possibly contributing to the diminished natriuretic response.
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PMID:Regulation of papillary plasma flow by angiotensin II. 343 Sep 49

The hepatic hemodynamic response to cardiogenic shock was investigated in a porcine model produced by pericardial tamponade to better understand the pathophysiology of postshock hepatic insufficiency. Reductions of cardiac output to 50 percent of baseline levels produced marked hepatic ischemia by causing disproportionate reductions in blood flow through the celiac and hepatic arteries and portal vein. These were due to selective vasoconstriction of the splanchnic resistance vessels that was mimicked without tamponade by the infusion of angiotensin II, ablated by angiotensin-converting enzyme blockade, unaffected by alpha-adrenergic ablation, and correlated closely with levels of plasma renin activity. The ischemic liver injury of cardiogenic shock appears to be largely due to an exquisite responsiveness of the splanchnic vascular smooth muscle to endogenously released angiotensin II.
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PMID:Pathophysiology of hepatic ischemia in cardiogenic shock. 351 57

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.
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PMID:Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF. 354 13

The nonocclusive component of ischemic colitis in anesthetized pigs was mimicked using cardiogenic shock produced by pericardial tamponade. Increases in pericardial pressure produced decreases in arterial pressure (PA) and cardiac output (CO), with corresponding rises in total peripheral resistance (i.e., cardiogenic shock). This was associated with marked reductions in blood flow through the inferior mesenteric artery (IMA), due primarily to disproportionate increases in IMA vascular resistance. Levels of plasma renin activity correlated closely with these changes in mesenteric hemodynamics. Confirmed, total alpha adrenergic blockade with phenoxybenzamine failed to block this selective mesenteric vasoconstriction, while ablation of the renin-angiotensin axis with captopril completely abolished it, thereby ameliorating the colonic ischemia. Central intravenous infusions of pathophysiologic levels of angiotensin II, without tamponade, mimicked the response to shock seen with tamponade alone. In an additional group of pigs, 4 hours of sustained shock (tamponade) followed by 2 hours of normotension (release of tamponade and resuscitation) produced lesions characteristic of ischemic colitis, including full-thickness mucosal ulceration. Such lesions were ameliorated significantly in pigs in which the renin-angiotensin system had been ablated by bilateral nephrectomy. Nonocclusive ischemic colitis appears to be mediated primarily by a remarkable sensitivity of the colonic vasculature to the renin-angiotensin axis.
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PMID:Pathogenesis of nonocclusive ischemic colitis. 371 27

In order to elucidate the relationship between the degree of autoregulatory loss and the intensity or the duration of ischemia, and the difference of locations in and around the ischemic focus, we used the canine thalamic infarction model and studied the sequential changes of rCBF and autoregulation during 6 hours following vascular occlusion. The value of rCBF was measured by the hydrogen clearance method and autoregulation was tested by raising the blood pressure with drip infusion of angiotensin II. In the center of ischemic focus, autoregulation was impaired after 1, 3 and 5 hours following occlusion in the animals with moderate ischemia. In the animals with mild and severe ischemia, autoregulation was preserved during occlusion, but in the latter we thought it false autoregulation. In the periphery of infarctic focus with severe ischemia, autoregulation was impaired after 3 and 5 hours following occlusion. Outside of the infarctic focus with severe ischemia, autoregulation was preserved during occlusion, but in 2 of 6 animals rCBF decreased despite of raising blood pressure and it was thought to be paradoxical response.
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PMID:[Sequential changes of autoregulation in experimental focal cerebral ischemia--pathophysiology at the center, periphery and outside of the focal cerebral ischemia]. 376 89

That local splanchnic ischemia is associated with the acute gastric "stress" erosions seen in shock is well established. The hemodynamic mechanism mediating that ischemia is unknown. Pericardial tamponade was produced in anesthetized pigs while hemodynamic parameters were monitored in the systemic circulation as a whole and in the vascular beds of the celiac and left gastric arteries, respectively. Stepwise increases in pericardial pressure produced progressive decreases in arterial pressure and cardiac output (i.e., reproducible, quantitable, and rapidly reversible levels of cardiogenic shock). This produced a profound reduction in blood flow in the celiac and gastric beds that was significantly disproportionate to the reduction in cardiac output. This was due to significant increases in celiac and gastric vascular resistance that were more than twice as great as those seen in the systemic circulation as a whole (i.e., selective splanchnic vasoconstriction). This response was abolished by ablation of the renin-angiotensin axis, whether by bilateral nephrectomy, captopril, or saralasin, and mimicked, without tamponade, by the infusion of angiotensin II. Levels of celiac artery blood flow and resistance correlated significantly with endogenous levels of plasma renin activity. On the other hand, this response was not abolished by confirmed alpha-adrenergic blockade (phenoxybenzamine) or by sympathectomy. In this model, cardiogenic shock produces regional splanchnic ischemia in the celiac and gastric vascular beds by inducing a severe and disproportionate vasospasm that is mediated primarily by the renin-angiotensin axis.
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PMID:Control of gastric vascular resistance in cardiogenic shock. 389 36

The effects of essential fatty acid (EFA) deprivation on the arachidonate content and phospholipid composition of different tissues are quite diverse. When C57B1 mice were placed on a fat-free diet, hepatic liquids were readily depleted of arachidonate. In contrast, the renal cortex tenaciously retained arachidonate, whereas surprisingly the heart showed a doubling of its content of arachidonate. This increase in cardiac arachidonate was due to a four-fold increase in arachidonylphosphatidylethanolamine (PE). The renal cortex showed preservation of its arachidonate content in PE, phosphatidylserine, and phosphatidylcholine. Only phosphatidylinositol was depleted of arachidonate in heart or renal cortex. Using an in vivo labeling technique, it was shown that the liver incorporated most of the [1-14C]arachidonate initially following intraperitoneal injection. Over 11 days, as levels of labeled arachidonate fell in liver, the EFA-deficient heart accumulated arachidonate selectively in PE (8-fold greater than control), and the EFA-deficient renal cortex accumulated arachidonate in PE, phosphatidylserine, and phosphatidylcholine (2-3-fold greater than control). This uptake was shown to be specific for arachidonate over 20:3(n-9). Despite the conservation of cardiac and renal arachidonate seen with EFA deficiency, prostaglandin production by the isolated perfused EFA-deficient heart and kidney was markedly decreased relative to control in response to specific agonist stimulation with angiotensin II, although it was equivalent to control in response to nonspecific stimulation by ischemia. These data suggest that the liver serves to supply other tissues with arachidonate in EFA deficiency, and that the heart and renal cortex both contain mechanisms to accumulate arachidonate selectively in certain phospholipids. However, phosphatidylinositol, which is uniquely depleted of arachidonate in heart and renal cortex with EFA deficiency, appears to be the principal source of arachidonate in response to receptor-mediated agonists.
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PMID:Paradoxical conservation of cardiac and renal arachidonate content in essential fatty acid deficiency. 393 63

Evidence indicates that after vascular occlusion, infusion of angiotensin II restores blood supply to ischemic tissues by stimulating the development of collateral circulation through a mechanism independent of the mechanical effects of increased blood pressure. To test this effect in focal cerebral ischemia, angiotensin II was intravenously administered for four hours to gerbils immediately after unilateral carotid ligation. Three different pressor doses, 50, 250, and 500 ng/kg/min, were used, and mortality rate was evaluated at 1 and 2 days after vascular occlusion. Two additional groups similarly prepared were infused either with saline or with the pressor agent metaraminol. There was a significant inverse relationship between the infusion dose of angiotensin II and mortality: the greater the infusion dose of angiotensin II, the lower the mortality rate. Infusion of metaraminol, at the dose chosen to mimic the pressor effect of the highest angiotensin II dose, yielded a mortality rate which was statistically indistinguishable from that obtained with saline infusion. It is concluded that the mortality rate after unilateral carotid occlusion is significantly reduced by intravenous administration of angiotensin II through mechanisms unrelated to its hypertensive action. Evidence suggests that this may occur by the enhancement of the development of collateral circulation and therefore the reduction of the severity of brain ischemia.
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PMID:Angiotensin II decreases mortality rate in gerbils with unilateral carotid ligation. 394 89

The unique architecture and organization of medullary vasculature permit regional regulation of medullary hemodynamics by vasoactive hormones and are conducive to the operation of the countercurrent multiplication system. Recent studies suggest that an increase in inner medullary blood flow causes medullary solute washout, which in turn decreases passive sodium transport in the thin ascending limb of Henle's loop. In canine models of chronic sodium retention accompanied by activation of the renin-angiotensin system, glomerular filtration rate (GFR), renal blood flow (RBF), and intracortical blood flow distribution were similar to those in normal dogs; however, papillary plasma flow (PPF) was markedly reduced and papillary tissue solute content was increased significantly both during hydropenia and after saline loading. During euvolemic diuresis with loop diuretics, there was an increased renin release associated with a marked reduction in PPF, despite an increase in total RBF. Direct intrarenal infusion of angiotensin II (AngII) (at a dose not affecting GFR and RBF) induced ipsilateral sodium retention, conservation of urinary concentration, and papillary ischemia. These studies provide evidence for regional regulation of medullary hemodynamics by AngII, possibly contributing to sodium retention in chronic salt-retaining states.
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PMID:Contribution of angiotensin to the control of medullary hemodynamics. 395 61

Fluid (sodium) reabsorption, total glucose efflux, and reabsorption of angiotensin II and insulin from the proximal convoluted tubule were studied in rats by in vivo microperfusion. After 35 min of total renal artery occlusion, function was assessed at two intervals, 0-1 h (early recovery, ER) and 2-4 h (late recovery, LR). Light and electron microscopic evaluation showed 60-75% loss of proximal convoluted tubule brush border membrane in ER and nearly complete restoration of brush border in LR. No other structural abnormalities were evident. Renal blood flow was unchanged from control during both ER and LR. During ER, fluid reabsorption was reduced to 29.8 +/- 5.2%, and total glucose efflux, at normal tubule loads, to 73.9 +/- 5.5% of control. However, angiotensin II and insulin reabsorption were unchanged. In LR, fluid reabsorption remained significantly reduced at 54.3 +/- 8.1% of control. Total glucose efflux from the proximal tubule was normal in LR at glucose loads of up to 400 pmol X min-1, but was significantly reduced at higher loads. Passive glucose efflux, measured in the presence of 10(-4)M phloridzin, was not altered by ischemia. Brief ischemia results in significant alterations in proximal tubular reabsorption of sodium and glucose, which correlate with a substantial loss of brush border during ER. However, despite restoration of cell morphology to normal in LR, transport defects for both sodium and glucose persist.
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PMID:Recovery of proximal tubular function from ischemic injury. 636 44


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