Effect of Ischemia on Renal Blood Flow in the Rat

Abstract

The effect of ischemia on renal blood flow (RBF) in the rat has been an unsettled question. This study used a totally extractable indicator, radioactive microspheres, with a reference arterial sample, to study RBF quantitatively 10 and 60 min after 1 h of unilateral renal artery clamping in anesthetized, heparinized rats. The results indicate that after release of the arterial clamp, the kidney is enlarged and exhibits an increase in renal vascular resistance. RBF to the contralateral non-ischemic kidney is not different from that of a time-control series.

Support of renal blood flow after ischaemic‐reperfusion injury by endogenous formation of nitric oxide and of cyclo‐oxygenase vasodilator metabolites

“…The model of I/R injury of the kidney used in this study results in haemodynamic alterations within the renal vasculature including a rise in RVR, a lb l i Table 1 Changes in (A) renal blood flow (RBF) and (B) renal vascular resistance (RVR) in rats subjected to 60 min ischaemia followed by 120 min of reperfusion Before 30 min 60 min 120 min fall in RBF, a loss of autoregulation (Kashgarian et al, 1976;Riley, 1978) and an impairment of the response to endothelium-dependent vasodilators (Conger et al, 1991). In the isolated erythrocyte-perfused kidney of the rat, 25 min of ischaemia followed by reperfusion is associated with a marked increase in RVR (Lieberthal et al, 1989).…”

“…The model of I/R injury of the kidney used in this study results in haemodynamic alterations within the renal vasculature including a rise in RVR, a lb l i Different groups of animals received vehicle (I/R, n = 6), (30 itg kg-' min-, i.v., n = 5), indomethacin (Indo, 5 mg kg-', i.v. bolus, n = 3), indomethacin and N0-nitro-L-arginine methyl ester (L-NAME) (Indo + L-NAME, n = 4), dexamethasone (3 mg kg-'; i.v., n = 6), L-arginine (1 or 3 mg kg-' min-'), or D-arginine (1 mg kg-' fall in RBF, a loss of autoregulation (Kashgarian et al, 1976;Riley, 1978) and an impairment of the response to endothelium-dependent vasodilators (Conger et al, 1991). In the isolated erythrocyte-perfused kidney of the rat, 25 min of ischaemia followed by reperfusion is associated with a marked increase in RVR (Lieberthal et al, 1989).…”

Effects of External Renal Hypothermia on Postischemic Hemodynamics

“…In the rabbit model renal cortical blood flow increases briefly in the early reperfusion pe riod [3,6], while renal blood flow in rats is reduced to 78% of normal after 1 h of normothermic ischemia [7], The postischemic increase in renal cortical blood flow seen after normothermic ischemia is absent after sham operation and after hypothermic ischemia. As the benefi cial effect of organ hypothermia in preventing acute post ischemic renal failure is well documented, one could argue whether the brief postischemic rise in blood flow could potentiate parenchymal damage or whether it con tributes to a physiologically useful response caused by metabolic changes.…”

Die pharmakologische Blockade des Renin-Angiotensin-Systems in der Prävention des postischämischen akuten Nierenversagens*

“…Das Nierenmark und insbesondere die Papillen sind somit trotz guter Durchblutung bereits unter normalen Bedingungen einem hypoxisch-hyperkapnischen Milieu ausgesetzt [35,36] [65]. Der Abfall des renalen Blutflusses wird mit 50 bis 80% angegeben [66,67]. Der renal vaskuläre Widerstand steigt an und ist wesentlich mit der präglomerulären Vasokonstriktion verknüpft [68].…”