SUMMARY We used angiographic and microsphere methods to evaluate the anatomic and functional features of renal collateral circulation in the rat. By the microsphere method, renal parenchymal blood flow was less than 1% of control 1 hour after occlusion of the main renal artery; 2.8% of control 1-2 weeks after arterial occlusion; and 1% of control 4-9 weeks after occlusion. Radiographic observations during chronic occlusion revealed numerous collateral vessels to the kidney. These vessels readily filled with angiographic contrast medium but the intrarenal circulation did not visualize. We conclude that collateral circulation to renal parenchyma is negligible after acute or chronic occlusion of the main renal artery in the rat. The rich anatomic plexus of collateral vessels has no functional significance and is unable to preserve viability of the parenchyma.MANY ANATOMICAL and radiographic studies demonstrate that collateral vessels are present after occlusion of the renal artery in the rat and the dog. "6 However, there are few measurements of the actual rate of blood flow through these collateral channels. To evaluate the functional significance of collateral circulation in the rat, we have visualized collateral vessels angiographically and quantitated nutrient flow to the renal parenchyma with microspheres. Although impressive collateral vessels develop during arterial occlusion, parenchymal blood flow is negligible. Methods MEASUREMENT OF RENAL BLOOD FLOW WITH MICROSPHERESFor chronic studies, male Sprague-Dawley rats, weighing 210-400 g and allowed free access to food and water, were anesthetized with methohexital (100 mg/kg). A left flank incision was made and the renal artery was carefully separated from the renal vein near its origin from the abdominal aorta. Care was taken not to disrupt perirenal structures. The renal artery was tied at two separate locations with 4-0 silk. The proximal tie was as close to the aorta as possible and was proximal to any identifiable branches of the renal artery. Any rats in which the entire kidney did not blanch uniformly were discarded. Five to 60 days later, these rats were anesthetized with Inactin (ethyl-(l-methyl-propyl)-malonylthiourea) (100 mg/kg, ip). A tracheostomy tube (PE 240) was inserted and the right jugular vein was cannulated with PE 50 tubing for infusion of heparinized saline at 0.028 ml/min (6 units of aqueous heparin/ml). A second PE 50 cannula was placed into the right femoral artery and connected to a pressure transducer and recorder. A third PE 50 cannula was placed into the left axillary artery and advanced to the junction of this artery and the aorta. Rats were maintained at normal body temperature throughout the experiment by use of thermostatically controlled heating coil and esophageal sensing probe. One-half hour after the above surgery had been completed, a timed 60-second free-flow collection of blood was begun from the right femoral artery cannula under oil into a preweighed plastic test tube. The total volume of blood collected was 1 ml or l...
SUMMARY Renal phospholipid metabolism was studied after ischemia was induced by occlusion of the left renal artery in the rat. There was no change in the rate of cellular ["C]choline uptake after 25 or 80 minutes of ischemia. However, [ u C]choline incorporation into phospholipid was two to three times greater in slices from the ischemic kidney than in slices from the contralateral control kidney. The increase occurred after 25 minutes of ischemia plus 15 minutes of reflow, and after 60 minutes of ischemia with or without reflow. When [ u C]choline was injected into rats after a 60-minute period of renal ischemia, the rate of incorporation into phospholipid in the ischemic kidney was almost twice that of the control kidney. These results were similar to those of the in vitro experiments. Since virtually all of the cellular phospholipids of the kidney are present in cellular membranes, renal ischemia affects membrane metabolism. The mean distribution ratio of a-aminoisobutyric acid in slices of kidneys ischemic for 60 minutes was similar to that of control slices DAMAGE to cell membranes is a prominent feature of renal ischemia. In rats, after occlusion of the renal artery for periods up to 1 hour, the damage is especially evident in the proximal tubular cells, which become denuded of brush border membranes (Reimer and Jennings, 1971a;Reimer et al., 1972;Venkatachalam et al., 1978). If the ischemic period is short, the membranes regenerate; with longer periods of ischemia, cellular necrosis ensues. Phospholipids are the basic structural component of cellular membranes. We therefore investigated membrane metabolism in renal ischemia by determining the rate of incorporation of [ u C]choline into phospholipid of ischemic rat kidneys. We also determined the transport of a-aminoisobutyric acid (AIB) in the kidneys, since the membrane damage might be expected to affect the membrane transport of metabolites. MethodsMale Sprague-Dawley rats, weighing 250-350 g (Charles River Breeding Laboratories, Inc.) and fed rat chow, were used. They were anesthetized with Inactin, 100 mg/kg body weight, placed on a heated board to maintain body temperature at 37°C, and continuously infused with heparinized saline (6 U aqueous heparin/ml 0.85% saline) into the left jugular vein at 28 fil/min. Tubing in the right femoral artery was attached to a Hewlett-Packard pressure transducer and recorder for continuous blood pressure measurements. Through a left flank incision, the left kidney and ureter were freed from surrounding fat, and the kidney was covered with cotton immersed in mineral oil at 37°C. The left renal artery was totally occluded with a modified aluminum Blalock clamp for periods of from 25 minutes to 3 hours and then released. Adequacy of clamping was assessed by blanching of the kidney and by the absence of a vascular flush after a venous injection of 50 jd of 5% lissamine green midway during the ischemic period. Adequacy of reflow after removal of the clamp was assessed by the return of normal color and by a vascular flush ...
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