Rabbit skeletal muscle contains 56% more ATP and 225% more creatine phosphate than rabbit cardiac muscle. With ischemia the per cent reduction in ATP and creatine phosphate is less in skeletal than cardiac muscle and ADP and AMP decrease in skeletal and increase in cardiac muscle, IMP is present in skeletal muscle and increases with ischemia, whereas it is absent in cardiac muscle but appears with ischemia. Adenosine, inosine, and hypoxanthine are absent in skeletal and cardiac muscle. Ischemia results in the appearance of adenosine, inosine, and hypoxanthine in cardiac muscle but only the latter two compounds appear in ischemic skeletal muscle. Although complete ischemia is required to demonstrate the presence of adenosine in cardiac muscle, the appearance of this nucleoside is nevertheless consistent with the hypothesis that under physiological conditions quantities of adenosine, undetectable by present methods, may play a role in the regulation of coronary blood flow.

A B S T R

Renal blood flow (RBF) and the distribution of cortical blood flow (microspheres) were measured in the dog after 90 min of total unilateral renal ischemia. RBF was 21% greater than control 2 min after release of the renal artery occlusion, and returned toward control 60 min later. At 2 min after release there was a small but significant increment in deep cortical blood flow which reverted to control by 60 min. When renal artery occlusion was maintained for 180 min, return of blood flow was blunted at 2 min after release of the occlusion, but was not significantly different from control within 10 min after release. Clearance rates of inulin and para-aminohippurate (Cin and Cpah) were 81 and 82% below control after release of occlusion. These data demonstrate that in the dog there is prompt and complete return of blood flow to or above control levels after complete renal artery occlusion. There was no evidence for the "no-reflow" phenomenon.

We evaluated the effects of hemodilution, expansion of intravascular volume, and expansion of interstitial volume on the distribution of cortical renal blood flow, utilizing the microsphere technique. Hemodilution without volume expansion (saline exchange) produced an increase in fractional blood flow in zone 1 (outermost zone) of the cortex from 34 ± 1% to 43 ± 2% and a decrease in fractional blood flow in zone 4 (innermost zone) from 16 ± 2% to 13 ± 2%. Hemodilution without volume expansion or a decrease in plasma protein concentration (isoncotic exchange) produced a similar redistribution in blood flow in zone 1 from 34 ± 2% to 41 ± 2% and in zone 4 from 14 ± 2% to 10 ± 1%. Hemodilution with intravascular volume expansion (hyperoncotic albumin infusion) also produced a superficial shift; blood flow in zone 1 increased from 27 ± 1% to 30 ± 1% and that in zone 4 decreased from 19 ± 2% to 15 ± 1%. Previous studies have demonstrated a redistribution to the juxtamedullary area after saline expansion. Our data demonstrate that hemodilution causes flow to redistribute to the superficial rather than the deep cortex. This superficial shift appears to be secondary to decreased hematocrit rather than to dilution of plasma proteins or expansion of intravascular volume. The deep shift in cortical blood flow which occurs during saline loading is presumably a consequence of expansion of interstitial volume. KEY WORDSvolume expansion dog radioactive microspheres rheology cortical renal blood flow axial streaming• Acute saline infusion increases blood flow to the inner cortex of the kidney proportionately more than it increases flow to the superficial zones (1-3). Among the changes during saline loading that could cause this redistribution of blood flow are: (1) hemodilution, (2) expansion of intravascular volume, and (3) expansion of interstitial volume. We designed experiments in dogs to study the separate effects of these changes on the distribution of cortical blood flow. We found that decreased hematocrit caused flow to redistribute to the superficial rather than the deep cortex. Dilution of plasma proteins and expansion of intravascular volume appeared to have no major effect on blood flow distribution. The deep shift of cortical blood flow during saline infusion is presumably aFrom the Departments of Medicine, Boston University School of Medicine, Boston City Hospital, and University Hospital, Boston University Medical Center, Boston, Massachusetts 02118.This study was supported by U. S. Public Health Service Grants AO 3-14004, AM 11733, and AM 05209 from the National Institutes of Health.Dr. Bruns' present address is Montefiore Hospital, Pittsburgh, Pennsylvania; Dr. Riley's present address is Veterans Administration Hospital, Wood, Wisconsin.Received November 29, 1973. Accepted for publication September 19, 1974. Circulation Research, Vol. 36, January 1975 consequence of expansion of the interstitial volume. MethodsDogs weighing 11-23 kg were anesthetized with sodium pentobarbital (30 mg/kg, iv) and ventila...

No 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.

1. The effect of infusion of ovine prolactin was studied in anaesthetized dogs pretreated with bromocryptine to reduce the release of endogenous prolactin. 2. Prolactin, injected intravenously and also directly into one kidney, resulted in a 12--18% increase in glomerular filtration rate (GFR) by both kidneys. 3. This increased GFR was not associated with any demonstrable changes in whole-kidney blood flow, distribution of intrarenal blood flow, fractional excretion of sodium or osmolar or free-water clearance. 4. We conclude that ovine prolactin produced an increase in GFR not dependent on an increase in whole-kidney plasma flow.

No abstract