Spectral analysis of spontaneous heart rate fluctuations were assessed by use of autonomic blocking agents and changes in posture. Low-frequency fluctuations (below 0.12 Hz) in the supine position are mediated entirely by the parasympathetic nervous system. On standing, the low-frequency fluctuations increase and are jointly mediated by the sympathetic and parasympathetic nervous systems. High-frequency fluctuations, at the respiratory frequency, are decreased by standing and are mediated solely by the parasympathetic system. Heart rate spectral analysis is a powerful noninvasive tool for quantifying autonomic nervous system activity.

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A method has been described for the measurement, by means of Kr 85 , of intrarenal nutrient blood flow distribution in the unanesthetized dog. Injection of the isotope into the renal artery is followed by a multi-exponential disappearance curve which can be obtained by external monitoring with a scintillation detector. In acute experiments autoradiographs have demonstrated that the first exponential component represents cortical blood flow; the second, outer medullary blood flow : the third, inner medullary blood flow; and the fourth, hilar and perirenal fat blood flow. The average cortical blood flow in 65 experiments in five kidneys of four nnanesthetized dogs was 472 ml/100 g/min, the outer medullary 132 ml/100 g/min, and the inner medullary 17 ml/100 g/min. Eighty per cent of the radioactivity was distributed initially to the cortex, 16% to the outer medulla, and 2% to the inner medulla. The hilar and perirenal fat, which receives approximately 2% of the initial radioactivity, was estimated to have a flow rate of 21 ml/100 g/min. In addition, a method for the rapid determination of serial cortical blood flow rates has been described. The importance of these findings has been discussed with reference to the anatomy of the kidney, and to the countercurrent concept as it applies to passive reabsorption of lipid soluble substances, and to the maintenance of an osmotic gradient.

Renal medullary blood flow was well maintained for several hours after blood loss which produced hypotension. Renal cortical blood flow was altered by trauma and mild hemorrhage even though blood pressure remained normal; rate of blood flow through the subcapsular, peritubular capillaries decreased to the level of that in the outer medulla. With further hemorrhage and the development of hypotension, rate of blood flow in large cortical areas was reduced to that of the outer medulla. With prolonged hypotension, the rate of blood flow in most of the cortex approached outer medullary rate and a single exponential could describe the flow in this combined area. Small regions of even slower flow rate began to appear in the outer cortex; patches of tissue appeared to be completely ischemic. The progression of cortical ischemia noted in these experiments may provide additional evidence for the pathogenesis of the patchy tubular necrosis noted in hemorrhagic shock.

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