During antidiuresis, sodium is concentrated in the papilla and medulla of mammalian kidneys as a result of active sodium reabsorption from medullary tubules and countercurrent flow through the loops of Henle and the medullary capillaries. It is clear from chemical (1) and cryoscopic (2, 3) analysis of sections of kidney, and from direct micropuncture (4-6), that under these circumstances the osmolality of medullary interstitial fluid is approximately that of collecting-duct urine and that sodium concentration rises progressively along a gradient from cortex to medulla.The precise role of antidiuretic hormone (ADH) in establishing and maintaining this gradient is not entirely clear, partly because comparable studies in the absence of vasopressin (i.e., during water diuresis) have been more difficult to accomplish. Ullrich, Jarausch and Drenckhahn demonstrated that the osmolality and sodium concentration of papillary water approached that of peripheral plasma in dogs during water diuresis (1, 7). That medullary interstitial fluid is actually hypertonic to plasma in the absence of ADH was suggested by the demonstration (8) that compression of the renal artery of one kidney during water diuresis led to production of hypertonic urine by that kidney. Recently, Bray reported that the

A decrease in the ability of the kidneys to excrete a highly concentrated urine is one of the earliest hallmarks of potassium depletion in animals and in humans (1). According to present views of the mechanism of the renal concentrating process (2), this might be the result of a) impairment of the countercurrent multiplier system by which a high concentration of sodium (and urea) is created and maintained in the interstitial space of the renal papilla, and/or b) decreased permeability of the walls of the collecting ducts and distal tubules to the back-diffusion of water. If the first alternative were correct, analysis of the renal papilla from potassium-deficient animals excreting a maximally concentrated urine should reveal a lower concentration of sodium than that present in the papilla of normal animals. Should the second mechanism be operative, the fall in maximum urinary osmolality observed in potassium deficiency might be entirely unassociated with a decrease in papillary sodium, or else would be out of proportion to it.In the present experiments samples of maximally concentrated urine and renal papilla, medulla and cortex from potassium-depleted rats and dogs were analyzed. By placing all animals on a sodium-free diet prior to sacrifice, difficulties in the interpretation of tissue analyses consequent to high concentrations of sodium in the urine were avoided. The results indicate that the * Aided by grants from the American Heart Association, the National Heart Institute, the Lawrence M. Gelb Foundation, and a contract (MD-116) with the Office of the Surgeon General, Department of the Army. concentration of sodium and total solutes in the renal papilla is indeed decreased by potassium depletion, though the decrease is not as great as the fall in maximum urinary osmolality. METHODS I. RatsWhite male Sprague-Dawley rats initially weighing 150 to 200 g were divided into the following groups. The composition of the diets is given in Table I.Group IE. Twenty-four animals were fed a low potassium diet for 29 days, followed by 5 days of a low sodium, low potassium diet before sacrifice.Group IC. Twenty-two rats received a normal diet for 23 days, followed by 5 days of a low sodium diet.Group IIE. Twenty-eight rats received a high sodium, low potassium diet for 6 days. Desoxycorticosterone acetate (DCA), 0.2 mg per rat, was injected subcutaneously daily for 5 days. Following this, a low sodium, low potassium diet was given for 9 days.Group IIC. Twenty-four animals received a high sodium diet for 6 days and a low sodium diet for 5 days.In order to obtain enough papillary tissue for accurate analysis, 3 or 4 animals were kept in a cage and analyses of urine, plasma and tissue were performed on pooled material.Twenty-four hours before sacrifice food and water were withheld. Twelve hours later 50 mU of vasopressin in oil was injected subcutaneously and micturition was induced. The rats were then placed in metabolism cages with screens so placed as to deflect feces, and urine was collected under oil for 12 hours. Alt...

The events of 11 September 2001 became the catalyst for many to shift their disaster preparedness efforts towards mass-casualty incidents. Emergency responders, healthcare workers, emergency managers, and public health officials worldwide are being tasked to improve their readiness by acquiring equipment, providing training and implementing policy, especially in the area of mass-casualty decontamination. Accomplishing each of these tasks requires good information, which is lacking. Management of the incident scene and the approach to victim care varies throughout the world and is based more on dogma than scientific data. In order to plan effectively for and to manage a chemical, mass-casualty event, we must critically assess the criteria upon which we base our response.This paper reviews current standards surrounding the response to a release of hazardous materials that results in massive numbers of exposed human survivors. In addition, a significant effort is made to prepare an international perspective on this response.Preparations for the 24-hour threat of exposure of a community to hazardous material are a community responsibility for first-responders and the hospital. Preparations for a mass-casualty event related to a terrorist attack are a governmental responsibility. Reshaping response protocols and decontamination needs on the differences between vapor and liquid chemical threats can enable local responders to effectively manage a chemical attack resulting in mass casualties. Ensuring that hospitals have adequate resources and training to mount an effective decontamination response in a rapid manner is essential.

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