The impact of medical care on the quality and length of life of the population has been poorly documented. The rapid growth of evidence of efficacy of therapy for individual medical conditions now offers the opportunity to create an inventory of benefits. A method for creating such an inventory is described, as is its application to a selection of condition-treatment pairs, chosen for their high incidence of prevalence, their serious outcomes, and the demonstrated efficacy of their treatment. An aggregate effect of medical care on life expectancy is found to be roughly five years during this century, with a further potential of two years. Although there is no overall index of quality of life analogous to life expectancy, our inventory demonstrates the enormous burden of pain, suffering, and dysfunction that afflicts the population for which medical care can provide a large measure of relief.

Studies have been made on the isolated urinary bladder of the toad, Bufo raarinus, in an attempt to evaluate gradients of chemical activity across the mucosal surfaces of the epithelial cells which would serve to maintain a net movement of sodium from the mucosal medium into the cells.

Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. This change is reflected in a decreased De resistance of the bladder; identification of the permeability barrier which is affected localizes the site of action of vasopressin on sodium transport. Cells of the epithelial layer were impaled from the mucosal side with glass micropipettes while current pulses were passed through the bladder. The resulting voltage deflections across the bladder and between the micropipette and mucosal reference solution were proportional to the resistance across the entire bladder and across the mucosal or apical permeability barrier, respectively. The position of the exploring micropipette was not changed and vasopressin was added to the serosal medium. In 10 successful impalements, the apical permeability barrier contributed 54 % of the initial total transbladder resistance, but 98 % of the total resistance change following vasopressin occurred at this site. This finding provides direct evidence that vasopressin acts to increase ionic mobility selectively across the apical permeability barrier of the transporting cells of the toad bladder. I N T R O D U C T I O NWhen the urinary bladder of the toad, Bufo marinus, is bathed by solutions containing Na +, the addition of vasopressin regularly causes a stimulation in the active transport of Na + from the mucosal to the serosal medium (8, 9). A variety of experimental approaches has provided evidence that the hormonal effect occurs at a mobility barrier early in the transport process, perhaps at the mucosal or apical face of the epithelial cell, and does not directly affect the step in transport at which metabolic energy production is coupled to the process (2,5,6,11 ). The hormonal effect on transport of Na + is regularly associated with a decrease in the DC resistance of the bladder (2). The present study was undertaken in order to determine directly the site of action of vasopressin on transport of Na + by localizing the region within the epithelial cell where vasopressin has its characteristic effect upon the resistance.