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A major impediment to the use of the objective structured clinical examination (OSCE) is that it is a labor-intensive and costly form of assessment. The cost of an OSCE is highly dependent on the particular model used, the extent to which hidden costs are reported, and the purpose of the examination. The authors detail hypothetical costs of running a four-hour OSCE for 120 medical students at one medical school. Costs are reported for four phases of this process: development, production, administration, and post-examination reporting and analysis. Costs are reported at two ends of the spectrum: the high end, where it is assumed that little is paid for by the institution and that faculty receive honoraria for work put into the examination; and the low end, where it is assumed that the sponsoring institution defrays basic costs and that faculty do not receive honoraria for their participation. The total costs reported for a first-time examination were $104,400 and $59,460 (Canadian dollars) at the high and low ends, respectively. These translate to per-student costs of $870 and $496. The cost of running an OSCE is high. However, the OSCE is uniquely capable of assessing many fundamental clinical skills that are presently not being assessed in a rigorous way in most medical schools.

Accurate assessment of clinical competence and performance in office practice is enhanced through a multi-tool approach. Two assessment tools that offer

A B S T R A C T Observations were made on the relation of the renin-angiotensin-aldosterone system and renal hemodynamic function to sodium balance in 43 pregnant dogs. Daily balance studies revealed that about 30-40% of ingested sodium was retained during the last half of pregnancy; during the same period, potassium balance was also positive but to a lesser extent. For groups of pregnant dogs, plasma renin activity (n = 14) and aldosterone secretion (n = 19) were significantly higher than normal; however, in some animals one or both functions were normal even though sodium retention was present. In contrast, plasma renin substrate concentration was consistently elevated during pregnancy in seven dogs. In a group of nine dogs in which both aldosterone secretion and plasma renin activity were measured, aldosterone secretion was elevated in the three dogs with the highest values for plasma renin activity; in two of the remaining six animals aldosterone secretion was elevated but plasma renin activity was normal or only slightly increased. The sequestration of sodium and water into the uterine contents was defined quantitatively in this study but evidence was lacking to support the idea that such changes led to renin release. The glomerular filtration rate (GFR) was significantly elevated throughout pregnancy but a significant decrease from the high level of mid-pregnancy occurred during the last half of pregnancy; this decrease in GFR probably contributed to the sodium retention. Administration of a large dose of deoxycorticosterone acetate (DOCA) to dogs in late pregnancy produced marked sodium retention but "escape" from the sodium-retaining steroid occurred. The data demonstrate that although increased activity of the renin-angiotensin-aldosterone system was frequently present during pregnancy, a normal rate of aldosterone secretion occurred. This finding and the observed "es-

Hepatic blood flow, hepatic extraction of renin, and hepatic clearance of renin were compared in normal conscious dogs, in dogs with constriction of the thoracic inferior vena cava (as a model of low-output heart failure), and in dogs with an aortic-caval fistula (high-output heart failure). Both "failure" preparations showed marked sodium retention. Renin was measured by methods described previously and expressed as nanograms of angiotensin produced during incubation per milliliter of plasma. Hepatic plasma flow was determined by the sodium sulfobromophthalein method. The dogs with low-output heart failure had a marked reduction in hepatic plasma flow, while those with high-output failure showed no significant change in this flow. Plasma renin was significantly elevated in both models of heart failure. Dogs with low-output failure had an increase (P<.05) in hepatic renin extraction from a normal value of 19.8% to 33.4%, while those with high-output failure showed a decrease in hepatic renin extraction to 11.9% (P<.01). The hepatic clearance of renin in low-output failure (104 ml/ min) was the same as the average normal value of 104 ml/min, while clearance of renin by the liver in high-output failure was reduced to 51 ml/min (P<.001). The data provide evidence that the decreased metabolism of renin contributes substantially to the increased plasma level of renin in experimental high-output heart failure. ADDITIONAL KEY WORDS hepatic extraction of renin sodium retention thoracic inferior vena caval constriction aortic-caval fistula plasma renin hepatic blood flow chronic venous congestion• In congestive heart failure, in decompensated cirrhosis of the liver, and in their experimental counterparts, elevated plasma renin levels (1-7) have been causally related in increased aldosterone secretion. The exact mechanisms which lead to an elevated plasma renin have not been clearly defined. Haecox, et al. (8) have demonstrated in anesthetized dogs that significant extraction or inactivation of renin is brought about by the liver. In view of the hepatic congestion associated with right heart failure, it was decided to investigate the role of the hepatic metabolism of renin in the elevated plasma renin levels found in experimental heart failure. Hepatic blood flow, hepatic renin extraction, and the hepatic clearance of renin were measured in normal conscious dogs and in conscious dogs with either constriction of the thoracic inferior vena cava or an aortic-caval fistula.Constriction of the thoracic inferior vena cava was used to produce a model of lowoutput heart failure. Although such animals are not in true congestive heart failure, it has been demonstrated that the salt and