In our attempt to design a method which would be more reliable than dietary survey interviews when estimating salt and protein intakes in a population survey, a urinalysis-related study was done on volunteers. Urinary sodium (Na), urea nitrogen (UN) and inorganic sulfate (SO₄), all indices of dietary salt, protein and sulfoamino acids, respectively, were confirmed to reflect the nutritional condition. Interaction between salt and protein was not observed at least at the dietary levels used in the present study (for salt, 0.33 and 0.1 g/kg body weight/day; for protein, 1.6 and 0.7 g/kg body weight/day). Excretion of components was delayed several days or more after dietary ingestion, and nutritional estimation by urinalysis, therefore, may not be so much affected by daily variables in the diet intake. Further, partial urine samples proved to have a highly significant correlation with 24-hour (hr) urine, as for urinary Na, potassium (K), SO₄, UN and their creatinine (Cr) ratios, thus indicating the availability of partial urine samples as substitutes for 24-hr urine specimens. Thus, urinalysis is a more readily facilitated, more scientific and more quantitative method for epidemiological nutritional surveys.

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Utility of urinalysis as a method for estimating dietary salt and protein intakes was examined in volunteers from farming and fishing villages in Japan and the data was compared to findings in a survey on diets. We found that partial urine samples and even a fasting single spot urine in the a.m. could serve as valid substitutes for 24-hour (hr) urine collections. Further, significant correlations were obtained between levels of salt in the diet estimated by survey interviews and urinary sodium (Na) and between interview-estimated dietary total or animal protein and urinary inorganic sulfate (SO₄). In comparative studies between farming and fishing villages, almost the same findings, higher salt in a farming village and higher animal protein in a fishing village, were obtained in the urinalysis and the survey on diets. These findings clearly indicate that urinalysis, as a method for estimating dietary salt and protein intake in population surveys, has distinct advantages.

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General medical examinations were performed in two rural areas of Shimane Prefecture in Japan, one was a farming village and the other a fishing village where incidences of death due to stroke differed, higher in the former and lower in the latter. Comparisons were made on salt and protein intake by analyzing fasting single spot urine collected in the morning and by blood tests. Urine samples were analyzed for sodium (Na), potassium (K), urea nitrogen (UN), inorganic sulfate (SO₄) and creatinine (Cr) and blood samples for cholesterol (Chl), trigly ceride (TG), hematocrit (Ht) and hemoglobin (Hb). Blood pressure, Na/Cr, Na/K and Ht were higher in the farming village and K/Cr, UN/Cr, SO₄/Cr, SO₄/UN, Chl and TG were higher in the fishing village. These findings indicate the higher salt intake and lower intake of K, animal protein and fat in the farming village. This typical dietary pattern of the Japanese may explain the higher incidence of hypertension and stroke in the farming village.

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We assessed to what extent sodium intake can be estimated from the sodium content of a spot-urine specimen (spot-UNa) collected within 4 hours after the first voiding upon awakening but before breakfast. Subjects were asked to collect spot-urine and 24-hour urine specimens other than the spot-urine for a 3-day period, either successively or intermittently. The coefficient of correlation between spot-UNa and urinary excretion of sodium in 24 hours (24-h UNa) collected on the first day was 0.47. When the coefficient of the variation of creatinine excretion in the spot-urine was above 20%, the sample was discarded as the "outlier", and in this case the coefficient of correlation was 0.725. A marked fluctuation of creatinine excretion in spot-urine was considered to represent technical errors at the time of the spot-urine collection. The coefficient of variation of intra-individual 24-h UNa exceeded 20%, suggesting that a single determination 24-h UNa does not represent the individual average of daily urinary excretion of sodium. It is concluded that the determination of a substantial number of spot-urine specimens to estimate daily salt ingestion of a given subject may be more reliable than a single determination of 24-h UNa, if the "outlier" of creatinine excretion in spot-urine specimen is excluded from the determination of spot-UNa. The average urinary excretion of sodium in 24 hours by the Japanese subjects investigated here was 218±67 mEq.

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Under various conditions of sodium balance, 1-sarcosine-8-isoleucine angiotensin II was infused into 15 normotensive controls and 82 patients with benign essential hypertension. Changes in mean blood pressure induced by the analogue were correlated with the logarithm of plasma renin activity (r = -0.763, p<0.001 for the controls; r = -0.776, p<0.001 for the patients). Although the coefficients of determination were much the same, 0.95 confidence limits of the regression line did not overlap at renin levels over 7 ng/ml/h. At those levels, a decrease in the mean blood pressure induced by the analogue was greater in the hypertensive patients. A pressure-renin index was defined as a product of the logarithm of plasma renin activity and the mean blood pressure measured before the analogue infusion. The correlation between the analogue effect and the pressure-renin index was highly significant (r = -0.763, p<0.001 for the controls; r = -0.777, p<0.001 for the hypertensive patients). The regression line (0.95 confidence limit) for the hypertensives coincided with that for the normotensives. Thus, the blood pressure level should be taken into account when attempting to evaluate plasma renin activity.

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The present study was attempted to determine whether a reduction in regional venous maximal coronary flow can indicate the presence of significant coronary stenosis. The great cardiac vein flow and the coronary sinus outflow were measured simultaneously in 8 open-chest dogs by a continuous thermodilution technique using a triple thermister catheter or two separate thermister catheters. The left anterior descending and circumflex coronary inflows were recorded using electromagnetic flow proves. Successive 70% and 90% stenoses of the coronary artery were produced using a calibrated constrictor. Maximal coronary flow was obtained during reactive hyperemic response after coronary occlusion for 8 sec. Coronary flow reserve was expressed as the ratio of maximal coronary flow to resting one. During 70% coronary arterial stenosis maximal coronary flow and coronary reserve decreased significantly in the great cardiac vein and the coronary sinus. Significant correlations were found between the flows in the left anterior descending artery and in the great cardiac vein (r = 0.81) and between those in the circumflex artery and in the coronary sinus minus the great cardiac vein (r = 0.79) throughout the periods of preocclusion, occlusion and reactive hyperemic response. There were no significant changes in heart rate and hemodynamics. Using continuous thermodilution techniques the inflows of the left anterior descending and the circumflex coronary arteries at a stenosis greater than 70% could be estimated from the changes in regional venous outflows.

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We investigated the mechanism of the reperfusion-accelerated mitochondrial dysfunction. To clarify this mechanism, we performed the following experiments using 40 mongrel dogs. Experiment I: Prostaglandin (PG) E and F₂α levels in the great cardiac vein (GCV) were examined before, during occlusion and after reperfusion of the left anterior descending coronary artery (LAD). Experiment II: Heart mitochondria were prepared from the normal area and the occluded or the reperfused area after 15 min of the LAD occlusion, or after 5 min of reperfusion following the occlusion with or without premedication of indomethacin. The PGE level in the GCV did not change significantly during occlusion, but increased significantly soon after reperfusion. Mitochondrial dysfunction was caused by occlusion and further accelerated by reperfusion. The PG E level in mitochondria isolated from the reperfused area increased significantly. Indomethacin significantly prevented both the increase in PG E and the acceleration of mitochondrial dysfunction by reperfusion. These results suggest that the increase in PG E level is closely related to the reperfusion-accelerated mitochondrial dysfunction, and that premedication with indomethacin significantly prevented the extension of mitochondrial dysfunction induced by coronary reperfusion.

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The difference in the electrophysiological properties between the subepicardial cells and the subendocardial cells (Purkinje fibers and ordinary myocardial cells) was examined in dogs using a microelectrode technique. The preparations were obtained one hour after coronary occlusion. Immediately after exposure to a hypoxic solution, spontaneous activities could be recorded in neither the subepicardial nor the subendocardial cells. The electrical activities induced by electrical stimulation disappeared 5-10 min after exposure to the hypoxic solution in the subepicardial cells, while they remained in the subendocardial cells. Vmax, action potential amplitude, action potential duration and resting membrane potential of the subendocardial cells were all reduced significantly in the hypoxic solution containing 7 mK K⁺ in contrast to those in the hypoxic solution containing 4 mM K⁺ (p<0.001). In the hypoxic solution containing 15 mM K⁺, all cardiac cells depolarized partially and became electrically quiescent in both normal and ischemic cardiac cells. These findings support the idea that during regional hypoxia and hyperkalemia resulting from acute coronary occlusion, heterogeneous changes in electrical activities occur between the subepicardium and the subendocardium in the ischemic regions.

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