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Biomedical subjects

S Arai

Publications and source records attributed to S Arai.

At least 487 records · Page 27Linked to original sources

Quantitative analysis of cardiac hypertrophy due to pressure load in reference to the relations of blood pressure, left ventricular weight and left ventricular capacity.

In almost all of the cases of cardiac hypertrophy due to sustained hypertension, left ventricular capacity is increased in proportion to increased left ventricular weight, even in the absence of manifest cardiac insufficiency. The condition is regarded as the general expression of cardiac response to pressure load, and the concept of "isomorphic hypertrophy" is proposed. Concentric hypertrophy of the current concept is observed only on rare special occasions, and its role in cardiac adaptation to pressure load is obscure. The increase in myocardial mass is sufficient to maintain the work done by a unit myocardial volume at a normal level. However, the calculation on pertinent models demonstrates that hypertrophied hearts of any type expel the normal stroke volume with smaller shortening of muscle fibers under larger stress, which is further elevated with the progress of cardiac contraction. Because the maximum force generated by muscle fibers declines with advancing cardiac contraction, hypertrophied hearts harbor a latent risk of mechanical insufficiency. Even under pressure load, ventricular dilation seems to precede the re-inforcement of ventricular wall in the development of cardiac hypertrophy. A common mechanism may be therefore assumed underlying the development and performance of all types of hypertrophied hearts, regardless of the difference in the character of physical loads.

Adult↗

Phytohemagglutinin-induced lymphocyte transformation in liver diseases and in asymptomatic HBsAg carriers.

Phytohemagglutin (PHA)-induced lymphocyte transformation was impaired in acute viral hepatitis. It was significantly correlated with grades of liver cell damage as shown by prothrombin time, GOT, or GPT. It was also lower in drug-induced hepatitis and in prolonged hepatitis than in controls. Of asymptomatic HBsAg carriers, only those with minimal hepatic change showed lower values in stimulation index as well as incorporated radioactivity.

Carrier State↗

Left ventricular stiffness and chamber geometry in the pressure-overloaded hypertrophied heart.

Pressure-overloaded hypertrophy of the left ventricle (LV) was produced by coarctation of the ascending aorta in 7 dogs. The overall mean weight of the left ventricle (LVW) was 7.86 +/- 1.49 (S.D.) g/kg body weight; (normal, 5.99 +/- 0.70 g/kg: p less than 0.05). After potassium arrest, pressure-volume (P-V) relationships were examined with the left ventricles isolated from the normals and from the dogs of left ventricular hypertrophy (LVH-dogs). In both groups, the P-V relationships could be expressed by an equation deltaV=a-be-cP throughout the range of filling pressure of 2.5 to 35 cmH2O, where deltav was the actual volume change of LV, P intraventricular pressure, and a, b and c constants. A sensitive index of LV stiffness, the half-inflation pressure (h), was defined as 1n (2b/a)/c. In hypertrophied hearts, h was 10.5 +/- 0.7 cmH2O; (normal 8.0 +/- 0.4 cmH2O; P less than 0.001). The ratio of LVW to LVVp=h (the left ventricular volume at h) in hypertrophy, which was related to the LV chamber geometry, was 3.1 +/- 0.6 in contrast with the normal value of 2.0 +/- 0.3. The development of concentric hypertrophy was thus demonstrated. Moreover, h was closely correlated with LVW/LVVp=h in both the normals and the LVH-dogs (r=0.83; p less than 0.01). On the other hand, an index of LV wall stiffness h/LVW/LVVP=h was relatively constant. Therefore, the increase of LV stiffness in the LVH-dogs was attributed to the change in chamber geometry.

Animals↗

Enzymatic modification for improving nutritional qualities and acceptability of proteins extracted from photosynthetic microorganisms Spirulina maxima and Rhodopseudomonas capsulatus.

The present study attempts to improve the proteins from a blue-green alga Spirulina maxima and a non-sulfur purple bacterium Rhodopseudomonas capsulatus through their peptic hydrolysis followed by plastein synthesis with papain. The former enzymatic process was effective in removing some photosynthetic pigments and flavors originating in the raw materials. The latter process was successful in incorporating limited amounts of methionine, lysine, and tryptophan, and thus to synthesize plasteins whose essential amino acid patterns resemble the FAO/WHO suggested pattern (1973). These plasteins had no colors and no flavors.

Amino Acids↗

The relation between experimentally induced pyelonephritis and hypertension.

Hypertension resulting from chronic pyelonephritis has been shown in clinical as well as experimental cases, although some authors deny that there is a pathogenic relationship between the two. To throw light on this problem the present authors conducted a series of experiments with mongrel dogs, in which chronic pyelonephritis was induced and postoperative changes in blood pressure and plasma renin activity were observed over a period of 3 months. The pyelonephritis infection was brought about by a method involving vesicoureteral reflux and ureteral dysfunction, as described in a previous paper. Preoperative and postoperative levels of systolic pressure wer compared, but no definit trends were found for the first 3 weeks after operation. At 30, 60 and 90 days the pressures were found to have risen by 21.2 plus or minus 11.2 mmHg, 21.7 plus or minus 14.6 mmHg and 17.1 plus or minus 16.7 mmHg, respectively. Thus there was a significant elevation (p smaller than 0.01). No appreciable change in the plasma renin activity was found, however, at any stage. From these results it was concluded that experimentally induced chronic pyelonephritis in dogs caused a rise in blood pressure. No connection between the pyelonephritis and the renin angiotensin system was found.

Animals↗

Pyelonephritis and hypertension.

Blood pressure changes were followed up for 1-12 years (average; 3.8 years) in 46 cases of confirmed postoperative chronic pyelonephritis which had undergone ureterocutaneostomy, nephrostomy or other urologic operations. Diastolic blood pressure levels averaged 82 mmHg before operation, and 89 mmHg in the chronic stage after the operation. The incidence of hypertension (over 100 mmHg diastolic pressure) was 7% before the operation, but rose to 30% in the chronic stage. Application of an "age- and sex-adjusted score" also served to confirm a mean increase in blood pressure through the development of chronic pyelonephritis. No correlation was found between renal function and blood pressure. Nor was there any definite relationship between family history of hypertension and high blood pressure. In the 14 cases observed for plasma renin activity, values were found to be in the normal range.

Adolescent↗

Analysis of diastolic pressure-volume relation of the canine left ventricle: half-inflation pressure as an index of left ventricular compliance.

A sensitive index was proposed for the determination of left ventricular compliance. In the isolated potassium-arrested canine left ventricle, the pressure-volume (P-V) relationship was expressed as deltaV=a-be-cP throughout the range of filling pressure from 0 to 40 cmH2O, where deltaV and P were the actual volume change and intraventricular pressure, and a, b and c were constants. Then, half-inflation pressure (h) was calculated from h=[ln(2b/a)]/c. Left ventricular weight (LVW), intraventricular volume (LVV), ventricular external radius (ro) and internal radius (ri) were obtained from the measurements on the left ventricle, fixed at a filling pressure of 10 cmH2O. Then, LVVp=h, ro and ri at h were calculated. In the normal canine hearts, h was well correlated to LVW/LVVp=h and [(ro-ri)/ri]p=h. On the other hand, h/LVW/LVVp=h and h/[(ro-ri)/ri]p=h were constant and independent of LVW within a range of 40 to 150 g. These ratios rose markedly in the state of rigor mortis. From these results, it was concluded that h/LVW/LVVp=h and h/[(ro-ri)/ri]p=h depended on the left ventricular wall stiffness. And h was influenced by changes in LVW/LVVp=h and [(ro-ri)/ri]p=h in the absence of changes in intrinsic muscle stiffness.

Animals↗