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Compared with WK, ADP-induced platelet aggregation was weaker in SHRSR, SHRSP, and especially in SHRSP with some symptoms of stroke (Apo-SHRSP). Bovine collagen-mediated platelet aggregation was also less in Apo-SHRSP. When collagens from the aortas of WK, SHRSR, SHRSP, and Apo-SHRSP were added to PRP from SHRSR, the aggregation in response to that from Apo-SHRSP was not so markedly changed. These findings might be partly related to the high incidence of stroke in SHRSP, either primarily or secondarily.

Stroke-resistant SHR (SHRSR) fed on high-cholesterol or high fat-cholesterol diets for 2 weeks, but not those on high fat diet, developed hypercholesterolemia and hyper β-lipoproteinemia as well as fat deposition in mesenteric arteries, which was prevented by an antihypertensive agent, hydralazine (8mg/dl in drinking water) and also by the dose of α1-blocker, prazosin HCl (20mg/dl) without antihypertensive effect. Thus, α1-receptor mediated mechanism appear to be involved in the development of acute arterial fat deposition in addition to hypertension and hypercholesterolemia.

Na+, K+-ATPase activity was measured in cultured smooth muscle cells from the aorta of male WKY, SHRSR and SHRSP at the age of 3-months. Na+, K+-ATPase activity in SHRSR showed significantly higher than that in SHRSP. WKY showed intermediate activity between SHRSR and SHRSP. Na+, K+-ATPase activities were dose-dependently inactivated by fatty acid-free bovine serum albumin in all strains, especially in SHRSP. However, Mg++-ATPase activities were not affected by the same treatment.

The chemical structures of the native oxides formed during various wet chemical treatments were measured nondestructively by changing the effective electron escape depth. The structures of the native oxides can be characterized by the distribution of suboxide Si3+ in the native oxide films. If Si3+ is correlated with Si-H bonds, the formation rate of the native oxide during the wet chemical treatment and the interface roughness produced by photoexcited dry etching through the oxide can be explained.

GT was examined in SHRSR at various ages. The GT was the lowest at the age of 2-3 months and improved at the age of 5-6 months. GT in SHRSR fed on a high fructose diet (HFD) or a high sucrose diet (HSD) was significantly lower as compared to that in SHRSR fed on a normal diet (ND).

It was suggested that VCG of 60 day-old WK rats were similar to that of 2-11 month-old human infants in angle and magnitude of the maximum QRS vector, except of the QRS loop rotation in the F plane. In comparison with human adult VCG, it was clear that the direction of the maximum QRS and P vector were deviated to -z direction in the LS and H plane in rats

Na loading accelerates urinary Ca excretion and this calciuretic effect of Na is possibly related to the aggravation of hypertension by Na loading in SHRSP. Our observation on Na-loaded SHRSP, so far indicated bones were more fragile, so that excess Na intake might be pathogenically involved in the development of osteoporosis. Therefore, Na-loaded SHRSP could be a good model for osteoporosis. On the other hand, Ca supplementation attenuated the development of severe hypertension and stroke in SHRSP. Since urinary Na excretion was increased in the group given the Casupplemented diet, the beneficial effect of Ca appeared to be ascribed to the acceleration of urinary Na excretion. Thus, it can be concluded under excess Na intake, enough Ca intake is important for the prevention not only of hypertensive diseases but also of osteoporosis.

In the present study, it became clear that β-blocker (propranorol) had effectively improved rCBF in adult SHRSP with sever hypertension in which rCBF was significantly lower than control WKY. Yamori and Horie's previous studies clarified the BP reduction in SHRSP with severe hypertension increased rCBF and prevented the development of cerebrovascular lesions (STROKE 8: 456, 1977). It is noteworthy that β-blocker, without reducing BP significantly in SHRSP with severe hypertension, increases rCBF significantly. Because of the high frequency of pulse rate over 400/min in conscious rats, blood flow in cerebral arteries near recurrent branchings is regarded as being nearly similar to steady flow. Since our previous hemorheological study demonstrated that pulsatile flow increased flow into recurrent branches and that the effect of pulsation was augmented with the increased pulse pressure (Niimi et al: JAP HEART J 20: 681, 1979), it is theoretically considered that β-blocker, which reduces heart rate without affecting BP and thereby increases pulse pressure, favourably increases the reduced blood flow into recurrent arteries especially under severe hypertension. The present experiment substantiated this hypothesis and suggested that β-blocker, even without reducing blood pressure markedly, would be useful for preventing cerebrovascular lesions caused by hypoxia due to reduced rCBF in the predilection sites of stroke fed by recurrent arteries.

SHRSP fed on the high protein diet showed significantly higher vascular reactivity than those fed on the high fat-cholesterol diet as determined by response in mean pressure, while response in pulse pressure showed the inverse relationship, indicating improvement of vascular elasticity in SHRSP fed on the high protein diet. These experimental results suggest that high protein diet may increase the vascular robustness in SHRSP

Amorphous-silicon field-effect transistors have been integrated into three-dimensional form for the first time, and the static as well as dynamic characteristics were evaluated. Inverters and nine-stage ring-oscillators fabricated on a fused silica substrate have two layers of FETs isolated by CVD SiO2. The inverters had step-like transfer characteristics and a small-signal gain of about 10 was obtained. The ring-oscillator experiment showed that the minimum proparation delay time per gate was about 60 µsec.

WITH DISCUSSION Although platelet function, determined by collagen or ADP-mediated aggregation, was decreased in SHRSP and SHRSR, the vascular collagens from SHRSP and SHRSR induced more extensive aggregation of platelets than that from WK. Changes in platelet volume distribution might reflect the functional changes or might be used as the indicator of not yet defined platelet alteration. Moreover, the impairment of fibrinolytic system (decreased plasminogen activator and increased plasmin inhibitor) was noted in SHRSP and SHRSR and this might be the cause of high incidence of thrombosis in SHRSP with hypertensive vascular damages

Methionine and taurine attenuated the development of severe hypertension in SHRSP. However cysteine had not such an effect. Methionine also decreased the incidence of stroke in SHRSP (43%) in comparison with the incidences in cysteine-treated and control SHRSP (88 and 89%, respectively). Methionine or taurine may reduce the blood pressure by modulating central blood pressure regulation

Isoelectric focusing method revealed that the heart and aorta, but not choroid plexus and the cultured vascular smooth muscle cells, had obvious differences in nonspecific esterase isozyme patterns.The separation of the nonspecific esterase isozymes which were electrophoresed in the starch gel was already established as a method to detect a genetic marker of SHR (LAB INVEST 22: 206, 1970), but the separation of the isozyme pattern of the cardiovascular system was not so sufficiently clear. In contrast to the starch gel electrophoresis, the separation of the isozyme pattern by the isoelectric focusing was sufficient. Therefore, this technique can be regarded as a good method for analyzing nonspecific esterase isozymes and for detecting genetic markers of hypertensive strains.Although the pathogenic relationship between the different isozyme pattern and hypertensive diseases is not yet known from the present study, such a clear genetico-biochemical differences is suggestive of the possible existance of genetic factor of hypertension in the heart and blood vessels of SHR and SHRSP.

No effect was observed on cerebrovascular atherogenesis after cervical sympathectomy in renal infarction hypertensive rats. These results suggest that denervation has no effect on atherogenesis in renal infarction hypertensive rats and the role of the nervous system is more important in the development of fat deposition in SHRSP which show greater susceptibility to genetic hypertension and atherogenesis

The noradrenergic fluorescence at the nerve terminals was augmented during the ontogenic development in the mesenteric arteries, cerebrobasal arteries and renal arteries of SHRSP. The finding suggests that the sympathetic aminergic neuron system may be altered genetically in SHRSP. The nervous system in young SHRSP may accelerate the vasomotion of systemic and cerebral afteries, leading to severe hypertensive vascular lesions observed in adult SHRSP

The authors propose a new photoexcited silicon-wafer cleaning technique, in which ultraviolet light irradiates the wafer through chlorine gas, followed by thermal treatment in a hydrogen ambient, to grow a high-quality epitaxial layer. The surface metal contaminants were removed through a thin native oxide without damaging the surface by photoexcited cleaning, and the remaining volatile chloride after the photoexcited cleaning at 150°C was removed by thermal treatment at 900°C. Further thermal treatment at 980°C removed even the thin native oxide and then made it possible to grow an epitaxial silicon layer. The SiO2 film formed using a conventional technique on the epitaxial silicon layer showed improved breakdown fields and a decrease of fixed-charge density. The results mean that a high-quality silicon-epitaxial layer has been realized by the cleaning procedure.

The erythrocyte membrane abnormality in SHRSP was detected by the method using a TPP+ sensitive electrode even before the development of hypertension. Therefore, such an abnormality does not seem to be secondary to the effect of hypertension but rather due to genetic abnormality. Similar tendency to the findings in SHRSP was observed in erythrocytes from men with genetic disposition to stroke. This method is simple enough to determine the characteristics of erythrocyte membrane within a short period and may hopefully contribute to the prescience and prevention of hypertensive diseases.

(1) In Experiment 2, the deformity or irregularity of QRS vector in VCG was ascertained to correspond to myocardial necrosis and fibrosis(2) In Experiment 1, myocardial lesions of SHRSP could be detected vectorcardiographically about 1 year of age. And, such myocardial lesions as diffuse fibrosis developed progressively but rather gradually, compared with "sudden onset" of the artificial myocardial infarction as demonstrated in Experiment 2Thus, vectorcardiographical or pathological study on the heart of SHRSP and its comparison with the surgically induced myocardial infarciton in WK demonstrated that the heart of old SHRSP could be used as the model of myocardial infarction

There was a closer relationship between the heart weight and the liver weight than between the heart weight and the brain weight in old SHRSP. However, in SHRSP heart weight to liver weight ratios were still greater than those in WK, indicating the cardiac hypertrophy is a more dominant characteristics in hypertensive state. Hypertrophied hearts of more than 2.2g in weight, all with cerebral stroke, corresponded also to the heaviest group of the liver in old SHRSP. Pathological examinations of the liver showed that the characteristic pathological finding in old SHRSP was the fibrous thickning of the wall of central vein ("central sclerosis") and a tendency toward fibrosis of the liver. Laboratory tests of 'very old' SHRSP showed increase in (a)BUN, (b)GOT and LDH and (c)GPT, which corresponded to (a)hypertensive renal vascular lesions (arterionecrosis, glomerular fibrosis and arteriosclerosis), (b)myocardial lesions (infarction and extensive perivascular fibrosis) and (s)liver damage due to congestion.These experimental studies indicate that cardiac hypertrophy in old SHR is closely related with the congestion of the liver which is also hemodynamically over-loaded in long-standing hypertensive state.

The erythrocytes from stroke-prone SHR (SHRSP) were more fragile than those from stroke-resistant SHR (SHRSR) or Wistar-Kyoto (WK) rats at the age of 2 months. After the chronic administration of saline (1% NaCl in drinking water), blood pressure in both SHRSR and WK was elevated, but the membrane fragility was not changed. Therefore, the membrane characteristics in SHRSP may not be related to their hypertension, but possibly to their stroke-proneness