Brown Norway Katholiek rats, which have very low levels of plasma kininogens, excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats fed low (0.3%) NaCI diets (131±4 mm Hg, n=12) was not different from that in normal rats. Two percent NaCI diets given from 7 weeks of age for 4 weeks caused rapid increases in blood pressure (167±4 mm Hg, n=12, 9 weeks old) in deficient rats, although the same diets induced no blood pressure increase in normal rats. Urinary excretion of active kallikrein and prokallikrein remained constant in both rat groups throughout NaCI loading. During this period, the deficient rats secreted less urine (9 weeks old, P<.05) and less urinary sodium (11 weeks old, P<.05). Serum levels of sodium in deficient rats were higher (/ > <.O5) than in normal rats at 9 weeks of age. Intracellular concentrations of sodium in the erythrocytes of deficient rats were higher (P<.05) than in normal rats throughout NaCI loading. Subcutaneous infusion of bovine low molecular weight kininogen with an osmotic pump in NaCI-loaded deficient rats induced a reduction (P<.01) in blood pressure and increases (P<.05) in urine volume and urinary sodium and kinin levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 or of aprotinin in NaCI-loaded normal rats induced a hypertensive response. This antagonist treatment reduced urine volume and urinary sodium. These results indicate that the lack of kinin generation observed in the kininogen-deficient rats was related through sodium retention to the hypertensive response to NaCI loading. (Hypertension. 1993;22:705-714.) KEY WORDS • hypertension, sodium-dependent • sodium, dietary • kininogens • bradykinin • aprotininT he blood pressure-lowering effects of urinary kallikrein injected intravenously have been described for more than six decades,' and bradykinin is well known to induce vasodilatation and an increase in renal blood flow and excretion of water and sodium from the kidney.2 Urinary kallikrein therefore has been thought to be involved in hypertension, and its reduction has been reported in human 36 and animal 717 experiments. On the other hand, it is widely accepted that sodium retention may be related to the pathogenesis of hypertension, although the precise mechanisms of its contribution to the elevation of blood pressure are still unclear. The causal relation between these three factors -urinary kallikrein, sodium retention, and hypertension-has not been verified. Recently, we reported that the kallikrein-kinin system may play a suppressive role in deoxycorticosterone acetate (DOCA)-salt hypertension.18 Using kininogendeficient Brown Norway Katholiek (BN-Ka) rats and normal rats of the same strain (Brown Norway Kitasato [BN-Ki]), we were able to demonstrate that the urinary kallikrein-kinin system may contribute to lowering of systemic blood pressure in the initial phase of the development of DOCA-salt hypertension in uninephrectomized ...

Perineural invasion is a potent prognostic factor in extrahepatic cholangiocarcinoma. Adjuvant chemotherapy may improve the overall survival of patients with perineural invasion.

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BackgroundMany techniques that compensate for locomotion problems in daily life using externally controlled stimulation have recently been reported. These techniques are beneficial for effortlessly supporting patients’ locomotive functions, but the users of such devices must necessarily remain dependent on them. It is possible that some individuals with gait impairment may be prevented recovering locomotive function. From a rehabilitation viewpoint, it may therefore be supposed that ideally, devices that can be used in daily life to improve the locomotive functions of the body itself should be proposed.MethodsWe evaluate the effectiveness of Walk-Mate, which has been used mainly as a gait compensation device, as a gait rehabilitation training device by analyzing improvement in locomotion before, during and after rehabilitation in hemiparetic patients and comparing it with a previous gait training method. Walk-Mate generates a model walking rhythm in response to a user’s locomotion in real time, and by indicating this rhythm using auditory stimuli, provides a technology that supports walking by reducing asymmetries and fluctuations in foot contact rhythm. If patients can use the system to learn a regulated walking rhythm, then it may also be expected to fulfil the functions of a gait rehabilitation training device for daily life.ResultsWith regard to asymmetry, significantly improvements were seen for compensatory movement during training using Walk-Mate, but improvements were not retained as rehabilitative results. Regarding fluctuations in the foot contact period, significant improvement was observed for compensatory movement during training and these significant improvements were retained as rehabilitative results. In addition, it became clear that such improvement could not be adequately obtained by the previously proposed training technique utilizing constant rhythmic auditory stimulation.ConclusionsWalk-Mate effectively compensated for locomotion problems of hemiparetic patients by improving gait rhythm both during and after training, suggesting that locomotive function can be effectively recovered in some patients. The interactive mechanism of Walk-Mate may be capable of simultaneously achieving the aims of gait compensation and gait rehabilitation training methods previously developed under individual frameworks. Walk-Mate is a promising technology for assisting the reintegration of disabled persons into society.