The effects of dietary magnesium (Mg) on pulmonary vascular reactivity and chronic hypoxic pulmonary hypertension were assessed in rats. The rats were fed high magnesium (H-Mg) diet or a regular diet for two months before the start of normobaric hypoxia, 10±0.5 % O₂ ventilation, 8 h/day, for 14 days runnning. The plasma level of Mg was significantly increased in the H-Mg group as compared to the controls. Mean pulmonary arterial pressure, pulmonary vascular reactivity to hypoxia and pulmonary vascular resistance were significantly lower in the rats fed H-Mg diet than in those fed regular diet. The weight ratios of the right ventricle to the ending body weight (RV/EBW) and to the left ventricle plus iterventricular septum (RV/LV+S) in the rats fed H-Mg diet were remarkably lower as well. No difference was observed in blood viscosity and hematocrit between the H-Mg group and the hypoxic control. The above findings suggest that dietary Mg can attenuate basic pulmonary resistance and hypoxic pulmonary vasoconstriction, thereby preventing the development of chronic hypoxic pulmonary hypertension and right ventricular hypertrophy.

Effects of cigarette smoke extract (CSE) and some vasoactive mediators on the production of PGI₂ and TXA₂ in normoxic and hypoxic pulmonary artery endothelial cells (PAECs) in culture were studied. The production of PGI₂ in PAECs was inhibited by hypoxia or verapamil, but promoted by angiotensin II (A II), noradrenaline (NE) or platelet activating factor (PAF), while that of TXA₂ slightly increased except when treated with PAF. The effect of A II, NE, PAF and verapamil, however, was not influenced by hypoxia. CSE inhibited the production of PGI₂ in normoxic PAECs but did not further reduce 6-keto-PGF_1α in hypoxic PAECs medium. The results suggested that a) the production of PGI₂ during hypoxia might be stimulated by vasoactive mediators produced during hypoxia, not by hypoxia directly; b) the production and release of PGI, were related to intracellular calcium, c) the augmented production of PGI₂ might be one of the mechanisms in the pulmonary vasodilating role of PAF: and d) prostaglandin production might be associated with the alteration of hypoxic pulmonary vasoreactivity after cigarette smoking.

Rabbits and rats were infected intratracheally with extracellular enzyme of Streptomyces thermohygroscopicus (H_9-4) by only one exposure, and lesions of the lung developed including mononuclear macrophage infiltration as well as bronchitis and vasculitis. The obvious damages in type I pneumocytes, endothelial cells of capillaries and arterioles in the lung were observed by electron microscopy. Immunofluorescent histochemistry examination revealed exudation of plasma fibronectin which might play an important role during the process of lesion repairing in lung. The experiment also confirmed that extracellular enzyme of Streptomyces thermohygroscopicus might directly damage the lung tissue. These experimental data may serve as valuable reference for studying the etiology and pathogenesis of farmer’s lung disease.

Impedance rheopneumogram (IRP) and right heart Swan-Ganz catheter examinations were simultaneously carried out in 63 patients. Two equations for calculating after-exercise-pulmonary-pressure (PAP_m) were obtanined by stepwise regressional analysis:

This is a new method for diagnosing latent pulmonary hypertension noninvasively.

Standard microelectrode techniques were used to study the effects of benzyltetrahydropalmatine (BTHP) on ouabain-induced delayed afterdepolarization (DAD) and triggered activity in isolated guinea papillary muscles. The results indicate that ouabain-induced DAD and triggered activity were abolished by BTHP 100 μmol/L. In anesthetized rabbit ECG heart rate was reduced in a dose-dependent manner from control value of 288±14 to 261±14 (BTHP 5 mg/kg) and 226±36 bpm (BTHP 10 mg/kg). P-R interval was prolonged. In His-bundle electrogram, H-V interval and V duration were not affected, but A-H interval was prolonged from 41±3 to 45±5 ms.

The effects of α-adrenergic receptor blockade during stellate ganglion stimulation on arrhythmias induced by repeated coronary artery occlusion in pigs under spontaneous breathing were studied. Prazosin, α₁-receptor blocker, did not have any effect on the early ischemic dysrhythmia. Yohimbin, which selectively blocks α₂-receptor, significantly increased the number of premature ventricular complexes (19±3→ 32±2 PVC;P<0.01), but produced no effects on the percentage of appearance of ventricular fibrillation (VF) and ventricular tachycardia (VT). However, nonselective α-receptor blocker phentolamine significantly reduced the number of premature ventricular complexes (30.5 ± 4.5→ 11 ±3 PVC;P<0.05), but did not affect the frequency of occurrence of VF and VT. The above results show that α-adrenergic mechanisms do not play any important role in the genesis of arrhythmias during ischemia in the pig model.

The effect of central renin-angiotensin system (RAS) on one-kidney Grollman hypertension during the maintaining phase and its mechanism were investigated in rats. The arterial blood pressure (ABP) and the content of angiotensin II (A II) and norepinephrine (NE) in brain regions was measured respectively. 4 weeks after operation the ABP was elevated significantly, and it sustained at high level 8 weeks post-operatively. However, ABP in the control group underwent no significant changes at the same period. The A II and the NE content in the brain regions of the operated group were significantly higher than in those of the age-matched control group. During the maintaining phase of hypertension captopril (150 μg/10 μ1) was injected into the lateral cerebroventricle at 0.5 h, 1.0 h and 1.5 h respectively, and ABP and content of A II and NE were determined at the corresponding time. The results showed that the above three parameters decreased consistently at 0.5 h and 1.0 h, and increased gradually at 1.5 h, suggesting that the central RAS might play an important role in the maintaining phase of onekidney Grollman hypertension in rats.

The experimental study was aimed at elucidating the effects of phentolamine and vasopressin used separately or in combination on hepatic and systemic hemodynamics in cirrhotic portal hypertensive dogs. The results showed that either of the two drugs used separately could lead to reduction in portal venous pressure and could also influence systemic hemodynamics or lower hepatic blood flow. When phentolamine in combination with vasopressin was administered, no side-effect could be found on hepatic and systemic hemodynamics, suggesting that the drugs used in combination could efficaciously decrease portal hypertension and counteract their respective side-effect. This combination therapy will be useful in treating bleeding from esophageal variceal rupture in cirrhotic patients with portal hypertension.

Macrophages were incubated with^125I-VLDL for 5 h in presence or absence of lipoprotein lipase (LPL) inhibitor, benzene boronic acid (BBA). Both the uptake and degradation of^125I-VLDL by macrophages were saturable, and the uptake and degradation curves were virtually identical. When macrophages were incubated with^125I-VLDL for 10 h in presence of BBA, the uptake and degradation of^125I-VLDL were still saturable. However, in absence of BBA, the uptake and degradation were no longer saturable. The results suggest that with macrophages incubated with VLDL for a shorter period, VLDL was taken up predominantly via receptor pathway, with a longer period of incubation, LPL played a striking role in uptake of VLDL.

Skin-visceral divergent projections of cholecystokinin (CCK)-containing dorsal root ganglion neurons were studied by combined technique of fluorescent double-labelling and immunohistochemistry. Fast blue (FB) and nuclear yellow (NY) were injected into the coeliac ganglion and the cutaneous branches of left 9th–11th intercostal nerves, respectively. Three kinds of neurons labelled with fluorescein were observed in T_9-11 dorsal root ganglia: FB-labelled neurons with blue-fluorescent cytoplasm; NY-labelled neurons with yellow-fluorescent nucleus and double-labelled neurons with blue cytoplasm and yellow nucleus. The double-labelled neurons were found to account for 2.8 % of total labelled neurons. The sections containing neurons labelled with fluorescein were stained by CCK-immunohistochemical procedure. Four kinds of neurons could be identified: NY-neurons with CCK-immunoreactivity (NY+CCK); FB-neurons with CCK-immunoreactivity (FB+CCK); NY+FB neurons with CCK-immunoreactivity (NY+FB+CCK); and neurons only CCK-positive. NY+FB+CCK tri-labelled neurons accounted for approximately 11.5 % of NY+FB double-labelled neurons, and for 0.4 % of all CCK-positive neurons. The findings clearly indicated that the peripheral processes of some sensory dorsal root ganglion neurons divergently project to both skin and visceral structure and contain CCK.

The diabetic patient with renal failure underwent simultaneous pancreaticoduodenal and renal transplantation. Duodeno-cystostomy was performed for the drainage of exocrine secretion. Immediately after grafting, the pancreatic and the renal graft regained normal function, and there was no operative complication whatever. The patient had functioning pancreatic graft and became insulin-independent for more than 3 months, although two transplanted kidneys were rejected. Immunosuppression consisted of cyclosporine A, azathioprine and prednisone. Our results suggest that hemorrheological parameters may serve as early indicators of acute rejection and be used to estimate the efficacy of anti-rejection and anti-coagulation therapy.

The aim of this paper is to continue the discussion on the defects of the structures of medical resources and their applicability at the present time, and then to design the qualitative networklike subsystem of the new research Quantitatively Medicine Simulating and Operating by Computer (QMSOC) and a five-library model of the new knowledge-base of QMSOC, Finally, a set of results from the primary functions of exploitation of pancreas-glucagon-insulin information by QMSOC are presented.