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Between 1982 and May 1993, we operated on 680 patients with combined valvular disease. Previous operations were including closed mitral commissurotomy in 87, and bioprosthetic valve replacement in mitral position in 15. The types of combined valve disease included mitral valve disease combined with functional tricuspid regurgitation (FTR) (245), with organic tricuspid disease (OTD) (10); mitral and aortic disease (258), combined with FTR (128), and with OTD (39). The early mortality was 4.7% in total 2.4% and 6.1% respectively in MVR or DVR plus tricuspid procedures. The main cause of early death was low cardiac output syndrome. The late mortality was 2.6% pt-yr, congestive heart failure and coagulant-related hemorrhage were the predominant causes of late death. We considered that FTR is the outcome of right ventricle decompensation, while tricuspid valve must be actively inspected intraoperatively, and must be corrected completely. OTD can be successfully repaired in most patients. Myocardial protection should be emphasized, and continuous perfusion of cold blood cardioplegia and controlled reperfusion of warm blood contained mannitol have marked effect.

Between Jan. 1982 and July, 1993, 102 patients with rheumatic giant heart disease (cardio-thoracic ratio > or = 0.8) underwent valve replacement. Heart functional class III was in 54 patients, and class IV in 48. Early mortality was 8.8%, late mortality 3.6%. We classified the patients into five types, based on the valvular lesions, dilated degree of each atrial and ventricular chamber: Type I, giant left atrium (LA); Type II, obvious enlargement of LA and left ventricle (LV); Type III; obvious enlargement of LA, right atrium and ventricule (RA and RV); Type IV; all chambers obviously dilated; Type V, giant LA and RA. Clinical results showed that this kind of classification can reflect kinds of diseased valves, pathophysiological changes and clinical characteristics, and postoperative early and late outcomes, also can offer useful suggestions to operative method selection, and has great clinical significance for perioperative management.

Various 3'-deoxy-3'-C-(hydroxymethyl)-, 3'-deoxy-3'-C-(fluoromethyl)-, 3'-deoxy-3'-C-(azidomethyl)-, and 3'-deoxy-3'-C-(aminomethyl)-substituted nucleosides (total 12 compounds) have been synthesized and evaluated against L1210, P388, S-180, and CCRF-CEM cells and HSV-1, HSV-2, and HIV-1 in culture. Only 3'-deoxy-3'-C-(hydroxymethyl)thymidine (36) was found to show significant anticancer activity against L1210, P388, S-180, and CCRF-CEM cells with ED50 values of 50, 5, 10, and 1 microM, respectively. None of these compounds demonstrated significant antiviral activity against HSV-1, HSV-2, or HIV-1. These compounds were also evaluated against thymidine kinases derived from HSV-I (strain KOS), HSV-2 (strain 333), and mammalian (K562) cells. The thymidine kinase (HSV-1 strain KOS) was inhibited significantly by both 3'-deoxy-3'-C-(hydroxymethyl)- and 3'-deoxy-3'-C-(fluoromethyl)thymidine.

Infusion of norepinephrine (NE) into humans and experimental animals induces diuresis by mechanisms that are not completely understood. Two series of experiments were performed to determine whether changes in plasma levels of vasopressin or changes in mean arterial pressure (MAP) are important-factors in NE-induced diuresis in conscious dogs. First, plasma vasopressin (PAVP) levels were measured in normal and cardiac-denervated conscious dogs during a 30-min intravenous infusion of NE (0.5 micrograms.kg-1.min-1). When NE was administered to normal dogs, urine flow increased from 0.3 +/- 0.1 to 0.9 +/- 0.4 ml/min. PAVP did not decrease, in spite of increases in mean arterial pressure (from 103 +/- 4 to 123 +/- 6 mm Hg) and left atrial pressure (from 5.2 +/- 0.9 to 8.6 +/- 1.4 mm Hg). The same dose of NE infused into cardiac-denervated dogs significantly increased urine flow (from 0.2 +/- 0.1 to 0.8 +/- 0.3 ml/min) and MAP (from 107 +/- 5 to 147 +/- 10 mm Hg), and decreased PAVP (from 1.8 +/- 0.3 pg/ml to 1.2 +/- 0.3 pg/ml). In the second series of experiments, NE was infused into cardiac-denervated dogs for 40 min. During the final 20 min of NE infusion, nitroprusside was infused to offset the pressor effect of NE by returning MAP to the initial control level. Urine flow increased during the first 20 min in which NE alone was given; however, when MAP was returned to the control level by nitroprusside infusion, urine flow also returned to the control level. PAVP increased from a control value of 3.6 +/- 0.6 to 18.9 +/- 3.8 pg/ml 15 min after the NP infusion had begun. We conclude that a decrease in PAVP is not required to elicit diuresis during NE infusion in normal conscious dogs and that the pressor effect of NE appears to play a major role in NE-induced diuresis.

Low-dose infusions of atriopeptin produce only a modest diuresis and natriuresis. However, these infusions also decrease atrial pressures, a change that has been postulated to elicit an antidiuretic and antinatriuretic reflex from cardiac receptors and thereby to attenuate the direct renal effects of atriopeptin. To determine whether the renal effects of intravenously administered atriopeptin might be attenuated by a cardiorenal reflex, we infused alpha-human atrial natriuretic peptide (alpha-hANP) into cardiac-denervated and sham-operated (normal) conscious dogs. Following a control period, alpha-hANP was infused into each dog at 12.5, 25, or 50 ng.kg-1.min-1 for 1 hr. Infusion of alpha-hANP at 50 ng.kg-1.min-1 produced similar decreases in left atrial pressure in both normal and cardiac-denervated dogs (peak changes, -1.6 +/- 0.8 vs -2.4 +/- 0.9 mm Hg, respectively). Increases in urine flow (peak changes, 0.13 +/- 0.05 vs 0.20 +/- 0.06 ml/min) and sodium excretion (peak changes, 56 +/- 22 vs 70 +/- 11 microEq/min) also were not different between groups. The lower doses of alpha-hANP also elicited renal and hemodynamic responses in the cardiac-denervated dogs that did not differ significantly from those in the normal dogs. These data indicate that the diuresis and natriuresis elicited by intravenously administered alpha-hANP are not attenuated by a cardiorenal reflex in conscious dogs.

The treatment of 65 cases (with 20 cases in the control group) of patients with post-hepatic cirrhosis by Extractum Semen Persicae (ESP) and cultivated Cordyceps Hyphae (CH) was reported, and the adjustment of the disorders of both cellular and humoral immune functions was investigated. The results indicated apparently that the restrained cellular immune function, among which the rate of lymphocyte transformation, the NK cell's function, CD8+ and CD4+ cells in the patients' group were lower than those in the healthy group. The CD8+ cell count was positively correlated with lymphocyte transformation rate and the humoral immune hyperfunction revealing that the levels of IgG, IgA, ssIgA and CIC of the patients were abnormally higher than those of healthy subjects, while level of C3 was negatively correlated with that of CIC. After the treatment, rate of transformation, function of NK cell, CD8+, CD4+ cells and the ratio of CD4+/CD8+ improved; levels of IgG, IgA, ssIgA and CIC reduced, while those of C4 and C3 rose. These results revealed the ESP and cultivated CH could modulate the cellular immune function, inhibit the humoral immune hyperfunction and increase serum complement level in patients with post-hepatitic cirrhosis, which were correlated to the improvement of hepatic function. Disorder of immune function was one of the important causes of liver cell necrosis, inflammatory cell infiltration and fibroplastic proliferation. The results showed that the drugs are of some value in the treatment of patients with post-hepatitic cirrhosis.

Homobrassinolide (2) and (22S, 23S)-22,23-epi-homobrassinolide (4) were synthesized from stigmasterol in seven steps respectively in 4.7% and 24.1% overall yields. The ratio of 2 to 4 is 1:5. The key step is the highly regioselective formation of the B-homo-7-oxa-lactone ring by oxidation of an enol silyl ether with 3-chloro-peroxybenzoic acid.

This study was designed to determine whether the increase in atriopeptin secretion induced by an intravenous infusion of norepinephrine is mediated directly by adrenergic receptor stimulation or indirectly by the associated increase in atrial pressure. Norepinephrine was infused at 0.5 microgram.kg-1.min-1 for 30 min into both sham-operated (intact) and cardiac-denervated conscious dogs. The infusion increased mean arterial pressure in all dogs. On the other hand, left atrial pressure increased from 5.0 +/- 0.7 to 9.6 +/- 1.6 mmHg (p less than 0.01) in intact dogs, but decreased from 5.5 +/- 1.0 to 2.0 +/- 0.7 (p less than 0.01) in cardiac-denervated dogs. Right atrial pressure changes followed similar trends, but were not significant in the intact group. Plasma atriopeptin increased from 73 +/- 12 to 110 +/- 18 pg/ml (p less than 0.01) as left atrial pressure increased in intact dogs and decreased from 79 +/- 15 to 54 +/- 10 pg/ml (p less than 0.01) as left atrial pressure decreased in cardiac-denervated dogs. The changes in plasma atriopeptin correlated closely with the changes in left atrial pressure (r = 0.941, p less than 0.001) and to a lesser extent with the changes in right atrial pressure (r = 0.413, p less than 0.05). These results suggest that the change in plasma atriopeptin induced by infusion of norepinephrine into conscious dogs is mediated by the concomitant change in atrial pressures.

Human endothelin, a 21-residue peptide produced by vascular endothelial cells, was infused intravenously into trained conscious dogs at a rate of 20 ng.kg-1.min-1 for 1 hr. Endothelin produced a renal vasoconstriction that persisted during a 40-minute recovery period. Sarafotoxin S6b, a closely related 21-residue peptide that has been isolated from the venom of the burrowing asp, was also infused into the same conscious dogs at 20 ng.kg-1.min-1. Sarafotoxin produced a renal vasodilation that persisted throughout the infusion; when the infusion ended, however, renal blood flow decreased rapidly to below control levels. Both endothelin and sarafotoxin produced marked decreases in urine osmolality even though plasma vasopressin remained normal, thus indicating that these peptides inhibit the antidiuretic effects of vasopressin. These results imply that a broad spectrum of structure-activity relationships may exist among analogues of this unique group of 21-residue peptides.