[Influence of lyophilized Radix Astragali powder injection on hemodynamics of dogs with myocardial ischemia].

In order to observe the influence of lyophilized Radix Astragali powder injection on hemodynamics and myocardial consumption of oxygen of dogs with myocardial ischemia, we establised the myocardial ischemia model by ligating the anterior descending branch of left coronary artery of 5 mongrel dogs. Then the drugs were administered intravenously, and the hemodynamic parameters and myocardial consumption of oxygen of the dogs were measured. All the Radix Astragali groups and Radix Salviae Miltiorrhizae Group (RSMG) showed significantly decreased heart rate (HR), diastolic blood pressure (DBP), mean arterial pressure (MAP) of dogs with myocardial ischemia in 5-30 min after drug administration (P < 0.05-0.01). All the Radix Astragali groups and the RSMG showed significantly lowered left ventricular end-diastolic pressure (LVEDP) of the dogs in 10 min-4 h after drug administration (P < 0.05-0.01). All the Radix Astragali groups displayed significantly increased maximum contraction velocity (+dp/dt(max)) of the dogs in 10 min after drug administration (P < 0.05-0.01). All the Radix Astragali groups and the RSMG displayed significantly increased cardiac output (CO) in 10 min-4 h after drug administration, in which the High Dose Group (HDG) of Radix Astragali displayed the highest statistical significance (P < 0.01). All the Radix Astragali groups and the RSMG exhibited significantly decreased peripheral resistance (TPR) and increased coronary blood flow (CBF) in 10 min-4 h after drug administration (P < 0.05-0.01). HDG showed significantly decreased myocardial work (MW) in 5 min-30 min after drug administration (P < 0.05-0.01). HDG and MDG exhibited significantly decreased oxygen uptake rate of the myocardium (MVo2) in 30 min-3 h after drug administration(P < 0.05-0.01). In summary, the lyophilized Radix Astragali powder injection can significantly benefit all the indexes and strengthen the heart function of the dogs with myocardial ischemia.

[The changes of hemodynamic parameters, pathology and c-kit mRNA expression in myocardium after acute myocardial infarction in rats].

This study was aimed to investigate the changes of hemodynamic parameters, pathology and c kit mRNA expression in myocardium after acute myocardial infarctionin (AMI) in rats, and to elucidate the relationship between these three kinds of changes. Sixty six adult male SD rats were randomly divided into normal group, Sham groups and ligation groups. The rat model of AMI was set up by ligating the left anterior descending artery. Hemodynamic parameters, pathological changes and c kit mRNA expression in myocardiam were examined. The results revealed that there were no statistically significant differences in hemodynamic parameters between normal group and Sham groups. Compared with the normal group, all ligation groups exhibited significantly decreased left ventricular systolic pressure (LVSP) and +/-dp/dtmax (P<0.01), and increased left ventricular end diastolic pressure (LVEDP, P<0.01). In the other ligation groups, compared with 6th hour group after ligation, there appeared striking increase of LVSP, LVEDP and +/-dp/dtmax (P<0.05). HE staining in myocardiam showed that there are necrosis and derangement at 24th hour group after ligation ,and a great number of inflammatory cells infiltration around the infarct zone at 3rd day group after ligation, and granulation tissue infiltrated into the infarct zone at 14th day group after ligation. In all five time points groups after ligation, the levels of c-kit mRNA expression were 0.99 fold, 1.06 fold, 1.46 fold, 1.91 fold and 2.67 fold, respectively, compared with Sham groups. The results suggest that cardiac stem cells in myocardium might contribute to the role of regenerating myocardium via self proliferation after acute myocardial infarction, but further investigation is still needed.

[A sharp rise in portal vein pressure, not arterial constriction, initiates bile salt-induced pancreatic microcirculatory disturbance].

It was reported that pancreatic arteries constricted during the early phase of bile salt-induced acute pancreatitis (AP), leading to pancreatic microcirculatory disturbance. We conducted this experiment to verify whether the above-mentioned finding was true. AP was induced with intraductal injection of taurodeoxyholate. Small pancreatic artery pressure in dogs was recorded. Functional capillaries were counted and calibrated by multiplying wet weight of pancreas. Pancreatic perfusion was measured with Laser Doppler flowmeter. Pancreatic arterioles of rats dilated during the initial 20 min of AP, and pancreatic arterial pressure declined during the early phase of AP in dogs (from 104.5 +/- 4.8 mmHg to 54.6 +/- 5.6 mmHg). The hematocrit of blood from inferior vena cava was significantly lower than that of portal vein at 5 min after pancreatitis induction. The "true" pancreatic functional capillary density increased. The early pancreatic microcirculatory disturbance coincided with a marked increase of portal vein pressure (PVP) as high as 9.18 +/- 0.78 mmHg. Reduction of PVP to baseline level was followed by a marked increase of pancreatic perfusion (by 1.4-fold). Arterial dilatation, but not constriction, occurred during the early phase of bile salt-induced AP. The pancreatic microcirculatory disturbance was due to a marked rise in PVP that greatly reduced the pressure difference in the pancreatic blood vessels and increased plasma extravasation which led. to local hemoconcentration.

[Studies of the possible mechanisms for protective effects of recombinant human growth hormone on intestinal mucosa barrier in rat sepsis].

OBJECTIVE: To investigate the protective effects of recombinant human growth hormone (rhGH) on intestinal mucosal barrier in rat sepsis and explore its possible mechanisms. METHODS: E. coli was injected intraperitoneally to produce rats sepsis models. Forty-two female SD rats were randomly divided into the control group (group C), sepsis group (group S) and treatment group (group T). Group S and group T were further divided into 1 d and 3 d subgroups (T1d,T3d, Sld, S3d), respectively. The expression of IGF-1 mRNA in liver, expression of Bcl-2 protein in intestine, bacteria translocation, the levels of growth hormone(GH) and insulin-like growth factor-1 (IGF-1) in plasma, and the histological appearance of intestine were determined dynamically by means of RT-PCR, radioimmunoassay, immunohistochemical staining and other corresponding methods, respectively. RESULTS: (1) rhGH could significantly attenuate intestinal mucosal injuries and ameliorate bacteria translocation on sepsis rats. (2) The levels of Bcl-2 protein expression in intestine in group T (T1d:2441 +/- 117; T3d: 3628 +/- 235) were obviously higher than those of group S (S1d: 321 +/- 36; S3d: 1873 +/- 57) (P < 0.01). (3) The plasma levels of GH in group T (T1d: 1.28 +/- 0.24 microg/L; T3d: 2.14 +/- 0.48 microg/L) increased markedly than those of group S (S1d: 0.74 -/+ 0.12 microg/L; S3d: 0.60 +/- 0.18 microg/L) (P < 0.01). (4) The plasma levels of IGF-1 in group T (Tld: 168.94 +/- 65.67 microg/L; T3d: 201.56 +/- 64.98 microg/L) elevated significantly than those of group S (Sld: 116.72 +/- 13.96 microg/L; S3d:107.50 +/- 23.53 microg/L) (P < 0.05). (5) The levels of liver IGF-1 mRNA in group T (Tld: 0.98 +/- 0.20; T3d: 1.76 +/- 0.17) were significantly higher than those in group S (S1d: 0.38 +/- 0.09; S3d: 0.46 +/- 0.10) (P < 0.01). CONCLUSION: rhGH conferred protective efficacy in maintaining the integrity of intestinal mucosal barrier against sepsis in rat. The possible mechanisms might involve the rhGH-diminished apoptosis of intestinal mucosa cells and the rhGH-maintained intestinal mucosa barrier via the roles of GH and IGF-1.