ABSTRACT
ObjectiveDahl salt-sensitive (Dahl/SS) rats are hereditary salt-sensitive hypertensive rats.Its pathogenesis is similar to that of human primary hypertension,CPB established in Dahl/SS rats provides an animal model for the study of CPB in patients with primary hypertension.MethodsMale 14-16 weeks old Dahl/SS rats weighing 360-390 g were fed with high salt (8％ NaCl) diet for 4 weeks before the experiment.Ten Dahl/SS rats were randomly divided into 2 groups ( n =5 each) according to the CPB time:groups Ⅱ and Ⅲ underwent CPB for 120 and 75 min respectively.Another 7 male 14-16 weeks old ordinary SD rats weighing 410-490 g undergoing CPB for 120 min were used as control group (group Ⅰ ).Anesthesia was induced with isoflurane inhalation.Orotraeheal intubation was performed.The animals were mechanically ventilated.Right jugular vein and tail artery were cannulated for venous drainage and arterial inflow from CPB circuit.Blood was oxygenated with a customized mini-oxygenator.Blood gases were analyzed and blood glucose concentration was determined.MAP was recorded before (baseline) and at 30 and 60 min of CPB and 30 and 90 min after CPB.The rate of changes in MAP and blood glucose concentration and survival rate at 7 d after termination of CPB were recorded.ResultsThere was no significant difference in blood gases among the 3 groups.The rates of change in MAP and blood glucose concentration were significantly higher during and after CPB in Dahl/SS rats than in control SD rats in a duration of CPB dependent manner.The survival rate at 7 d after CPB was 7/7 (in group Ⅰ ),1/5 (in group Ⅱ ) and 4/5 (in group Ⅲ ) respectively.ConclusionA model of 75 min CPB is established successfully in Dahl/SS rats.
ABSTRACT
Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.