Table 1.
Parameters of vagus nerve stimulation on rats with ischemia heart disease.
Figure 1.
The schematic representation of the experimental set up.
During the experiment, the distal end of right vagus nerve was stimulated. A polyethylene catheter (PE) catheter was inserted into the left femoral artery to monitor the blood pressure. Another PE catheter was inserted into the right carotid artery to measure the changes of left ventricular pressure. The intense of vagal stimulation was controlled by the computer which was connected with the simulator. The signal of vagal stimulation was output by the stimulator and was displayed in the computer.
Figure 2.
Uniform design protocol and schematic representation of the protocols of study.
(A) Factors and levels in the uniform design experiments. (B) Experiment of protocol. After initial surgical preparation, all rats were allowed 30 minutes (min) stabilization. Rats in each group were then treated a bolus injection of phenylephrine (5 µg/kg, i.v.) via the right femoral vein to measure baroreflex sensitivity (BRS). After this, all rats were allowed to stabilize over a 30-minute period before left anterior descending (LAD) artery ligation. Acute myocardial infarction (AMI) was induced by 240 min of LAD artery ligation. In MI group, the rats were just received LAD without VNS. In the G1–G6 group, vagus nerve stimulation (VNS) was performed immediately after the LAD artery ligation. Different vagal stimulation parameters following LAD artery ligation was also demonstrated in experiment protocol.
Figure 3.
Time courses of heart rates (HR) change during acute myocardial infarction in rats with or without vagal simulation.
The baseline values obtained just before LAD ligation are shown at time 0. (A) HR change in rats with AMI. Myocardial ischemia alone caused an increase initially then a progressively decrease in HR. (B–G) HR change in rats during AMI with vagal stimulations. HR was reduced from 1% to 45% compared to the baseline level. After the cessation of vagal stimulations, HR tends to increase back to the baseline level (n = 12 for each group).
Figure 4.
Effects of vagal stimulation on serum enzyme activity and infarction size following acute myocardial infarction in MI and G1–G6 group.
(A) Lactate dehydrogenase (LDH), (B) creatine kinase (CK), (C) cTnT activity in the serum (n = 8 for each group). (D) Changes of myocardial infarction size (percentage risk area) by VNS. (n = 8 for each group). Data are expressed as mean ± SEM Data are the mean ± SEM. *P<0.05 compared with MI control group.
Figure 5.
Effects of vagus nerve stimulation (VNS) on cardiac function in MI and G1–G6 group.
MAP, mean arterial pressure; HR, heart rate; LVSP, left ventricular systolic pressure; LVEDP, left ventricular end-diastolic pressure; ±dP/dt, maximum slope of systolic pressure increment and diastolic pressure decrement. Data are the mean ± SEM (n = 8 for each group). *P<0.05 compared with MI control group.
Figure 6.
Effects of vagus nerve stimulation on myocardial and plasma level of tumor necrosis factor-α (TNF-α) in MI and G1–G6 group.
(A) Representative blots and densitometric analyses of TNF-α protein expression, normalized against GADPH. (B) Arterial blood levels of TNF-α, as determined by ELISA. Data are the mean ± SEM (n = 8). *P<0.05 compared with MI group.
Figure 7.
Impacts of vagal stimulation on baroreflex sensitivity (BRS) change.
BRS was quantitated as slope of a line generated from the relationship of R-R interval during increases in arterial pressure. (A) The BRS baseline level in each group at the stabilization period. (B) The BRS levels in each group at the end of experiment. The levels of BRS were obviously higher in G1, G2 and G3 compared with the MI group. Data are the mean ± SEM (n = 8). *P<0.05 compared with MI group.
Figure 8.
Representative blot and densitometric analyses of α7-nicotinic receptor protein from the myocardial.
The levels of α7-nicotinic receptor were increased significantly in G1, G2 and G3 compared with the MI group. Data are the mean ± SEM (n = 8). *P<0.05 compared with MI group.