Drug administration and LL-ES of ARVGP
The HF dogs were anesthetized with an intraperitoneal injection of 3%
sodium pentobarbital (30 mg/kg) and then ventilated with room air
(DDH-1, NO. 3529 PLA, Henan, China). The right femoral vein was
cannulated to infuse normal saline at
100-200
mL/h to replace spontaneous fluid loss. An electrocardiogram lead II was
monitored throughout the study. After the chest was opened through a
left fourth intercostal thoracotomy, the pericardium was opened and sewn
to the chest wall to cradle the heart. A custom electrode with eight
metal electrode heads (Henan Huanan Medical Science & Technology Co.,
Zhengzhou, China) was sewed tightly on the surface of ARVGP to stimulate
the neurons. The thirty HF dogs were subsequently divided randomly into
control, drug administration, and LL-ES groups, and then the chest was
closed. Dogs underwent no treatment in the baseline open chest status.
Then different modifications were performed as follows: Dogs in the
control group received a placebo
(starch,1g,qd ) for 1 w,while dogs in the drug group were administered a
mixed powder of drugs including
metoprolol(6.25mg,bid),
perindopril(2mg,qd), furosemide(20mg,bid),spironolactone(20mg,bid), and
digoxin(0.125g,qd) for 1w. Simultaneously, dogs in the LL-ES group
underwent 12h (immediate) and 1 w (short-term) of LL-ES ARVGP, which was
embedded in the adipose tissues surrounding the root of the aorta and
connected to the aorta by the mesangial ligament, as described in our
previous study [6]. The lowest voltage level that induced any
slowing of the sinus rate or
atrial
ventricular conduction (measured by the A-V interval) was
considered
as the threshold. Approximately10% below the threshold was then chosen
as the voltage for LL-ES. During LL-ES, the sinus rate and A-V interval
were monitored to ensure that the stimulation voltage was below the
threshold [7]. The study protocol can be seen in the flow chart
(Figure 1).