Heterogeneous cardiac sympathetic innervation in heart failure after myocardial infarction of rats

Abstract

We examined cardiac neuronal function and beta-receptor with a dual-tracer method of [(131)I]meta-iodobenzylguanidine (MIBG) and [(125)I]iodocyanopindolol (ICYP) in rat heart failure after myocardial infarction (MI). In rats with MI, left ventricular (LV) systolic function decreased, and LV dimension and right ventricular (RV) mass increased gradually. MIBG accumulations of the noninfarcted LV (remote region) and RV decreased by 15% at 1 wk compared with sham-operated rats, and these accumulations were restored by 71% and 56%, respectively, at 24 wk compared with age-matched sham rats despite sustained depletion of myocardial norepinephrine contents in these regions. ICYP accumulation of the remote region and of the RV did not decrease at any stages. Myocardial MIBG distribution was heterogeneous at 1 wk when it was lower in the peri-infarcted region than in the remote region, associated with reduced ICYP accumulation in the peri-infarcted region. The heterogeneous distribution of both isotopes disappeared at 12 wk. Thus cardiac sympathetic neuronal alteration was coupled with downregulation of beta-receptors in rat heart failure after MI. The abnormal adrenergic signaling occurred heterogeneously in terms of ventricular distribution and time course after MI.

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

“…Although the present study confirms peri-infarct hyperinnervation (Cao, et al, 2000a;Cao, et al, 2000b), other studies have reported reduced cardiac sympathetic innervation after infarction (Barber, et al, 1983;Igawa, et al, 2000;Li, et al, 2004). These differences may be related to the extent of infarction as larger infarcts can result in frank congestive heart failure, and this has been linked to cardiac NGF depletion and diminished sympathetic axon density (Kaye, et al, 2000;Qin, et al, 2002).…”

Effects of the Angiotensin-converting Enzyme Inhibitor Enalapril on Sympathetic Neuronal Function and .BETA.-adrenergic Desensitization in Heart Failure after Myocardial Infarction in Rats.

“…Experimental animals: Male Wistar rats weighing 300-350 g were used for the induction of MI, that was produced by ligation of the left coronary artery under ether anesthesia as reported previously. 19) Briefly, the left coronary artery was ligated approximately 2-3 mm from its origin with a suture (6-0 silk). With this method, the 24-hour survival rate was 57% in the infarcted rats.…”

Brief Episode of Myocardial Ischemia Before Prolonged Ischemia Attenuates Cardiac Sympathetic Nerve Injury

“…7 Briefly, under ether anesthesia, a left thoracotomy was performed to expose the heart. The left coronary artery was ligated 2-3 mm from its origin with a 5-0 Prolene suture (Ethicon Inc, Somerville, NJ, USA) for 30 min and then the ligature was released (non-PC group).…”

“…7 Briefly, 3 days after the induction of myocardial ischemia, 1.85 MBq of 131 I-MIBG (radiochemical purity >98%, specific activity 7.4 GBq/mg, Daiichi Radioisotope Laboratory, Chiba, Japan) was injected via the external jugular vein under pentobarbital anesthesia (30 mg/kg, ip). The heart was removed 3 h later.…”

“…7 The circumference of the LV was divided into 6 equal segments at the level of papillary muscles, and the ischemic region (IR) was put on the LV anterior segment and the remote region (RR), the interventricular septum, as described in the previous study. 8 The myocardial tracer uptake in IR and RR was normalized as a percentage of the administered dose per gram of heart tissue (%kg dose/g) using 131 I-labeled graded standards.…”