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LOM ablation prevented acute myocardial infarction-induced VAs with the same efficiency as LSG ablation, potentially by blocking the sympathetic pathway from the LSG to the heart.

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Distinct sympathetic activation as represented by left stellate ganglion high-frequency spike discharge activity protected against bradycardia and hypotension in a canine model of vasovagal syncope. Our findings may have therapeutic implications.

The identification and treatment of androgen-independent prostate cancer are both challenging and significant. In this work, high-throughput deformability cytometry was employed to assess the effects of two anti-cancer drugs, docetaxel and enzalutamide, on androgen-sensitive prostate cancer cells (LNCaP) and androgen-independent prostate cancer cells (PC-3), respectively. The quantified results show that PC-3 and LNCaP present not only different intrinsic physical properties but also different physical responses to the same anti-cancer drug. PC-3 cells possess greater stiffness and a smaller size than LNCaP cells. As the docetaxel concentration increases, PC-3 cells present an increase in stiffness and size, but LNCaP cells only present an increase in stiffness. As the enzalutamide concentration increases, PC-3 cells present no physical changes but LNCaP cells present changes in both cell size and deformation. These results demonstrated that cellular physical properties quantified by the deformability cytometry are effective indicators for identifying the androgen-independent prostate cancer cells from androgen-sensitive prostate cancer cells and evaluating drug effects on these two types of prostate cancer.

Cardiac sympathetic tone overdrive is a key mechanism of arrhythmia. Cardiac sympathetic nerves denervation, such as LSG ablation or renal sympathetic denervation, suppressed both the prevalence of VAs and the incidence of SCD. Accumulating evidence demonstrates the ligament of Marshall (LOM) is a key component of the sympathetic conduit between the left stellate ganglion (LSG) and the ventricles. The present study aimed to investigate the roles of the distal segment of LOM (LOMLSPV) denervation in ischemia and reperfusion (IR)-induced VAs, and compared that LSG denervation. Thirty-three canines were randomly divided into group 1 (IR group, n = 11), group 2 (LOMLSPV Denervation + IR, n = 9), and group 3 (LSG Denervation + IR, n = 13). Hematoxylin-Eosin (HE) and Immunohistochemistry staining revealed that LOMLSPV contained bundles of sympathetic but not parasympathetic nerves. IR increased the cardiac sympathetic tone [serum concentrations of noradrenaline (NE) and epinephrine (E)] and induced the prevalence of VAs [ventricular premature beat (VPB), salvo of VPB, ventricular tachycardia (VT), VT duration (VTD) and ventricular fibrillation (VF)]. Both LOMLSPV denervation and LSG denervation could reduce the cardiac sympathetic tone in Baseline (BS) [heart rate variability (HRV)]. Compared with group 1, LOMLSPV denervation and LSG denervation similarly reduced sympathetic tone [NE (1.39±0.068 ng/ml in group 2, 1.29±0.081 ng/ml in group 3 vs 2.32±0.17 ng/ml in group 1, P<0.05) and E (114.64±9.22 pg/ml in group 2, 112.60±9.69 pg/ml in group 3 vs 166.18±15.78 pg/ml in group 1, P<0.05),] and VAs [VT (0±3.00 in group 2, 0±1.75 in group 3 vs 8.00±11.00 in group 1, P<0.05) and VTD (0 ± 4 s in group 2, 0±0.88s in group 3 vs 10.0 ± 22.00s in group 1, P<0.05)] after 2h reperfusion. These findings indicated LOMLSPV denervation reduced the prevalence of VT by suppressing SNS activity. These effects are comparable to those of LSG denervation. In myocardial IR, the anti-arrhythmic effects of LOMLSPV Denervation may be related to the inhibition of the expression of NE and E.

Background Atrial ganglionated plexus (GP) ablation was proved to have therapeutic effects on vasovagal syncope. The study aimed to investigate whether selective ablation of only right anterior GP (ARGP) and right inferior GP (IRGP) was effective in a canine model of vasovagal syncope. Methods Seventeen mongrel dogs were divided into control (N = 10) and ablation group (N = 7). Bilateral thoracotomy was performed at the fourth intercostal space and ARGP and IRGP were ablated in the ablation group. A bolus of veratridine (15 ug/kg) was injected into the left atrium to induce vasovagal reflex. Surface electrocardiogram and blood pressure (BP) were continuously monitored. Heart rate (HR) variability was calculated to represent cardiac autonomic tone. Results Veratridine injection induced vasovagal reflex in all dogs. HR decreased from 149 ± 17 to 89 ± 33 beats/min (P < 0.001) in the control group, while in the ablation group HR decreased from 141 ± 35 to 125 ± 34 beats/min (P = 0.032). The postveratridine HR in the ablation group was significantly higher than that in the control group (P = 0.045). A significantly less intense HR decrease was observed in the ablation group compared with control (–17 ± 16 vs –61 ± 34 beats/min, P = 0.006). Significant BP decreases were induced in both the groups (all P < 0.01), while no evident differences in postveratridine BP and the extent of BP decreases were found between the groups. HR variability revealed significant decrease in cardiac vagal tone after ablation [high‐frequency power, 0.50 (0.17–1.05) vs 6.28 (0.68–8.99) ms2, P = 0.005]. Conclusions Selective ablation of ARGP + IRGP weakened cardiac parasympathetic control and significantly attenuated the cardioinhibitory response in an animal model of vasovagal reflex. This ablation strategy might be effective for vasovagal syncope with evident cardioinhibitory response.

Introduction Our recent study found that selective ablation of the distal part of the ligament of Marshall (LOMLSPV) could suppress ventricular arrhythmias (VAs) during acute myocardial infarction (AMI). This study was to investigate the possible underlying mechanisms. Methods Dogs were randomly divided into the sham‐operated group (SO; n = 6), AMI group (AMI; n = 8) and the group undergoing LOMLSPV ablation ahead of AMI (LOMD+AMI; n = 8). Incidence of VAs, serum levels of malondialdehyde (MDA) and superoxide dismutase (SOD), expression of connexin (Cx43), Bcl‐2, Bax, caspase‐3, tumor necrosis factor (TNF)‐α, interleukin‐6 (IL‐6), and high mobility group box (HMGB)1 were compared. Anatomic and immunostaining examinations of LOM LSPV were performed. Results Compared with the AMI group, incidence of VAs was reduced in the LOMD+AMI group. Compared with the SO group, Cx43, SOD, and Bcl‐2 were decreased, MDA, Bax, caspase‐3, TNF‐α, IL‐6, and HMGB1 were increased in the MI group, and all the alterations were significantly restrained in the LOMD+AMI group. A visual nerve fiber communication between the left stellate ganglion (LSG) and LOM and abundant sympathetic nerve bundles distribution in LOMLSPV were revealed. Conclusions LOMLSPV ablation could suppress VAs during AMI. The possible mechanism may be associated with disconnection of the sympathetic conduit from LSG to the ventricles. Preservation of Cx43, inhibition of cardiac oxidative stress, apoptosis, and inflammation may be involved.