scholarly journals Interaction between Endothelin-1 and Left Stellate Ganglion Activation: A Potential Mechanism of Malignant Ventricular Arrhythmia during Myocardial Ischemia

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Zhenya Wang ◽  
Shuyan Li ◽  
Huanzhu Lai ◽  
Liping Zhou ◽  
Guannan Meng ◽  
...  

Endothelin-1 (ET-1) is synthesized primarily by endothelial cells. ET-1 administration in vivo enhances the cardiac sympathetic afferent reflex and sympathetic activity. Previous studies have shown that sympathetic hyperactivity promotes malignant ventricular arrhythmia (VA). The aim of this study was to investigate whether ET-1 could activate the left stellate ganglion (LSG) and promote malignant VA. Twelve male beagle dogs who received local microinjections of saline (control, n=6) and ET-1 into the LSG (n=6) were included. The ventricular effective refractory period (ERP), LSG function, and LSG activity were measured at different time points. VA was continuously recorded for 1 h after left anterior descending occlusion (LADO), and LSG tissues were then collected for molecular detection. Compared to that of the control group, local ET-1 microinjection significantly decreased the ERP and increased the occurrence of VA. In addition, local microinjection of ET-1 increased the function and activity of the LSG in the normal and ischemic hearts. The expression levels of proinflammatory cytokines and the protein expression of c-fos and nerve growth factor (NGF) in the LSG were also increased. More importantly, endothelin A receptor (ETA-R) expression was found in the LSG, and its signaling was significantly activated in the ET-1 group. LSG activation induced by local ET-1 microinjection aggravates LADO-induced VA. Activated ETA-R signaling and the upregulation of proinflammatory cytokines in the LSG may be responsible for these effects.

2021 ◽  
Vol 104 (3) ◽  
pp. 506-511

Ventricular arrhythmias are usually well controlled with medical management, cardiac implantable electronic devices, or catheter ablation. However, the refractory ventricular tachycardia or fibrillation (VT/VF) is life threatening and challenging. The authors reported a case series of left stellate ganglion blocks (LSGB) in patients with refractory VT/VF, who failed pharmacological treatment and multiple traditional cardiac interventions. Five patients underwent six LSGB. Four patients had significant decreased in ventricular arrhythmia burden. Among the responders, the LSGB suppressed significant VT/VF for three to seven days. Blocks did not only temporary suppress ventricular arrhythmia, but also stabilized the condition and served as a bridge to definitive treatment such as EP ablation or heart transplantation. There was no significant hemodynamic change or devastating side effects. The outcome from the present case series suggested that LSGB could be an effective treatment and a lifesaving intervention frintractable VT/VF. Keywords: Stellate ganglion block, Refractory ventricular tachycardia, Sympathectomy


1995 ◽  
Vol 269 (2) ◽  
pp. R287-R293 ◽  
Author(s):  
N. Yamaguchi

The aim of the present study was to investigate if either dihydropyridine-sensitive L-type Ca2+ channels or cholinergic receptor-mediated mechanisms are implicated in endothelin-1 (ET)-induced adrenal catecholamine (CA) secretion in anesthetized dogs. ET was locally administered to the left adrenal gland via the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography method. In the control group, local infusion (1 min, 0.5 ml/min) of ET (the fixed total dose of 0.5 microgram given to the gland or approximately 0.0197 microgram/kg of body weight) resulted in a sharp increase in the basal CA output, followed by a rapid decline, and a relatively slow secondary response lasted over a period of 15-30 min. In the second group treated with nifedipine (5 micrograms or approximately 0.207 microgram/kg) similarly administered 10 min before ET infusion, the ET-induced first steep increase in CA output was significantly attenuated by approximately 75% (P < 0.05, n = 6). In dogs similarly receiving either pentolinium (1 mg or approximately 0.041 mg/kg) or atropine (0.5 mg or approximately 0.018 mg/kg), the ET-induced CA response remained unchanged. The results indicate that ET-induced adrenal CA release was largely mediated by the activation of dihydropyridine-sensitive L-type Ca2+ channels. Furthermore, neither nicotinic nor muscarinic receptors were functionally implicated in the CA response to ET. The study suggests the existence of noncholinergic mechanisms involved in the secretory action of ET on the adrenal medulla in the dog in vivo.


2017 ◽  
Vol 20 (2) ◽  
pp. 93 ◽  
Author(s):  
Alessandra Cury Machado ◽  
Denise Belucio Ruviere ◽  
Renata Zoccal Novais ◽  
Carlos Roberto Emerenciano Bueno ◽  
Elerson Gaetti Jardim Jr ◽  
...  

<p><strong>Objective:</strong> To evaluate <em>in vivo </em>tissue reaction to the extract of araçá (<em>Psidium cattleianum</em>) associated with inactivated microorganisms. <strong>Material and Methods:</strong> A 0.1 mL suspension was used containing Porphyromonas gingivalis, Prevotella intermedia, <em>Fusobacterium nucleatum, Enterococcus faecalis, Peptostreptococcus micros</em>, and <em>Porphyromonas endodontalis,</em> which were inactivated by heat and mixed into a 1.0 mL saline (control group), an aqueous solution, or a hydroalcoholic extract of araçá. Eighteen male rats (<em>Rattus norvegiccus</em>) under general anesthesia received 0.2 mL of 1% intravenous Evans blue. Thirty minutes later, 0.1 mL of one of the associations was injected into the animals’ dorsal region. The animals were euthanized after 3 and 6 hours, and the materials obtained were placed in formamide for 72 hours then analyzed in a spectrophotometer (λ=630 hm). For the morphological analysis, 30 rats received polyethylene tubes implants with the extracts or the saline with the associations in the dorsal region and euthanized after 7 and 30 days to be analyzed according to an inflammation cell score. <strong>Results:</strong> No significant difference (p&gt;0.05) was observed in the edema among groups. The optical microscopy results showed a repair in the 30-day-period, which was higher when compared to the 7-day-period (p&lt;0.0001). Nevertheless, in the 7-day-period, the hydroalcoholic extract presented a significant response compared to the aqueous extract (p=0.05) and a trend for better results than the control group. <strong>Conclusion: </strong>The aqueous and hydroalcoholic araçá extracts associated with inactivated microorganisms showed similar responses to control, indicating no interference on the toxic effects of the bacterial components in tissue repair.</p><p><strong>Keywords</strong></p><p>Anaerobic bacteria; Edema; Inflammation; Plant extracts; <em>Psidium.</em></p>


2015 ◽  
Vol 27 (1) ◽  
pp. 246 ◽  
Author(s):  
H. Fernandes ◽  
L. Schefer ◽  
F. C. Castro ◽  
C. L. V. Leal

Melatonin is a pineal hormone related to the control of the circadian cycle, besides the reproductive seasonality of some animal species, and has shown positive effects on oocyte maturation and embryo development. The aim of this study was to assess the effects of melatonin on in vivo and in vitro maturation of mouse oocytes. Female F1 hybrids (C57BL/6 × CBA; n = 8 per group/treatment) were used in 3 different treatments (trt) groups: (I) in vivo trt: mice received 2 different doses of melatonin injections, 10 and 20 mg kg–1 per IP including a saline control dose (0 mg kg–1 per IP) for 4 days along with ovarian stimulation trt of 5 IU of eCG IP, followed by 5 IU of hCG IP 48 h later, and cumulus-oocyte complexes (COC) were collected 16 h after hCG; (II) mice received a similar in vivo melatonin trt, but ovarian stimulation trt was only 5 IU of eCG, no hCG, and COC were collected after 48 h and subsequently matured in vitro with 0.5 µg mL–1 of FSH for 16 h; (III) in vitro maturation of oocytes: COC were collected 48 h after 5 IU of eCG and maturated in the presence of 3 different doses of melatonin (10–9, 10–6, and 10–3 M) or 0.5 µg mL–1 of FSH (control) for 16 h. In vitro-maturing oocytes were in incubated at 37°C, 5% CO2, and 95% humidity. Maturation rates were evaluated according to the presence of the first polar body under an inverted microscope. Statistical analyses were performed by ANOVA followed by Tukey's test (4 replicates). In the first treatment, 20 mg kg–1 of melatonin showed the highest in vivo maturation rate, 80.3% (61/76), while 10 mg kg–1 of melatonin was 62.4% (53/85) and the saline control group was 69.4% (77/111), but differences were not significant (P > 0.05). For in vitro maturation of oocytes from animals previously treated with melatonin, the 10 mg kg–1 of melatonin group had the highest maturation rate, 53.2% (99/186), in comparison with the saline and 20 mg kg–1 of melatonin groups, which showed 46.6 (88/189) and 39.0% (85/218), respectively; again, no differences were detected (P > 0.05). In the last treatment, the maturation rates increased from 48.9 (43/88) to 53.7 (51/95) and 56.0% (56/100) as the melatonin concentrations decreased from 10–3, 10–6, and 10–9 M, respectively. The control group had the highest rate of 57.3% (55/96), but no statistical differences were observed (P = 0.706). In conclusion, under the conditions studied, melatonin was unable to improve the maturation rate neither after in vivo nor in vitro treatment. However, during in vitro maturation, melatonin alone was as efficient as FSH in promoting maturation in murine oocytes, indicating its potential effect on stimulating meiosis. Therefore, the role of melatonin in stimulating meiosis needs further investigation.Acknowledgments to FAPESP for fellowship (HF) and funding (CLVL).


Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Silvia I García ◽  
Ludmila S Peres Diaz ◽  
Maia Aisicovich ◽  
Mariano L Schuman ◽  
María S Landa

Cardiac TRH (cTRH) is overexpressed in the hypertrophied ventricle (LV) of the SHR. Additionally in vivo siRNA-TRH treatment induced downregulation of LV-TRH preventing cardiac hypertrophy and fibrosis demonstrating that TRH is involved in hypertrophic and fibrotic processes. Moreover, in a normal heart, the increase of LV TRH expression alone could induce structural changes where fibrosis and hypertrophy could be involved, independently of any other system alterations. Is well-known the cardiac hypertrophy/ fibrotic effects induced by AII, raising the question of whether specific LV cTRH inhibition might attenuates AII induced cardiac hypertrophy and fibrosis in mice. We challenged C57 mice with AII (osmotic pumps,14 days; 2 mg/kg) to induce cardiac hypertrophy vs saline. Groups were divided and , simultaneously to pump surgery, injected intracardiac with siRNA-TRH and siRNA-Con as its control. Body weight, water consume and SABP were measured daily. As expected, AII significantly increased SABP (p<0.05) in both groups treated , although cardiac hypertrophy (heart weight/body weight) was only evident in the group with the cardiac TRH system undamaged, suggesting that the cardiac TRH system function as a necessary mediator of the AII-induced hypertrophic effect. As hypothesized, we found an AII-induced increase of TRH (p<0.05) gene expression (real-t PCR) confirmed by immunofluorescence that was not observed in the group AII+siRNA-TRH demonstrating the specific siRNA treatment efficiency. Furthermore, AII significantly increase (p<0.05) BNP (hypertrophic marker), III collagen and TGFB (fibrosis markers) expressions only in the group with AII with the cardiac TRH system intact. On the contrary, the group with AII and the cTRH system inhibited, shows genes expressions similar to the saline control group. We confirmed these results by immunofluorescence. Similar fibrotic results were observed with NIH3T3 cell culture where we demonstrated that AII induced TRH gene expression (p<0.05) and its inhibition impedes AII-induced increase of TGFB and III/I collagens expressions telling us about the role of the cTRH in the AII fibrosis effects. Our results point out that the cardiac TRH is involved in the AII-induced hypertrophic and fibrotic effects.


2007 ◽  
Vol 102 (3) ◽  
pp. 1273-1280 ◽  
Author(s):  
Jaime F. Mata ◽  
Talissa A. Altes ◽  
Jing Cai ◽  
Kai Ruppert ◽  
Wayne Mitzner ◽  
...  

The apparent diffusion coefficients (ADCs) of hyperpolarized 3He and 129Xe gases were measured in the lungs of rabbits with elastase-induced emphysema and correlated against the mean chord length from lung histology. In vivo measurements were performed at baseline and 2, 4, 6, and 8 wk after instillation of elastase (mild and moderate emphysema groups) or saline (control group). ADCs were determined from acquisitions that used two b values. To investigate the effect of b value on the results, b-value pairs of 0 and 1.6 s/cm2 and 0 and 4.0 s/cm2 were used for 3He, and b-value pairs of 0 and 5.0 s/cm2 and 0 and 10.0 s/cm2 were used for 129Xe. At 8 wk after instillation, the rabbits were euthanized, and the lungs were analyzed histologically and morphometrically. ADCs for the rabbits in the control group did not change significantly from baseline to week 8, whereas ADCs for the rabbits in the emphysema groups increased significantly ( P < 0.05) for all gas and b-value combinations except 129Xe with the b-value pair of 0 and 5.0 s/cm2. The largest percent change in mean ADC from baseline to week 8 (15.3%) occurred with 3He and the b-value pair of 0 and 1.6 s/cm2 for rabbits in the moderate emphysema group. ADCs (all b values) were strongly correlated ( r = 0.62–0.80, P < 0.001) with mean chord lengths from histology. These results further support the ability of diffusion-weighted MRI with hyperpolarized gases to detect regional and global structural changes of emphysema within the lung.


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