Zobrazit v EDS

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

Uloženo v:
Podrobná bibliografie
Název: Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways
Autoři: Ok Soo Kim, Hyo Sup Shim, Young Jun Oh, Yong Seon Choi, Sungwoo Ryoo, Sungwon Na, Tae Dong Kweon
Přispěvatelé: Sungwon Na, Ok Soo Kim, Sungwoo Ryoo, Tae Dong Kweon, Yong Seon Choi, Hyo Sup Shim, Young Jun Oh, Kweon, Tae Dong, Kim, Ok Soo, Na, Sung Won, Shim, Hyo Sup, Oh, Young Jun, Choi, Yong Seon
Zdroj: Hypertension. 63:309-315
Informace o vydavateli: Ovid Technologies (Wolters Kluwer Health), 2014.
Rok vydání: 2014
Témata: Male, Blood Pressure, Local/pharmacology, Rats, Sprague-Dawley, 0302 clinical medicine, Cardiomegaly/drug therapy, Ropivacaine, Anesthetics, Local, Blood Pressure/physiology, 2. Zero hunger, Ganglia, Sympathetic, Monocrotaline, Pulmonary/metabolism, Superior Cervical Ganglion/metabolism, Superior Cervical Ganglion/drug effects, Sympathetic/metabolism, 3. Good health, Amides/pharmacology, Hypertension, Cardiomegaly/metabolism, Cardiomegaly/physiopathology, autonomic pathways, Autonomic Nerve Block, Monocrotaline/pharmacology, Nitric Oxide Synthase Type III, Arginase/antagonists & inhibitors, pulmonary, Hypertension, Pulmonary, Oxidative Stress/drug effects, Oxidative Stress/physiology, Cardiomegaly, Superior Cervical Ganglion, Nitric Oxide, Blood Pressure/drug effects, 03 medical and health sciences, nitric oxide, Animals, Sympathetic/physiopathology, Anesthetics, sympathetic nervous system, Arginase, Pulmonary/drug therapy, Nitric Oxide Synthase Type III/metabolism, Superior Cervical Ganglion/physiopathology, Autonomic Nerve Block/methods, Amides, Arginase/metabolism, Rats, Oxidative Stress, Nitric Oxide/metabolism, Ganglia, Sympathetic/drug effects, Sprague-Dawley
Popis: It has been recognized that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH), and abnormal sympathetic hyperactivity leads to worsening of PAH via endothelial dysfunction. The purpose of this study was to examine whether sympathetic ganglion block (SGB) can treat PAH by increasing the availability of nitric oxide (NO). PAH was induced in rats by 50 mg/kg of subcutaneous monocrotaline. After 2 weeks, daily injections of ropivacaine into the left superior cervical ganglion were repeated for 14 days (monocrotaline-SGB group). Monocrotaline group received sham SGB with saline, whereas control group received saline instead of monocrotaline. PAH was evident in monocrotaline group, with right ventricular systolic pressures (47±4 mm Hg) that were higher than those of controls (17±2 mm Hg), whereas SGB significantly attenuated monocrotaline-induced PAH (35±4 mm Hg). The right/left ventricular mass ratios exhibited similar changes to those seen with right ventricular pressures. Heart rate variability showed significantly higher sympathetic activity in the monocrotaline group. Microscopy revealed a higher proportion of muscular arteries with thicker medial walls in the monocrotaline group, which was attenuated by SGB. Monocrotaline induced arginase hyperactivity, which was in turn decreased by SGB-induced endothelial NO synthase activation. SGB restored monocrotaline-induced hypoactivity of superoxide dismutase. In conclusion, SGB could suppress PAH and the remodeling of pulmonary arteries via inactivation of arginase and reciprocal elevation of NO bioavailability, thus attenuating disproportionate hyperactivation of the sympathetic nervous system.
Druh dokumentu: Article
Popis souboru: 309~315
Jazyk: English
ISSN: 1524-4563
0194-911X
DOI: 10.1161/hypertensionaha.113.01979
Přístupová URL adresa: https://www.ahajournals.org/doi/pdf/10.1161/HYPERTENSIONAHA.113.01979
https://pubmed.ncbi.nlm.nih.gov/24324044
https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.113.01979
https://pubmed.ncbi.nlm.nih.gov/24324044/
https://www.ncbi.nlm.nih.gov/pubmed/24324044
https://hyper.ahajournals.org/content/63/2/309
https://hyper.ahajournals.org/content/hypertensionaha/63/2/309.full.pdf
https://ir.ymlib.yonsei.ac.kr/handle/22282913/99281
Rights: CC BY NC ND
Přístupové číslo: edsair.doi.dedup.....bf2a4a7a3173bb9ca857c7ee330c16a6
Databáze: OpenAIRE
Popis
Abstrakt:It has been recognized that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH), and abnormal sympathetic hyperactivity leads to worsening of PAH via endothelial dysfunction. The purpose of this study was to examine whether sympathetic ganglion block (SGB) can treat PAH by increasing the availability of nitric oxide (NO). PAH was induced in rats by 50 mg/kg of subcutaneous monocrotaline. After 2 weeks, daily injections of ropivacaine into the left superior cervical ganglion were repeated for 14 days (monocrotaline-SGB group). Monocrotaline group received sham SGB with saline, whereas control group received saline instead of monocrotaline. PAH was evident in monocrotaline group, with right ventricular systolic pressures (47±4 mm Hg) that were higher than those of controls (17±2 mm Hg), whereas SGB significantly attenuated monocrotaline-induced PAH (35±4 mm Hg). The right/left ventricular mass ratios exhibited similar changes to those seen with right ventricular pressures. Heart rate variability showed significantly higher sympathetic activity in the monocrotaline group. Microscopy revealed a higher proportion of muscular arteries with thicker medial walls in the monocrotaline group, which was attenuated by SGB. Monocrotaline induced arginase hyperactivity, which was in turn decreased by SGB-induced endothelial NO synthase activation. SGB restored monocrotaline-induced hypoactivity of superoxide dismutase. In conclusion, SGB could suppress PAH and the remodeling of pulmonary arteries via inactivation of arginase and reciprocal elevation of NO bioavailability, thus attenuating disproportionate hyperactivation of the sympathetic nervous system.
ISSN:15244563
0194911X
DOI:10.1161/hypertensionaha.113.01979