• Title/Summary/Keyword: Heart atria

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Peroxisome proliferator-activated receptor γ is essential for secretion of ANP induced by prostaglandin D2 in the beating rat atrium

  • Zhang, Ying;Li, Xiang;Liu, Li-Ping;Hong, Lan;Liu, Xia;Zhang, Bo;Wu, Cheng-Zhe;Cui, Xun
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.3
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    • pp.293-300
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    • 2017
  • Prostaglandin $D_2$ ($PGD_2$) may act against myocardial ischemia-reperfusion (I/R) injury and play an anti-inflammatory role in the heart. Although the effect of $PGD_2$ in regulation of ANP secretion of the atrium was reported, the mechanisms involved are not clearly identified. The aim of the present study was to investigate whether $PGD_2$ can regulate ANP secretion in the isolated perfused beating rat atrium, and its underlying mechanisms. $PGD_2$ (0.1 to $10{\mu}M$) significantly increased atrial ANP secretion concomitantly with positive inotropy in a dose-dependent manner. Effects of $PGD_2$ on atrial ANP secretion and mechanical dynamics were abolished by AH-6809 ($1.0{\mu}M$) and AL-8810 ($1.0{\mu}M$), $PGD_2$ and prostaglandin $F2{\alpha}$ ($PGF2{\alpha}$) receptor antagonists, respectively. Moreover, $PGD_2$ clearly upregulated atrial peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) and the $PGD_2$ metabolite 15-deoxy-${\Delta}12$, 14-$PGJ_2$ (15d-$PGJ_2$, $0.1{\mu}M$) dramatically increased atrial ANP secretion. Increased ANP secretions induced by $PGD_2$ and 15d-$PGJ_2$ were completely blocked by the $PPAR{\gamma}$ antagonist GW9662 ($0.1{\mu}M$). PD98059 ($10.0{\mu}M$) and LY294002 ($1.0{\mu}M$), antagonists of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling, respectively, significantly attenuated the increase of atrial ANP secretion by $PGD_2$. These results indicated that $PGD_2$ stimulated atrial ANP secretion and promoted positive inotropy by activating $PPAR{\gamma}$ in beating rat atria. MAPK/ERK and PI3K/Akt signaling pathways were each partially involved in regulating $PGD_2$-induced atrial ANP secretion.

The Influence of Simplified Surgical Procedures on the Surgical Treatment for Atrial Fibrillation with using the Cut-and-Sew Technique (절개봉합법을 이용한 심방세동 수술의 중단기 결과)

  • Choi, Jong-Bum;Kim, Jong-Hun;Lee, Mi-Kyung;Lee, Sam-Youn;Kim, Min-Ho;Kim, Kong-Su
    • Journal of Chest Surgery
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    • v.41 no.3
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    • pp.313-319
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    • 2008
  • Background: The Cox maze-III procedure is considered as the most effective surgical treatment for atrial fibrillation. Because this procedure takes a long time and it complicates the concomitant cardiac surgery, some surgeons perform a left atrial maze procedure or pulmonary vein isolation only to reduce the operation time. This study was performed to evaluate how the modified procedures, with using cut-and-sew techniques, can influence the treatment of atrial fibrillation. Material and Method: Between Feb 1999 and June 2005, 40 patients (17 males and 23 females) with organic heart disease and atrial fibrillation underwent the Cox maze-III procedure (23), the left atrial maze procedure (10) or pulmonary vein isolation (7). The cut-an-sew technique was used to ablate the atrial wall, but cryoablation was used instead of the cut-and-sew technique for the coronary sinus and the inferior wall between the pulmonary vein and the mitral annulus. Result: After a mean follow-up period of $50.0{\pm}21.6$ months, all (100%) of the 23 patients who underwent the Cox maze-III procedure had regular sinus or atrial rhythm conversion, and 7(70%) of 10 with a left atrial maze procedure and 4(57.1%) of 7 with pulmonary vein isolation had regular sinus or atrial rhythm conversion (p=0.002). Conclusion: To obtain a high conversion rate from atrial fibrillation to a regular sinus rhythm or a regular atrial rhythm, the standard Cox maze-III procedure should be performed in both atria. The limited modified procedures like the left atrial maze procedure or pulmonary vein isolation may reduce the cure rate of atrial fibrillation.