Yoshimura Aritada, Ohmori Takahiro, Hirao Daiki, Kishimoto Miori, Iwanaga Tomoko, Miura Naoki, Suzuki Kazuhiko, Fukushima Ryuji
Animal Medical Center, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Japan.
Cooperative Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, Fuchu, Japan.
Front Vet Sci. 2022 Jul 15;9:925847. doi: 10.3389/fvets.2022.925847. eCollection 2022.
Heart failure cause hypoperfusion-induced damage to abdominal organs due to decreased cardiac output (CO). Using a model dog with heart failure caused by rapid ventricular pacing (RVP), we have previously demonstrated that a decrease in CO reduces pancreatic blood flow (PBF). Furthermore, we have revealed that pancreatic acinar cell atrophy, which is a change in the pre-stage of pancreatitis was caused. However, the mechanism by which pancreatic acinar cell atrophy was caused in RVP dogs remains unknown. This study aimed to clarify the association between cardiac function, PBF, and histopathological changes in pancreatic acinar cells by administrating pimobendan, which increase CO, to RVP dogs. RVP dogs were divided into the control group (no medication, = 5) and the pimobendan group (pimobendan at 0.25 mg/kg BID, = 5). Non-invasive blood pressure measurement, echocardiography, and contrast-enhanced ultrasonography for PBF measurement were performed before initiating RVP and at 4 weeks after initiating RVP (4 weeks). At 4 weeks, the decreases in CO, mean blood pressure and PBF due to RVP were suppressed in pimobendan group. Furthermore, histopathological examination showed no changes in pancreatic acinar cells in the pimobendan group. Overall, it was clarified that the decrease in PBF due to cardiac dysfunction was a direct cause of pancreatic acinar cell atrophy. This suggests that maintaining PBF is clinically important for treating dogs with heart failure. In addition, these findings offer a reliable basis for developing new therapeutic strategies for heart failure in dogs, that is, pancreatic protection.
心力衰竭由于心输出量（CO）降低导致腹部器官因灌注不足而受损。我们之前使用快速心室起搏（RVP）诱导心力衰竭的模型犬，证明了CO降低会减少胰腺血流（PBF）。此外，我们还发现引发了胰腺炎前期的变化——胰腺腺泡细胞萎缩。然而，RVP犬胰腺腺泡细胞萎缩的发生机制尚不清楚。本研究旨在通过给RVP犬服用可增加CO的匹莫苯丹，阐明心功能、PBF与胰腺腺泡细胞组织病理学变化之间的关联。RVP犬被分为对照组（未用药，n = 5）和匹莫苯丹组（匹莫苯丹0.25 mg/kg，每日两次，n = 5）。在开始RVP前以及开始RVP后4周（4周）进行无创血压测量、超声心动图检查以及用于测量PBF的超声造影检查。4周时，匹莫苯丹组中因RVP导致的CO、平均血压和PBF降低受到抑制。此外，组织病理学检查显示匹莫苯丹组胰腺腺泡细胞无变化。总体而言，明确了心脏功能障碍导致的PBF降低是胰腺腺泡细胞萎缩的直接原因。这表明维持PBF对治疗心力衰竭犬具有临床重要性。此外，这些发现为开发针对犬心力衰竭的新治疗策略，即胰腺保护，提供了可靠依据。
