Centhaquine Increases Stroke Volume and Cardiac Output in Patients with Hypovolemic Shock

Aman Khanna, Krish Vaidya, Dharmesh Shah, Amaresh K. Ranjan, Anil Gulati
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Abstract

Background: Centhaquine is a resuscitative agent that acts on alpha-2B adrenergic receptors to enhance venous return in hypovolemic shock. The effect of centhaquine on cardiac output in patients with hypovolemic shock has not been reported. Methods: Trans-thoracic echocardiography was utilized to measure stroke volume (SV), cardiac output (CO), left ventricular outflow tract-velocity time integral (LVOT-VTI), left ventricular outflow tract diameter (LVOTd), heart rate (HR), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS) and inferior vena cava (IVC) diameter before (0 min) and after centhaquine (0.01 mg/kg, iv infusion over 60 min) treatment (60 min, 120 min, and 300 min) in 12 randomly selected patients with hypovolemic shock enrolled in a prospective, multicenter, open-label phase IV clinical study (NCT05956418) of centhaquine in patients with hypovolemic shock. Results: A significant increase in SV (mL) was observed after 60, 120, and 300 minutes of centhaquine treatment. CO (mL/min) increased significantly at 120 and 300 min despite a decrease in HR at these times. A significant increase in IVC diameter and LVOT-VTI (mL) at these time points was observed, which indicated increased venous return. The LVEF and FS did not change, while the mean arterial pressure (MAP, mmHg) increased in patients after 120 and 300 minutes of centhaquine treatment. Positive correlations between IVC diameter and SV (R2 = 0.9556) and between IVC diameter and MAP (R2 = 0.8928) were observed, which indicated the effect of centhaquine mediated increase in venous return on SV, CO, and MAP. Conclusions: Centhaquine mediated increase in venous return appears to play a critical role in enhancing SV, CO, and MAP in patients with hypovolemic shock; these changes could be pivotal for reducing shock-mediated circulatory failure, promoting tissue perfusion, and improving patient outcomes. Trial registration: The phase IV trial reported in this study has Clinical Trials Registry, India; ctri.icmr.org.in, CTRI/2021/01/030263; clinicaltrials.gov, NCT05956418.
春雷喹能增加低血容量性休克患者的每搏容量和心输出量
背景:百服宁是一种复苏药物,可作用于α-2B肾上腺素能受体,促进低血容量休克患者的静脉回流。有关 centhaquine 对低血容量性休克患者心输出量的影响尚未见报道:方法:利用经胸超声心动图测量低血容量性休克患者在使用 centhaquine(0.01 mg/kg,静脉输注)之前(0 分钟)和之后的每搏输出量(SV)、心输出量(CO)、左室流出道-速度时间积分(LVOT-VTI)、左室流出道直径(LVOTd)、心率(HR)、左室射血分数(LVEF)、左室缩短分数(FS)和下腔静脉直径(IVC)。01 mg/kg,静脉输注 60 分钟)治疗前(60 分钟、120 分钟和 300 分钟)和治疗后(60 分钟、120 分钟和 300 分钟),随机挑选了 12 名低血容量休克患者,他们参加了一项关于 centhaquine 治疗低血容量休克患者的前瞻性、多中心、开放标签 IV 期临床研究(NCT05956418):结果:在使用 centhaquine 治疗 60 分钟、120 分钟和 300 分钟后,观察到 SV(毫升)明显增加。尽管心率在 120 分钟和 300 分钟时有所下降,但一氧化碳(毫升/分钟)在这两个时间段仍明显增加。在这些时间点观察到 IVC 直径和 LVOT-VTI(毫升)明显增加,这表明静脉回流增加。患者的 LVEF 和 FS 没有变化,而平均动脉压(MAP,mmHg)在使用 centhaquine 120 分钟和 300 分钟后有所增加。观察到 IVC 直径与 SV(R2 = 0.9556)之间以及 IVC 直径与 MAP(R2 = 0.8928)之间呈正相关,这表明仙喹介导的静脉回流增加对 SV、CO 和 MAP 有影响:结论:仙喹介导的静脉回流增加似乎在提高低血容量休克患者的 SV、CO 和 MAP 方面发挥了关键作用;这些变化对于减少休克介导的循环衰竭、促进组织灌注和改善患者预后至关重要:本研究中报告的 IV 期试验已在印度临床试验注册中心注册;ctri.icmr.org.in,CTRI/2021/01/030263;clinicaltrials.gov,NCT05956418。
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