Effects of Ulinastatin on Myocardial Ischemia-Reperfusion Injury, Cardiac Function, and Serum TNF-α and IL-10 Levels in Patients Undergoing Cardiac Valve Replacement under Cardiopulmonary Bypass

Abstract

Background. Myocardial ischemia-reperfusion injury (MIRI) is a very common adverse reaction after cardiac valve replacement (CVR) under cardiopulmonary bypass, which seriously affects the rehabilitation and prognosis of patients. Objective. The prevention and treatment of MIRI are a hotspot of modern medical research, and this study is aimed at providing reliable reference and guidance for future clinical prevention and treatment of MIRI by analyzing the effects of ulinastatin (UL) on cardiac function and MIRI of patients after CVR. Methods. A total of 104 patients undergoing CVR under cardiopulmonary bypass in our hospital were selected as research participants. Among them, 52 patients treated with UL were assigned to the observation group, and the rest 52 patients given the same amount of normal saline were assigned to the control group. The cardiopulmonary bypass status, postoperative status, cardiac function, inflammatory response, oxidative stress response, and hemodynamics were observed and compared between the two groups. In addition, clinical efficacy and safety and patient prognosis were compared. Results. Through experimental analysis, we found that UL had no significant effect on the clinical efficacy, safety, and prognosis of patients after surgery ( P > 0.05 ) but had obvious protective effects on cardiopulmonary bypass status, cardiac function, inflammation, oxidative stress, and hemodynamics ( P < 0.05 ). Conclusion. UL can effectively prevent the occurrence of MIRI after CVR under cardiopulmonary bypass, which is worthy of clinical application.

Ulinastatin Improves Endothelial Cells Injury, Attenuating Cardiac Ischemia/Reperfusion Injury via Suppressing Tissue kallikrein-kinin System Activation

“…Endothelial dysfunction and inflammatory response are crucial hallmarks of the pathophysiology of cardiac IRI [30]. UTI, a proteinase inhibitor with anti-inflammatory properties, has been shown to be beneficial for patients undergoing CABG surgery [15,16]. Here, we extended insights into reperfusion-induced endothelial barrier dysfunction and established an interlink among UIT, the KKS, EC injury and inflammation in response to cardiac reperfusion for the first time.…”

Ulinastatin Ameliorates Cardiac Ischemia/Reperfusion Injury via Inhibiting the tissue kallikrein-kinin system

“…We hypothesized that UIT might reduce cardiac damage in response to reperfusion injury since UIT can improve cardiac blood vessel barrier function, alleviate cardiac edema formation, and protect against heart failure 15, 16 . First, we determined the cardioprotective effect of UIT in vivo in a mouse acute cardiac I/R model with 45 minutes of ischemia followed by 24 hours of reperfusion ( Figure 1A ) and found that the infarct size relative to the area at risk (INF/AAR) in mice treatment of UIT (before the onset of reperfusion) decreased from 71.0±3.1% to 23.5±3.0%, concomitantly with similar AARs ( Figure 1B-D ).…”

“…UTI can suppress various serine proteases and protect EC against neutrophil-mediated injury 14 . Moreover, recent studies have found that UTI protects against I/R 15, 16 and may be favorable for those patients undergoing cardiac surgery with cardiopulmonary bypass 17 . However, the current understanding of the role of UIT on cardiac I/R is limited.…”

Ulinastatin ameliorated streptozotocin-induced diabetic nephropathy: Potential effects via modulating the components of gut-kidney axis and restoring mitochondrial homeostasis

“…Ulinastatin, a urinary trypsin inhibitor (UTI), is a glycoprotein derived from human urine. Due to its inhibitory effect on cytokines and other proinflammatory mediators, UTI was used in many clinical trials to treat patients with acute pancreatitis [ 17 ] and protecting kidneys in patients with septic shock [ 41 ] and ischemia [ 40 ]. Furthermore, because of its anti-inflammatory properties, UTI may have had beneficial effects on the gut barrier in the early stages of sepsis [ 20 ] as well as on isoflurane-induced cell apoptosis and mitochondrial damage in vitro [ 24 ].…”