We aimed to established an interlink among the kallikrein-kinin system (KKS), endothelial dysfunction and cardiac inflammation in response to cardiosurgery , using clinic investigation.
The KKS, which is located on the vascular endothelium, plays a pivotal role in maintaining cardiovascular homeostasis. Tissue kallikrein (TK), a serine protease and a key enzyme of the KKS, is responsible for cleaving low-molecular-weight kininogen into bradykinin and kallidin. Under normal physiological conditions, the activation of the B2 receptor (B2R)/endothelial nitric oxide synthase (eNOS) signaling pathway leads to the transient release of nitric oxide (NO), resulting in cardiovascular protection. However, during reperfusion injury, the activation of the B1 receptor (B1R)/inducible nitric oxide synthase (iNOS) pathway leads to excessive NO production, promoting inflammation and cellular injury. Therefore, it is hypothesized that the KKS plays a critical role in the early stages of reperfusion injury during cardiac surgery with cardiopulmonary bypass.
Study Type
OBSERVATIONAL
Enrollment
308
Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
Wuhan, Hubei, China
survival
survival and KKS related factors levels
Time frame: 24 hours
Cardiac function
echocardiography and Myo-cardial enzymonram
Time frame: 24 hours
POD-postoperative delirium
Confusion Assessment Method for the ICU (CAM-ICU)
Time frame: 7 days
survival
survival and clinical symptom
Time frame: 28 days
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.