Protective effect of CDP-choline on hypotension and tissue injury in septic shock model

Abstract

Summary: CDP-choline is an endogen molecule and also a drug that is used in several trauma and ischemic conditions. It has been demonstrated that it improves the hemodynamic parameters in different shock models and prevents tissue damage in rats. The current study tested the effect of CDP-choline on hypotension, inflammation and tissue injury induced by septic shock model in rats. Twenty-four adult, male Spraque-Dawley rats, weighing 250-300 g were used. Septic shock was induced by cecal ligation-incision (CLI). CDP-choline (100 mg/kg) injected intravenously (i.v.) at the 180 th minute of the experiment. The animals were observed for 180 minutes after the injection, then blood and tissue samples were obtained for cytokine measurements and histological examinations, respectively. The cecal ligation-incision decreased arterial pressure and increased heart rate. Intravenous injection of CDP-choline reversed hypotension and increased arterial pressure up to control levels within the first 60 minutes without changing the increase in heart rate. The effect lasted for 3 hours. CDP-choline attenuated the increases in TNF-α, IL-1β and IL-6 levels in septic shock. Moreover, the drug exerted protective effects for the injury induced by septic shock in lungs, liver and kidney tissues; whereas this effect was not present on spleen. In conclusion, the present data suggested that intravenous CDP-choline administration can improve the deteriorations in hemodynamic and inflammatory parameters and can prevent the tissue injury in septic shock-induced by CLI in rats.

Plausible use of citicoline as an adjuvant in central nervous system infections: A case report and review of the literature

“…As previously demonstrated, in a murine model of septic shock, induced by cecal ligation-incision, citicoline intravenous injection at a dose of 100 mg/kg at the 180th min after shock induction is capable of reversing hypotension and recovering arterial pressure to control levels in 60 min after the injection. This appeared to be due to the attenuation in TNF-α, IL-1β and IL-6 levels (43). Cecal ligation and puncture was also used in cyclophilin D knockout (CypD KO) mice in order to research whether the mitochondrial permeability transition pore (MPTP), whose induction sensitivity is controlled by CypD, causes neuronal dysfunction, apoptosis and cell death in sepsis-associated encephalopathy (SAE).…”