ArticleExperimental and therapeutic medicine2018
Cholecystokinin octapeptide inhibits the inflammatory response and improves neurological outcome in a porcine model of cardiopulmonary resuscitation.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Vitamin C Improves the Outcomes of Cardiopulmonary Resuscitation and Alters Shedding of Syndecan-1 and p38/MAPK Phosphorylation in a Rat Model.Journal of the American Heart Association · 2022Article
- Hypothermia for Cardioprotection in Patients with St-Elevation Myocardial Infarction: Do Not Give It the Cold Shoulder Yet!Journal of clinical medicine · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that cholecystokinin octapeptide (CCK8) induces hypothermia and inhibits the systemic inflammatory response in septic shock in rat and murine models. The present study aimed to ascertain whether CCK8 induced hypothermia and improved the neurological outcomes in a porcine model of cardiopulmonary resuscitation (CPR). Ventricular fibrillation was induced and left untreated for 10 min in 12 male Bama miniature pigs. Defibrillation was attempted after 5 min of CPR. At 5 min following resuscitation, the pigs were randomized and equally assigned into the CCK8 or the control group. CCK8 was continuously infused for 1 h at a dose of 44.4 µg/kg/h and a rate of 20 ml/h in the CCK8 group. Body temperature, hemodynamic measurements and post-resuscitation myocardial function were monitored in the first 4 h following CPR. Neuron specific enzyme (NSE), S100B protein, tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured at baseline and 4, 12 and 24 h following resuscitation. The neurological deficient score (NDS) was recorded and cerebral samples were collected for terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling assay and integrated optical density (IOD) analysis at 24 h following CPR. The results revealed that hypothermia was not induced by CCK8; however, post-resuscitation NSE, S100B, IL-6 and TNF-α were significantly decreased, and NDS and IOD were significantly improved in the CCK8 group compared with the control group (P<0.05). The present study revealed that in a porcine model of CPR, CCK8 does not induce hypothermia, but inhibits the inflammatory response and significantly improves neurological outcomes.
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