Centrally acting cholecystokinin induces depressor circulatory effects in haemorrhage-shocked rats
 
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1
Katedra i Zakład Fizjologii, Wydział Nauk Medycznych w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach
 
2
Wydział Lekarski, Uniwersytet Medyczny im. Piastów Śląskich we Wrocławiu
 
 
Corresponding author
Jerzy Jochem   

Katedra i Zakład Fizjologii, Wydział Nauk Medycznych w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach, ul. Jordana 19, 41-808 Zabrze
 
 
Ann. Acad. Med. Siles. 2021;75:18-23
 
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Cholecystokinin (CCK) is a peptide gastrointestinal hormone involved in the stimulation of lipid and protein digestion as well as a neurotransmitter/neuromodulator in the central nervous system. After intravenous administration, it induces a resuscitating effect in rats subjected to haemorrhagic shock. Since CCK is able to directly and indirectly affect the cardiovascular centre function, the aim of the study was to examine the action of the sulphated octapeptide form of CCK (CCK-8) given intracerebroventricularly (icv) in the sympathoinhibitory phase of haemorrhagic shock.

Material and methods:
Studies were carried out in male Wistar rats anaesthetized with ketamine/xylazine (100 mg/kg + 10 mg/kg, intramuscularly) and subjected to irreversible haemorrhagic shock (0% survival at 2 h) with a mean arterial pressure (MAP) of 20–25 mmHg. At 5th min of critical hypotension, the rats were injected icv with CCK-8 (5, 15 nmol) or saline (5 μl).

Results:
Haemorrhage led to a decrease in pulse pressure (PP), heart rate (HR) as well as increases in renal (RVR) and mesenteric vascular resistance (MVR). In the control group injected with saline, there were no significant increases in the measured cardiovascular parameters, and the survival time was 32.5 ± 5.1 min. CCK-8 induced dose-dependent decreases in MAP, PP and HR accompanied by increases in RVR and MVR, and also shortened the survival time in comparison to the control animals.

Conclusions:
Centrally acting CCK-8 induces depressive circulatory effects in haemorrhage-shocked rats.

FUNDING
This research was supported by the Medical University of Silesia, Katowice grant (KNW-1-035/N/7/O).
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