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The dopaminergic system is able to modulate the central histamine-induced pressor effect in hemorrhage-shocked rats
1
Department of Physiology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, Katowice, Poland
2
Faculty of Medicine, Wroclaw Medical University, Poland
3
Dipartimento di Scienze Biomediche, Metaboliche e Neuroscienze, Sezione di Farmacologia e Medicina Molecolare, Università di Modena e Reggio Emilia, Modena, Italy
Corresponding author
Jerzy Jochem
Katedra i Zakład Fizjologii, Wydział Nauk Medycznych w Zabrzu ŚUM, ul. Jordana 19, 41-808 Zabrze
Katedra i Zakład Fizjologii, Wydział Nauk Medycznych w Zabrzu ŚUM, ul. Jordana 19, 41-808 Zabrze
Ann. Acad. Med. Siles. 2025;79:418-424
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Histamine administered intracerebroventricularly (icv) induces a resuscitating effect in hemorrhage-shocked rats. Dopamine receptors are present in neuronal pathways involved in central cardiovascular regulation; therefore, the aim of the study was to examine the effects of pre-treatment with dopamine receptor antagonists on histamine-induced cardiovascular effects in hemorrhagic shock.
Material and methods:
Male Wistar rats subjected to a reversible hemorrhagic hypotension with mean arterial pressure (MAP) of 30–35 mmHg were anaesthetized with ketamine/xylazine (100 mg/kg + 10 mg/kg, intraperitoneally). Immediately after bleeding terminated, the animals were pre-treated icv with dopamine receptor antagonists or saline; 5 min later they were treated icv with histamine (50 nmol) or saline.
Results:
Hemorrhagic hypotension was accompanied by decreases in pulse pressure (PP), heart rate (HR), and mesenteric blood flow (MBF). Histamine induced increases in MAP, HR, and MBF, with a decrease in PP as compared to the control group. Pre-treatment with the dopamine D4 receptor antagonist L-745,870 potentiated histamine-induced MAP and MBF changes, with no influence on PP or HR. There were neither the influence of the other dopamine receptor antagonists on histamine-mediated action nor the effects of dopamine receptor antagonists given alone in the control groups.
Conclusions:
Dopamine, acting via D4 receptors, is able to modulate the central histamine-induced pressor effect in hemorrhage-shocked rats.
Histamine administered intracerebroventricularly (icv) induces a resuscitating effect in hemorrhage-shocked rats. Dopamine receptors are present in neuronal pathways involved in central cardiovascular regulation; therefore, the aim of the study was to examine the effects of pre-treatment with dopamine receptor antagonists on histamine-induced cardiovascular effects in hemorrhagic shock.
Material and methods:
Male Wistar rats subjected to a reversible hemorrhagic hypotension with mean arterial pressure (MAP) of 30–35 mmHg were anaesthetized with ketamine/xylazine (100 mg/kg + 10 mg/kg, intraperitoneally). Immediately after bleeding terminated, the animals were pre-treated icv with dopamine receptor antagonists or saline; 5 min later they were treated icv with histamine (50 nmol) or saline.
Results:
Hemorrhagic hypotension was accompanied by decreases in pulse pressure (PP), heart rate (HR), and mesenteric blood flow (MBF). Histamine induced increases in MAP, HR, and MBF, with a decrease in PP as compared to the control group. Pre-treatment with the dopamine D4 receptor antagonist L-745,870 potentiated histamine-induced MAP and MBF changes, with no influence on PP or HR. There were neither the influence of the other dopamine receptor antagonists on histamine-mediated action nor the effects of dopamine receptor antagonists given alone in the control groups.
Conclusions:
Dopamine, acting via D4 receptors, is able to modulate the central histamine-induced pressor effect in hemorrhage-shocked rats.
FUNDING
The study was supported by a grant (KNW-1-063/N/8/0) from the Medical University of Silesia, Katowice, Poland.
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