Related Experiment Videos
Trigeminally induced cardiovascular reflex responses in spinalized rats.
S Ideguchi1, H Hotta, A Suzuki
1Department of Anesthesiology, Faculty of Dentistry, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan. ideguchi.dane@dent.med.tmd.ac.jp
Journal of the Autonomic Nervous System
|March 4, 2000
Summary
Noxious orofacial stimulation in spinalized rats increases heart rate via vagal nerve activity and blood pressure through vasopressin release, independent of direct sympathetic pathways.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Autonomic Nervous System Regulation
Background:
- Trigeminal nerve stimulation impacts cardiovascular functions.
- The role of the spinal cord in mediating these reflexes is not fully understood.
Purpose of the Study:
- To investigate the cardiovascular effects of orofacial noxious stimulation in rats with intact and spinalized (C2 level) spinal cords.
- To elucidate the neural pathways involved in these cardiovascular responses.
Main Methods:
- Experiments were conducted on urethane-anesthetized rats, both spinal cord-intact and acutely spinalized at the C2 level.
- Cardiovascular parameters including heart rate (HR) and mean arterial pressure (MAP) were monitored.
- Pharmacological interventions included bilateral vagotomy, methylatropine (muscarinic antagonist), and OPC-21268 (vasopressin V1 receptor antagonist).
Main Results:
- In spinal cord-intact rats, orofacial pinching increased HR and MAP, mediated by sympathetic efferent nerves.
- In C2-spinalized rats, HR increase was abolished by vagotomy or methylatropine, indicating vagal cholinergic involvement.
- MAP increase in spinalized rats was abolished by OPC-21268, suggesting vasopressin-mediated vasoconstriction.
Conclusions:
- Trigeminal nerve stimulation can elicit cardiovascular reflexes even after spinalization.
- Heart rate elevation is mediated by reduced vagal cholinergic activity.
- Blood pressure elevation is mediated by vasopressin release from the pituitary gland.