Lahlou S, Demenge P
Laboratoire de Physiologie et Pharmacologie, URA CNRS 1287, Faculté de Pharmacie, Université Joseph Fourier, La Tronche, France.
Cardiovasc Res. 1993 Feb;27(2):222-30. doi: 10.1093/cvr/27.2.222.
The cardiovascular responses to transient intrathecal administration of dopamine agonists were studied daily in chronically prepared rats that had been spinally transected or were sham operated. The goals were (1) to determine the group differences in evoked heart rate and arterial pressure responses and (2) to determine, within the transected group, whether or not the long term responses could be dissociated. The hypothesis tested is that cord transection releases a tonic inhibition of cardiovascular responsiveness independently of the mechanism of receptor hypersensitivity.
Changes in mean aortic blood pressure and heart rate induced by intrathecal administration of the mixed D1/D2 dopamine receptor agonist apomorphine (150 nmol per rat) were measured in conscious rats during a 10 d experimental period following spinal transection.
Complete spinal transection did not affect aortic pressure but increased basal heart rate values by about 33% with respect to normal rats (p < 0.001). When apomorphine was injected caudally to the section (at T9-T10) but not rostrally (at T2-T4), it induced a 50% greater and an 800% more long lasting decrease in mean aortic pressure and a 230% greater and 70% more long lasting decrease in heart rate in spinal than in sham operated rats. These increases in cardiovascular responses were corroborated by a leftward shift of the apomorphine dose-response curves. They were also found after intrathecal administration of highly selective D1 and D2 receptor agonists fenoldopam (50 nmol per rat) and quinpirole (150 nmol per rat), and were specifically blocked by intrathecal haloperidol (27 nmol per rat), a non-selective dopamine antagonist.
Complete spinal transection induces different increases in hypotensive and bradycardic responses to the stimulation of caudally located spinal dopamine receptors which could be due to the destruction of a tonically inhibiting spinal system rather than to hypersensitivity of the dopamine receptors.
在长期制备的脊髓横断或假手术大鼠中，每日研究对鞘内注射多巴胺激动剂的心血管反应。目标是：（1）确定诱发心率和动脉压反应的组间差异；（2）在横断组内确定长期反应是否可以分离。所检验的假设是脊髓横断可独立于受体超敏机制释放对心血管反应性的紧张性抑制。
在脊髓横断后的10天实验期内，测量清醒大鼠鞘内注射混合的D1/D2多巴胺受体激动剂阿扑吗啡（每只大鼠150 nmol）所诱导的平均主动脉血压和心率变化。
完全脊髓横断不影响主动脉压，但与正常大鼠相比，基础心率值增加约33%（p < 0.001）。当在脊髓节段尾侧（T9 - T10）而非头侧（T2 - T4）注射阿扑吗啡时，与假手术大鼠相比，脊髓损伤大鼠的平均主动脉血压降低幅度大50%且持续时间长800%，心率降低幅度大230%且持续时间长70%。阿扑吗啡剂量 - 反应曲线左移证实了这些心血管反应的增强。在鞘内注射高选择性D1和D2受体激动剂非诺多泮（每只大鼠50 nmol）和喹吡罗（每只大鼠150 nmol）后也发现了这种情况，并且可被鞘内注射非选择性多巴胺拮抗剂氟哌啶醇（每只大鼠27 nmol）特异性阻断。
完全脊髓横断导致对尾侧脊髓多巴胺受体刺激的降压和心动过缓反应出现不同程度的增强，这可能是由于紧张性抑制脊髓系统的破坏而非多巴胺受体超敏所致。
