부산대학교 도서관

The aims of this study were to examine effects of urinary bladder distension (UBD) on T3–T4 spinal neurons receiving cardiac and somatic noxious inputs and to determine the pathway involved in transmitting urinary bladder inputs to thoracic spinal segments. Extracellular potentials of single T3–T4 neurons were recorded in pentobarbital anesthetized male rats. Either bradykinin solution (10−5 M) or an algogenic mixture (adenosine 10−3 M, bradykinin, histamine, serotonin, prostaglandin E2 10−5 M each) was administered intrapericardially. UBD was produced by saline inflation (0.5–2.0 ml, 20 s). Of 487 neurons tested for responses to UBD, 70 were inhibited and 37 were excited. Seventy-six out of 336 neurons received convergent input from UBD and heart; 69/76 viscerovisceral convergent neurons had somatic fields. Spinal transection at rostral C1 abolished UBD inhibition in 5/9 neurons; whereas transections at L1–L2 abolished UBD inhibition in 3/3 cells tested. Results showed that T3–T4 spinal neurons processing cardiac and somatic nociceptive information were primarily inhibited by input from the urinary bladder through either supraspinal structures or direct intraspinal pathways. [Copyright &y& Elsevier]