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| Year : 1985 | Volume
: 1
| Issue : 1 | Page : 4-10 |
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A review of the role of opioid peptides in vesicourethral function and the possible clinical use of opiate antagonists in patients with a neurogenic bladder due to acute and chronic spinal cord injuries.
AK Goswami, S Vaidyanathan, AK Goel, MS Rao, CM Pathak, K Rao, PL Sharma
Department of Urology, Postgraduate Institute of Medical Education and Research, Chandigarh-160012
Correspondence Address:
A K Goswami
Department of Urology, Postgraduate Institute of Medical Education and Research, Chandigarh-160012
 Source of Support: None, Conflict of Interest: None  | Check |
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Opioid peptides have recently been shown to control bladder reflexes by tonic enkephalinergic inhibitory mechanisms in both the brain and the spinal cord. Intraperitoneal administration of naloxone, an opiate antagonist, to ananesthetised chronic spinal cats enhanced reflex contraction of the urinary bladder and induced micturition. The effects of naloxone and thyrotropin-releasing hormone (TRH), another opioid antagonist devoid of the anti-nociceptive property, were investigated in patients with a neurogenic bladder due to acute and chronic spinal cord injuries. Naloxone (0.4 mg i.v.) decreased the intravesical volume at which detrusor reflex occurred from 498 to 346 ml in patients with chronic neurogenic bladder due to suprasacral spinal lesions. A significant rise in detrusor pressure during bladder distension (15 plus minus 6 cm H2O) and a decrease in compliance (17 plus minus 6 ml/cm H2O) were observed, following intravenous administration of 10 mg of naloxone to eight traumatic paraplegics in spinal shock. TRH (2 mg i.v.) produced a significant rise in detrusor pressure along with a significant decrease in bladder compliance in 7 patients with spinal cord injury during the spinal shock phase. A significant reduction in the intravesical volume at which the detrusor reflex occurred (113 plus minus 29 ml), together with a decrease in compliance by 3 plus minus 2 ml/cm H2O was observed in six patients with chronic neurogenic bladder following 2 mg of TRH administered intravenously. The plasma beta-endorphin levels in six cases of spinal cord injury during the spinal shock phase was 28.7 plus minus 3.53 pmol/l as compared to 5 less than pmol/l in the adult healthy volunteers in this laboratory. TRH (2 mg i.v.) decreased plasma beta endorphin level to 6.3 plus minus 1.49 pmol/l at 120 min in the spinal cord-injured. In conclusion, opioid antagonists, naloxone and TRH hold promise in facilitating detrusor contraction in patients of both acute and chronic spinal cord injuries. |
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