The effect of Lipo prostaglandin E1 on cauda equina blood flow in patients with lumbar spinal canal stenosis: myeloscopic observation

Yone, Kazunori; Sakou, Takashi; Kawauchi, Yoshihisa

doi:10.1038/sj.sc.3100780

Cited by 34 publications

(16 citation statements)

References 8 publications

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“…Since it can be assumed that the impaired intraradicular blood flow is improved by the drug in patients whose NIC responds to administration of PGE1, this agent can be used for screening and staging of the disease. Yone et al [82] have reported that when lipo-PGE1 was injected intravenously in 11 LCS patients during surgery, symptoms were alleviated in 6 patients with dilation of vessels running along the cauda equina, but not in 5 patients with no change of their vessels. Dezawa et al [83] observed the movement of red blood increased intraradicular blood flow in the normal nerve root without compression, but the increase of blood flow observed in the compressed region of the nerve root exhibiting Wallerian degeneration was transient and not sustained (Figures 10 and 11).…”

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confidence: 99%

Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis

Kobayashi

2014

WJO

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Spinal nerve roots have a peculiar structure, different from the arrangements in the peripheral nerve. The nerve roots are devoid of lymphatic vessels but are immersed in the cerebrospinal fluid (CSF) within the subarachnoid space. The blood supply of nerve roots depends on the blood flow from both peripheral direction (ascending) and the spinal cord direction (descending). There is no hypovascular region in the nerve root, although there exists a so-called water-shed of the bloodstream in the radicular artery itself. Increased mechanical compression promotes the disturbance of CSF flow, circulatory disturbance starting from the venous congestion and intraradicular edema formation resulting from the breakdown of the blood-nerve barrier. Although this edema may diffuse into CSF when the subarachnoid space is preserved, the endoneurial fluid pressure may increase when the area is closed by increased compression. On the other hand, the nerve root tissue has already degenerated under the compression and the numerous macrophages releasing various chemical mediators, aggravating radicular symptoms that appear in the area of Wallerian degeneration. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis. However, investigations in the clinical setting have shown that PGE1 is effective in some patients but not in others, although the reason for this is unclear.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Lumbar canal stenosis; Cauda equine; Nerve root; Prostaglandin E1; Blood flow Core tip: The radicular symptoms associated with degenerative disease of the lumbar spine are reported to be attributable to a combination of mechanical nerve root compression and resultant circulatory disturbance. Disturbance of blood flow in the cauda equina and nerve roots is reported to play an important role in the mechanism of intermittent claudication in patients with lumbar canal stenosis. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis with intermittent claudication. However, investigations in the clinical setting have shown that lipo-PGE1 is effective in some patients but not in others, although the reason for this is unclear.Kobayashi S. Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis. World

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confidence: 99%

Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis

Kobayashi

2014

WJO

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“…Thus, compared with PTH, which cannot be administered orally due to its peptide nature, EP4A may be superior in terms of possible clinical oral use in the patients. Several forms of PG drugs have already been used in the clinical setting such as those to increase circulation in the case of obstructive arteritis (Makita et al 1997) or lumbar canal stenosis (Yone et al 1999). Together, these observations suggest that orally administrated EP4A may be safe and effective in combination with inhibition of OPN action.…”

Section: Discussionmentioning

confidence: 66%

Osteopontin deficiency enhances anabolic action of EP4 agonist at a sub-optimal dose in bone

Kato

Kitahara

Rittling³

et al. 2007

Journal of Endocrinology

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Osteoporosis is one of the most widespread and destructive bone diseases in our modern world. There is a great need for anabolic agents for bone which could reverse this disease, but few are available for clinical use. Prostaglandin E receptor (EP4) agonist (EP4A) is one of the very few anabolic agents for bone in rat, but its systemic efficacy against bone loss at sub-optimal dose is limited in mice. As osteoblasts are regulated by extracellular matrix proteins, we tested whether deficiency of osteopontin (OPN), a secreted phosphorylated protein, could modulate the effects of EP4A (ONO-AE1-329) treatment at 30 mg/kg body weight, a sub-optimal dose, for 5 days/week for 4 weeks. OPN deficiency enhanced the anabolic effects of EP4A on bone volume.Histomorphometric analysis indicated that EP4A increased mineral apposition rate as well as bone formation rate in OPN-deficient but not in wild-type mice. Neither OPN deficiency nor EP4A altered osteoclast parameters. Importantly, OPN deficiency enhanced the direct anabolic action of EP4A locally injected onto the parietal bone in inducing new bone formation. Combination of OPN deficiency and EP4A treatment caused an increase in mineralized nodule formation in the cultures of bone marrow cells. Finally, OPN deficiency enhanced anabolic action of EP4A in the mice subjected to ovariectomy. These data indicate that OPN deficiency enhances the actions of EP4A at sub-optimal dose.

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“…Several authors have reported that PGE1 also enhanced blood ow in the cauda equina. 22,23 Upon consideration of these facts, we believe that PGE1 may be e ective in simultaneously reducing hypertension and restoring spinal blood¯ow.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of spinal cord blood flow during prostaglandin E1-induced hypotension with power Doppler ultrasonography

et al. 2001

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Study design: Intraoperative power Doppler ultrasonography was used to evaluate the spinal cord blood¯ow in cervical spondylotic myelopathy patients during hypotensive anesthesia. Objective: To evaluate the e ect of prostaglandin E1 (PGE1) induced hypotension on spinal cord blood¯ow (SBF) during spinal surgery. Summary and background data: Hypotension is frequently induced to decrease blood loss during surgery and to diminish the need for blood transfusion. Prostaglandin E1 (PGE1) is reported to maintain cerebral, liver, and renal blood¯ow during surgery. However, there are few reports on spinal cord blood¯ow. Methods: Eleven patients underwent laminoplasty for cervical spondylotic myelopathy. After a French door type laminoplasty was carried out, hypotension was induced with PGE1. Before and during hypotension, we evaluated blood¯ow in the anterior spinal cord artery by determining the pulsatility index (PI) and resistance index (RI) using power Doppler ultrasonography. Results: Before hypotension, the mean blood pressure was 80 mmHg. The blood pressure decreased to 60 mmHg using PGE1 (P50.01), although the PI and RI were signi®cantly higher than before hypotension (PI, P=0.0076 RI, P=0.02). Conclusion: The pulsatility and resistance indices during hypotension were signi®cantly higher than before hypotension, suggesting that the autoregulation of the anterior spinal cord artery and anterior spinal cord blood¯ow were maintained with hypotension using PGE1. Prostaglandin E1 may be a useful drug for hypotensive anesthesia in spinal surgery. Spinal Cord (2001) 39, 31 ± 36

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The effect of Lipo prostaglandin E1 on cauda equina blood flow in patients with lumbar spinal canal stenosis: myeloscopic observation

Cited by 34 publications

References 8 publications

Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis

Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis

Osteopontin deficiency enhances anabolic action of EP4 agonist at a sub-optimal dose in bone

Evaluation of spinal cord blood flow during prostaglandin E1-induced hypotension with power Doppler ultrasonography

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