ﺯﻣﻴﻨﻪ ﻭ ﻫﺪﻑ: ﻣﻄﺎﻟﻌـﺎﺕ ﺗﺠـﺮﺑﻲ ﻧﺸﺎﻥ ﻣﻲ ﺩﻫـﺪ ﻛﻪ ﺩﺭ ﻣﻴﻠﻮﻣﻨﻨﮕﻮﺳﻞ ﺿﺎﻳﻌﺔ ﺣﺎﺻﻠﻪ، ﺍﺧﺘﻼﻝ ﺍﻭﻟﻴﻪ ﻋﺼﺒﻲ ﻧﻴﺴﺖ ﺑﻠﮑﻪ ﺁﺳﻴﺐ ﺍﻛﺘﺴﺎﺑﻲ ﺑﺎﻓـﺖ ﻋﺼﺒﻲ ﻭ ﻧﺎﺷﻲ ﺍﺯ ﺗﻤـﺎﺱ ﺑﺎﻓﺖ ﻋﺼﺒﻲ ﻧﺨﺎﻉ ﺑﺎ ﻣﺎﻳﻊ ﺁﻣﻨﻴﻮﺗﻴﻚ ﻣﻲ ﺑﺎﺷﺪ. ﺩﺭ ﻣﻄﺎﻟﻌﺔ ﺣﺎﺿﺮ ﺗﺄﺛﻴـﺮ ﻣﺎﻳﻊ ﺁﻣﻨﻴﻮﺗﻴﻚ ﺑﺮ ﺗﻐﻴﻴـﺮﺍﺕ ﻫﻴﺴﺘﻮﭘﺎﺗﻮﻟـﻮﮊﻳﻚ ﻧﺨﺎﻉ ﺟﻨﻴﻦ ﮔـﻮﺳﻔﻨﺪ ﻣﺒﺘﻼ ﺑﻪ
ﻣﻴﻠﻮﻣﻨﻨﮕـﻮﺳﻞ ﺑﺮﺭﺳﻲ ﻣﻲ ﺷﻮﺩ.
ﻣﻮﺍﺩ ﻭ ﺭﻭﺵ ﻫﺎ: ﺩﺭ ﻳﻚ ﻣﻄﺎﻟﻌﺔ ﺗﺠـﺮﺑﻲ ﺑﺎﻟﻴﻨﻲ 10 ﺟﻨﻴﻦ ﮔﻮﺳﻔﻨﺪ ﺩﺭ ﺩﻭ ﮔﺮﻭﻩ 5 ﺗﺎﻳﻲ ﻣـﻮﺭﺩ ﻭ ﺷﺎﻫـﺪ ﺑﺮﺭﺳﻲ ﺷﺪﻧﺪ. ﺑﺎ ﺍﺳﺘﻔﺎﺩﻩ ﺍﺯ ﺟﺮﺍﺣﻲ ﺟﻨﻴﻦ ﺩﺭ ﺭﻭﺯ 90-
100 ﺣﺎﻣﻠﮕﻲ ﮔﻮﺳﻔﻨﺪ )150 -145 ﺭﻭﺯ ﻃﻮﻝ ﺣﺎﻣﻠﮕﻲ(، ﺩﺭ ﻧﺎﺣﻴﺔ ﻛﻤﺮﻱ ﺩﺭ ﺳﻄﺢ L2-L4 ﻻﻣﻴﻨﻜﺘـﻮﻣﻲ ﺍﻧﺠﺎﻡ ﻭ ﺩﻭﺭﺍﻣﺘـﺮ ﺑﺎﺯ ﺷﺪ. ﺩﺭ ﮔﺮﻭﻩ ﻣﻮﺭﺩ ﺩﻳﻔﻜـﺖ ﺑﺎﺯ ﮔـﺬﺍﺷﺘﻪ ﺷﺪ ﺗﺎ ﻧﺨـﺎﻉ ﺩﺭ ﻣﻌـﺮﺽ ﻣﺎﻳﻊ ﺁﻣﻨﻴﻮﺗﻴﻚ ﻗﺮﺍﺭ ﮔﻴﺮﺩ ﻭ ﺩﺭ ﮔﺮﻭﻩ ﺷﺎﻫﺪ ﺑﻼﻓﺎﺻﻠﻪ ﭘﻮﺳﺖ ﺭﻭﻱ ﺩﻳﻔﻜﺖ ﺗﺮﻣﻴـﻢ ﺷﺪ. ﭘﺲ ﺍﺯ ﺍﻧﺠﺎﻡ ﺳﺰﺍﺭﻳﻦ ﻧﺰﺩﻳﻚ ﺗﺮﻡ، ﻧـﻮﺯﺍﺩﺍﻥ ﺗﺤﺖ ﺍﺭﺯﻳﺎﺑﻲ ﻫﺎﻱ ﺑﺎﻟﻴﻨﻲ ﻭ ﻣﻮﺭﻓﻮﻟﻮﮊﻳﻚ )ﭘﺎﺭﺍﭘﻠﮋﻱ ﻭ ﭘﺎﺭﺍﭘﺎﺭﺯﻱ ـ ﺑﻲ ﺍﺧﺘﻴـﺎﺭﻱ ﺩﻓـﻊ ﺍﺩﺭﺍﺭ ﻭ ﻣـﺪﻓﻮﻉ ﻭ ﭘﺎﺗﻮﻟـﻮﮊﻱ ﻧﺨـﺎﻉ ﻭ ﻋﻀﻼﺕ ﺍﺳﻔﻨﻜﺘﺮﻳﮏ ﻣﻘﻌـﺪ ﻭ
ﺭﮐﺘﻮﻡ ﻭ ﺭﺍﻥ( ﻗﺮﺍﺭ ﮔﺮﻓﺘﻨﺪ.
ﻳﺎﻓﺘﻪ ﻫﺎ: ﺩﺭ ﺍﺭﺯﻳﺎﺑﻲ ﺑﺎﻟﻴﻨﻲ ﺩﺭ ﮔـﺮﻭﻩ ﻣﻮﺭﺩ )5 ﺑﺮﻩ( ﻫﻤﻪ ﻧﻮﺯﺍﺩﺍﻥ ﺩﭼﺎﺭ ﭘﺎﺭﺍﭘﻠﮋﻱ ﻳﺎ ﭘﺎﺭﺍﭘﺎﺭﺯﻱ، ﺑﻲ ﺍﺧﺘﻴﺎﺭﻱ ﺍﺩﺭﺍﺭ ﻭ 4 ﻣﻮﺭﺩ ﺩﭼﺎﺭ ﺑﻲ ﺍﺧﺘﻴﺎﺭﻱ ﻣـﺪﻓﻮﻋﻲ ﺑﻮﺩﻧﺪ ﺩﺭ
ﺣﺎﻟﻴﻜﻪ ﺩﺭ ﮔﺮﻭﻩ ﺷﺎﻫﺪ ﻓﻘﻂ ﻳﻚ ﻣﻮﺭﺩ ﭘﺎﺭﺍﭘﺎﺭﺯﻱ ﻭﺟﻮﺩ ﺩﺍﺷﺖ )0/048=P( ﻭ ﺗﻤﺎﻡ ﻧﻮﺯﺍﺩﺍﻥ ﺍﺧﺘﻴﺎﺭ ﺩﻓﻊ ﻣﺪﻓﻮﻉ )0/04=P( ﻭ ﺍﺩﺭﺍﺭ )0/008=P( ﺩﺍﺷﺘﻨﺪ.
ﺩﺭ ﮔﺮﻭﻩ ﻣﻮﺭﺩ ﺩﺭ ﺗﻤﺎﻡ ﻧﻮﺯﺍﺩﺍﻥ ﻋﻀﻼﺕ ﻃﻮﻟﻲ ﺭﻛﺘﻮﻡ، ﻋﻀﻼﺕ ﺍﺳﻔﻨﻜﺮﻳﻚ ﻭ ﺭﺍﻥ ﺗﻜﺎﻣﻞ ﻛﺎﻣﻞ ﻧﺪﺍﺷﺘﻪ ﻭ ﺩﺭﺟـﺎﺗﻲ ﺍﺯ ﺁﺗﺮﻭﻓﻲ ﺩﺍﺷﺘﻨﺪ ﻭﻟﻲ ﺩﺭ ﮔﺮﻭﻩ ﺷﺎﻫﺪ
ﺗﻤﺎﻡ ﻧﻮﺯﺍﺩﺍﻥ ﺗﻜﺎﻣﻞ ﻧﺮﻣﺎﻝ ﻋﻀﻼﺕ ﻓﻮﻕ ﺭﺍ ﺩﺍﺷﺘﻨﺪ 0/008=P(.
ﺗﻐﻴﻴﺮﺍﺕ ﻫﻴﺴﺘﻮﭘﺎﺗﻮﻟﻮﮊﻳﻚ ﻧﺨﺎﻉ ﺷﺎﻣﻞ ﺍﺩﻡ ـ ﻛﻠﺴﻴﻔﻴﻜﺎﺳﻴﻮﻥ ﻓﻮﻛﺎﻝ، ﻓﻴﺒﺮﻭﺯ ﻭ ﭘﺮﻭﻟﻴﻔﺮﺍﺳﻴﻮﻥ ﺳﻠﻮﻝ ﻣﻮﻳﺮﮔﻲ ﺩﺭ ﮔﺮﻭﻩ ﻣﻮﺭﺩ ﻭﺟﻮﺩ ﺩﺍﺷﺖ ﻛﻪ ﺩﺭ ﮔـﺮﻭﻩ ﺷﺎﻫﺪ
ﻣﺸﺎﻫﺪﻩ ﻧﺸﺪ. ﺗﻌـﺪﺍﺩ ﺳﻠﻮﻝ ﻫﺎﻱ ﮔﺎﻧﮕﻠﻴـﻮﻧﻲ ﻧﺨﺎﻉ ﺩﺭ ﮔﺮﻭﻩ ﺷﺎﻫﺪ ﺑﻄﻮﺭ ﻗﺎﺑﻞ ﺗﻮﺟﻬﻲ ﺑﺎﻻﺗﺮ ﺍﺯ ﮔﺮﻭﻩ ﻣﻮﺭﺩ ﺑﻮﺩ )0005 /0
چكيده لاتين :
ntroduction & Objective: Experimental studies in myelomeningocele (MMC) suggested that the primary malformation is not neural but neural tissue damage is acquired as a result of exposure of neural tissue to amniotic fluid (AF). In this study the effects of amniotic fluid on spinal cord and histopathologic changes in fetal sheep with MMC were evaluated.
Materials & Methods: In an experimental clinical trial,10 fetal sheep in two group 5 cases and 5 controls were studied. In sheep at 90-100 days gestational age (term = 145-150 days) in lumbar area skin and paraspinal soft tissues excised and laminectomy was the performed at L2 – L4 and we opened duramater. In case group fetal sheep was dorsally with nonclosed dura and thus with open exposure of the spinal cord to amniotic fluid (AF) and in control group immediately the skin was closed. Lambs were delivered near term by cesarean section. They were assessed clinically and morphologically for paraplegia, paraparesia, urine and stool incontinency, pathology of spinal cord, thigh and rectal muscles and anal sphincter muscles.
Results: In case group, all lambs (n=5) had a complete or incomplete flaccid sensorimotor paraplegia, were incontinent for urine and 4 animals were incontinent of stool but only one lamb in control group (n=4) had paraparesia (P=0.048) and all lambs were continent for urine and stool.
In case group, all lambs had a hypoplastic longitudinal muscles in rectum but well developed circular muscles. Anal sphincter muscles did not develop normally but in control group all lambs had well developed longitudinal and circular muscles and anal sphincter muscles developed normally (P=0.008).
Spinal histopathologic changes were edema, focal calcification, fibrosis and capillary cell proliferation in case group but in control group were not seen. The number of ganglion cells was significantly higher in the control group, comparing with case group (P< 0.0005).
Conclusions: Exposure of MMC to AF, causes structural neural tissue damage that can be prevented by fetal surgery with repair of the MMC.