Tadaomi-Alfonso Miyamoto1, Koho-Julio Miyamoto2, Nobuhisa Ohno3. 1. Research Department, Kokura Memorial Hospital, 1-1 Kifunecho, Kokurakita-ku, 802, Kitakyushu-shi, Japan. 2. Second Department of Physiology, Uiversity of Ryukyus School of Medicine, Okinawa, Japan. 3. Department of Cardiovascular Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Abstract
PURPOSE: To develop a neurologic scoring (NS) system to objectively assess CNS function shortly after spinal cord ischemia. METHODS: Spinal cord ischemia was induced by temporarily clamping the infrarenal aorta in 27 rabbits anesthetized with isoflurane/N2O/O2 without muscle relaxants. Animals were divided ito group I, normothermic ischemia [I-a, 11 min (n=8); I-b, 12 min (n=8)], and group II, 60 min hypothermic ischemia targeted to II-a, 29.5°C (n=5), and II-i, 30.0°C (n=6). Postischemic neurologic function was scored from 0 to 6. RESULTS: Seventy-five percent of each group I subgroup ended with paraplegia. Function in the I-b group tended to be worse than in I-a (NS=1.7vs 1.9P>0.05). Hypothermia of 29.9±0.1°C protected partially (NS=2.8), whereas 29.4±0.1°C resulted in significantly higher NS, starting at 150 min (P<0.05vs IIi) with total recovery 5.5 hours (P<0.0001) post re-perfusion. CONCLUSIONS: Protection of the spinal cord from ischemia can be objectively quantitated by our system. Protection strategies can be compared within 6 h of the ischemia-insult.
PURPOSE: To develop a neurologic scoring (NS) system to objectively assess CNS function shortly after spinal cord ischemia. METHODS:Spinal cord ischemia was induced by temporarily clamping the infrarenal aorta in 27 rabbits anesthetized with isoflurane/N2O/O2 without muscle relaxants. Animals were divided ito group I, normothermic ischemia [I-a, 11 min (n=8); I-b, 12 min (n=8)], and group II, 60 min hypothermic ischemia targeted to II-a, 29.5°C (n=5), and II-i, 30.0°C (n=6). Postischemic neurologic function was scored from 0 to 6. RESULTS: Seventy-five percent of each group I subgroup ended with paraplegia. Function in the I-b group tended to be worse than in I-a (NS=1.7vs 1.9P>0.05). Hypothermia of 29.9±0.1°C protected partially (NS=2.8), whereas 29.4±0.1°C resulted in significantly higher NS, starting at 150 min (P<0.05vs IIi) with total recovery 5.5 hours (P<0.0001) post re-perfusion. CONCLUSIONS: Protection of the spinal cord from ischemia can be objectively quantitated by our system. Protection strategies can be compared within 6 h of the ischemia-insult.
Authors: A J du Plessis; R A Jonas; D Wypij; P R Hickey; J Riviello; D L Wessel; S J Roth; F A Burrows; G Walter; D M Farrell; A Z Walsh; C A Plumb; P del Nido; R P Burke; A R Castaneda; J E Mayer; J W Newburger Journal: J Thorac Cardiovasc Surg Date: 1997-12 Impact factor: 5.209
Authors: C K Rokkas; S Sundaresan; T A Shuman; R S Palazzo; T Nitta; G J Despotis; T C Burns; T H Wareing; N T Kouchoukos Journal: J Thorac Cardiovasc Surg Date: 1993-12 Impact factor: 5.209