Role of ischemia in rats with spinal cord injury induced by decompression sickness.
The microsphere technique was used to determine whether blood flow to the central nervous system and various organs is impaired in rats with spinal cord injury induced by decompression sickness. For this purpose cannulas were placed in the left ventricle of the rats for the injection of microspheres and in the tail artery as the reference site for withdrawal of blood for the calculation of cardiac output (CO) and blood flow (BF) and for measurement of blood pressure (BP) and heart rate (HR). The rats were then subjected to a simulated dive that by electrophysiologic criteria rapidly (within 60 min after diving) induces severe neurologic deficits in the cord. Microspheres were used to determine CO and BF before and at 10, 60, and 180 min after diving. CO, BP, and HR were not affected by diving. BF to various regions of the brain, heart, bone, and fat was also not affected by diving. BF decreased in the lung (40%) and skeletal muscle (50%) and increased in spinal cord (20%) at 10 min after diving. At 60 and 180 min after diving the only alterations seen were increases in hepatic arterial and portal BF. Analysis of the distribution of cardiac output showed that diving induced changes that essentially paralleled the BF changes described above. We conclude that perfusion in the central nervous system is maintained in rats with spinal cord injury induced by decompression sickness. These results indicate that ischemia does not play a role in the pathophysiology of neuronal injury in this model of decompression sickness.
Marzella
L
L
Department of Pathology, School of Medicine, University of Maryland, Baltimore 21201, USA.
Yin
A
A
D000818:Animals; D003665:Decompression Sickness / Q000503:physiopathology*; D006439:Hemodynamics; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D008863:Microspheres; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000098:blood supply; D013119:Spinal Cord Injuries / Q000209:etiology* / Q000503:physiopathology