Effect of hyperbaric oxygen on the expression of nitric oxide synthase mRNA in cortex after acute traumatic cerebral injury / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effect of hyperbaric oxygen (HBO) treatment on the expression of nitric oxide synthase (NOS) mRNA in cortex after acute traumatic cerebral injury, and to study the mechanism of HBO on brain injury.</p><p><b>METHODS</b>Acute traumatic brain injury model was established with rest received free fall injury method in SD rats. 0.25 MPa HBO treatment was used 1 h or 12 h after brain injury and the cortex was isolated 6 h or 24 h after brain injury respectively. The expression of mRNA coding for nNOS, eNOS or iNOS were assayed using reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The expression of nNOS, eNOS and iNOS mRNA were significantly decreased in 0.25 MPa HBO treatment groups than those in acute cerebral injury groups (P < 0.01). The amount of nNOS, eNOS and iNOS mRNA was significantly lower in HBOT 24 h group than those in HBOT 6 h group (P < 0.05, P < 0.01). There was no significantly difference among nNOS, eNOS and iNOS mRNA in 0.25 MPa normoxic hyperbaric nitrogen groups and acute cerebral injury groups (P > 0.05).</p><p><b>CONCLUSION</b>HBO may exert significant effects on the expression of nNOS mRNA/iNOS mRNA and protect cortical neuronal from traumatic cerebral injury.</p>

Changes of glycine uptake of synaptosomes of rat spinal cord in 0.7 MPa (7ATA) air pressure / 中国应用生理学杂志

<p><b>AIM</b>To study changes of function of transmitter glycine in nitrogen narcosis.</p><p><b>METHODS</b>Synaptosomes of rat spinal cord were prepared. Glycine uptake of synaptosomes of rat spinal cord in 0.7 MPa (7ATA) hyperbaric air pressure was observed by the methods of isotope.</p><p><b>RESULTS</b>Glycine uptake slowed down and took a longer period of time to reach saturation in 0.7 MPa (7ATA). The maximum glycine uptake was lessened. Vm was diminished, but Km was increased. Vm rose in 0.7 MPa (7ATA) when corticosterone was added.</p><p><b>CONCLUSION</b>When nitrogen narcosis arose in 0.7 MPa (7ATA), the function of transporters of glycine re-uptake was reduced, the affinity of glycine for transporters subsided. Corticosterone was conductive to the recovery of the function of glycine transporters of high affinity.</p>