Burned spinal cord in acidotic cerebrospinal fluid during subarachnoid hemorrhage: Experimental study.

OBJECTIVE: We investigated the effect of carotid body ischemia-induced cerebrospinal fluid acidosis on spinal cord during subarachnoid hemorrhage (SAH). METHODS: Twenty-three hybrid rabbits were divided into three groups: control (n = 5), Sham (injected with 0.5 ml isotonic) (n = 6), and the SAH (n = 12) (injected with 0.5 ml autologous blood into the 4th ventricle) and then monitored for 3 weeks. Cerebrospinal fluid pH and degenerated ependymal cell density and volume of cervical central canal were analyzed. RESULTS: The mean cervical central canal volumes, degenerated ependymal cells densities, and cerebrospinal pH values were 1.056 ± 0.053 mm3-6 ± 2 per mm2-7.342 ± 0.034, 1.321 ± 0.12 mm3-35 ± 9 per mm2-7.314 ± 0.056, and 1.743 ± 0.245 mm3-159 ± 24 per mm2-7.257 ± 0.049 in the Control, Sham, and SAH groups, respectively. The more degenerated carotid body neuron density induced decreased cerebrospinal fluid pH values (p < 0.0001) could result in the more ependymal cells desquamation (p < 0.0005) and central canal dilatation (p < 0.00001). CONCLUSION: Increased neurodegeneration of carotid bodies can reduce cause cerebrospinal fluid pH-induced ependymal cell degeneration and central canal dilatation following SAH.

OBJETIVO: El objetivo de este estudio fue investigar el efecto de la isquemia inducida del cuerpo carotideo por la acídosis de líquido cefalorraquídeo en la médula espinal durante una hemorragia subaracnoidea (SAH). METODO: Conejos híbridos (n = 23) fueron divididos en Control (n = 5), Sham (inyectados con 0.5 mil de solución isotónica) (n = 6), y SAH (n = 12) (inyectados en el 4º ventrículo con 0.5 ml de sangre autológa) y monitoreados por tres semanas. Se analizaron: El pH del líquido cerebro espinal, la densidad de las células ependimarias y el volúmen del canal cervical central. RESULTADOS: La media del volumen del canal cervical central, la densidad de las células ependimarias degeneradas y los valores de pH fueron 1.056 + 0.053 mm3-6 + 2 per mm2-7.342 + 0.034, 1.321 + 0.12 mm3-35 + 9 per mm2-7.314 + 0.056 y 1.743 + 0.245 mm3-159 + 24 per mm2-7.257 + 0.049 en los grupos Control, Sham y SHA, respectivamente. La mayor densidad inducida de la neurona del cuerpo carotideo degenerado, disminuyó los valores de pH del líquido cefalorraquideo lo que podría dar como resultado un aumento en la descamación de las células ependimarias asi como la dilatación del canal central. CONCLUSIÓN: Un aumento en la neurodegeneración del cuerpo carotideo puede reducir la degeneración de los ependimocitos y la dilatacióm del canal central siguiendo SAH.

First definition of burned choroid plexus in acidic cerebrospinal fluid-filled brain ventricles during subarachnoid hemorrhage: Experimental study.

Blood and cerebrospinal fluid (CSF) acidosis is the most troubling complication in subarachnoid hemorrhage (SAH) if carotid body (CB) networks are disrupted. However, histopathological examination of the choroid plexus (CP) in acidic CSF has not been evaluated so far. In this study, we aimed to investigate the CP in acidic CSF following SAH. Twenty-eight rabbits were used. Five rabbits were used to analyze CB network (control group; n = 5); seven rabbits were injected 1 mL of saline (Sham group; n = 7); and the rest 16 rabbits were given 1 mL of autologous arterial blood inject into the cisterna magna to create SAH (SAH group; n = 16). Blood and CSF pH values were recorded before/during/after the experimental procedures. Nuclear darkening, cellular shrinkage and pyknosis suggested the presence of apoptosis of epithelial cells of CP. The densities of normal and degenerated epithelial cells of CPs were estimated using stereological methods. The relationship between the pH values and degenerated epithelial cell densities of CPs were statistically compared by Mann-Whitney U-test. The pH values of blood were estimated as 7.359 ± 0.039 in the control group, 7.318 ± 0.062 in the Sham group, 7.23 ± 0.013 in the SAH group. CSF pH values were 7.313 ± 0.028 in the control group, 7.296 ± 0.045 in the Sham group, and 7.224 ± 0.012 in the SAH group. Degenerated epithelial cell density of CP was 25 ± 7 in the control group, 226 ± 64 in the Sham group, and 2115 ± 635 in the SAH group. There was a considerable link between CSF pH values and degenerated epithelial cells of CP (P < 0.0001). This study shows that CB insult causes acidosis of CSF as well as cellular degeneration of CP during SAH. This is the first description of this in the literature.