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Updated: Dec 26, 2025
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
First definition of burned choroid plexus in acidic cerebrospinal fluid-filled brain ventricles during subarachnoid
Tuba Demirci1, Mehmet D Aydin2, Ozgur Caglar3
1Department of Histology and Embryology, Medical Faculty of Ataturk University, Erzurum, Turkey.
Insights
Subarachnoid hemorrhage (SAH) can cause cerebrospinal fluid (CSF) acidosis, leading to choroid plexus (CP) epithelial cell degeneration. This study reveals a significant link between reduced CSF pH and CP cell damage following SAH.
Area of Science:
- Neuroscience
- Pathology
- Physiology
Background:
- Acidosis in blood and cerebrospinal fluid (CSF) is a significant complication of subarachnoid hemorrhage (SAH), particularly when carotid body (CB) networks are compromised.
- The histopathological effects of acidic CSF on the choroid plexus (CP) have not been previously investigated.
Purpose of the Study:
- To investigate the histopathological changes in the choroid plexus (CP) in response to acidic cerebrospinal fluid (CSF) following experimental subarachnoid hemorrhage (SAH).
- To establish the relationship between CSF acidosis and epithelial cell degeneration in the CP after SAH.
Main Methods:
- Subarachnoid hemorrhage (SAH) was induced in 16 rabbits by injecting autologous arterial blood into the cisterna magna.
- Control (n=5) and sham (n=7) groups were used for comparison.
- Blood and CSF pH were measured, and choroid plexus epithelial cells were analyzed for apoptosis and degeneration using stereological methods.
Main Results:
- SAH induction led to significant acidosis in both blood (pH 7.23 ± 0.013) and CSF (pH 7.224 ± 0.012) compared to control and sham groups.
- A strong correlation was found between decreased CSF pH and increased density of degenerated choroid plexus epithelial cells (P < 0.0001).
- The density of degenerated CP epithelial cells was markedly higher in the SAH group (2115 ± 635) compared to control (25 ± 7) and sham (226 ± 64) groups.
Conclusions:
- Carotid body (CB) insult during subarachnoid hemorrhage (SAH) contributes to cerebrospinal fluid (CSF) acidosis.
- Acidic CSF conditions result in significant cellular degeneration of the choroid plexus (CP) epithelium.
- This study provides the first evidence linking SAH-induced CSF acidosis to choroid plexus pathology.
Abstract:
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.
