Related Experiment Video
Updated: May 5, 2026
Isolated Lung Perfusion System in the Rabbit Model
Published on: July 15, 2021
Effect of experimental pneumococcal meningitis on respiration and circulation in the rabbit
Abstract:
Pathophysiological studies in bacterial meningitis in man have been limited by clinical variability and the necessity for immediate therapy. After the development of a reliable animal model of pneumococcal meningitis, we studied respiration and circulation in 25 anesthetized New Zealand white rabbits during untreated pneumococcal meningitis and in 33 healthy controls. In meningitis, we found increased lactic acid in cerebrospinal fluid (CSF). Increased ventilation, perhaps due to CSF lactic acid accumulation, resulted in respiratory alkalosis; the concomitant lowering of Pco(2) acted as a homeostatic mechanism to restore pH toward normality in the CSF. Hyperventilation increased with the duration of the illness. Cardiac output was also increased with decreased peripheral vascular resistance but with only slight reduction in mean systemic and pulmonary arterial pressures. In the final hour of life, peripheral vascular resistance fell further; ventilation declined and then abruptly ceased while cardiac activity continued. Lactic acid accumulation in the CSF, found in both experimental and human pneumococcal meningitis, may cause the hyperventilation found in this disease and may contribute to death.
Insights
This study on pneumococcal meningitis in rabbits found that increased lactic acid in cerebrospinal fluid (CSF) caused hyperventilation and respiratory alkalosis, contributing to death. These findings offer insights into bacterial meningitis pathophysiology.
Area of Science:
- Neurology
- Infectious Diseases
- Physiology
Background:
- Bacterial meningitis research is hampered by clinical variability and urgent treatment needs.
- A reliable animal model of pneumococcal meningitis was developed for controlled study.
- Previous studies lacked detailed insights into respiratory and circulatory changes during meningitis.
Purpose of the Study:
- To investigate the pathophysiological changes in respiration and circulation during untreated pneumococcal meningitis.
- To determine the role of cerebrospinal fluid (CSF) lactic acid in disease progression.
- To elucidate the mechanisms leading to respiratory failure and death in pneumococcal meningitis.
Main Methods:
- Utilized an established animal model of pneumococcal meningitis in anesthetized New Zealand white rabbits.
- Monitored respiratory parameters (ventilation, Pco2) and circulatory functions (cardiac output, vascular resistance, arterial pressures).
- Analyzed CSF for lactic acid accumulation and correlated findings with disease duration and outcome.
Main Results:
- Elevated lactic acid levels were observed in the CSF of rabbits with meningitis.
- Increased ventilation led to respiratory alkalosis, with Pco2 changes attempting to normalize CSF pH.
- Hyperventilation intensified as the illness progressed; cardiac output increased with decreased vascular resistance.
- In the terminal stages, peripheral vascular resistance dropped, ventilation ceased, but cardiac activity persisted.
Conclusions:
- CSF lactic acid accumulation is a key factor in the hyperventilation observed in pneumococcal meningitis.
- The observed physiological changes, particularly respiratory and circulatory dysfunction, contribute significantly to mortality.
- This animal model provides valuable data for understanding human pneumococcal meningitis pathophysiology.
