Related Experiment Videos
Effects of prolonged supratentorial mass expansion on regional blood flow and cardiovascular parameters during the
Insights
Intracranial hypertension triggers the Cushing response (CR) through progressive brain ischemia. This response involves initial bradycardia, followed by tachycardia, and is driven by peripheral vasoconstriction.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Cerebrovascular Regulation
Background:
- The Cushing response (CR) is a critical indicator of increased intracranial pressure.
- Understanding the central nervous and cardiovascular mechanisms of the CR is vital for managing intracranial hypertension.
Purpose of the Study:
- To investigate the central nervous and cardiovascular mechanisms underlying the Cushing response during intracranial hypertension.
- To elucidate the relationship between progressive cerebrospinal ischemia and cardiovascular changes.
Main Methods:
- Utilized a canine model with a continuously expanding epidural supratentorial balloon to induce intracranial hypertension.
- Measured regional cerebral blood flow, cardiac output, and vascular resistance using radioactive microspheres.
- Continuously monitored heart rate, arterial blood pressure, and ECG.
Main Results:
- Progressive ischemia of the brain, from cerebrum to spinal cord, correlated with distinct cardiovascular changes.
- Initial bradycardia occurred with lower pons ischemia, shifting to tachycardia with lower medulla oblongata ischemia.
- Mean arterial pressure peaked at 245 mm Hg but decreased as ischemia reached the spinal cord; cardiac output consistently fell.
Conclusions:
- The study suggests that the initial bradycardia in the CR is due to increased vagal discharge.
- Peripheral vasoconstriction appears to be the primary driver of the vasomotor component of the Cushing response.
- The findings highlight the intricate interplay between brain ischemia and cardiovascular regulation during elevated intracranial pressure.
Abstract:
To clarify the central nervous and the cardiovascular mechanisms mediating the Cushing response (CR) during intracranial hypertension, the effects of continuous and prolonged expansion of an epidural supratentorial balloon was studied in six dogs. Regional cerebral blood flow, cardiac output, extracerebral tissue blood flow and regional vascular resistance were measured with radioactive microspheres before and during the CR while heart rate, arterial blood pressure and ECG were continuously recorded. The results showed that balloon expansion led progressively to cerebrospinal ischemia beginning in the cerebrum and progressing to the pons, medulla oblongata and spinal cord in an orderly rostro-caudal fashion. This progressing ischemia was closely associated with patterned and stereotyped changes in cardiovascular indices. Thus, respiration ceased, heart rate decreased, blood pressure increased and cardiac output fell when the ischemia appeared in the lower pons. Further advancement of the ischemic front to the lower medulla oblongata led to an abrupt switch-over from bradycardia to tachycardia, which persisted until the experiment was terminated. Since bradycardia disappeared when ischemia reached the vagal cardiomotor nucleus, the initial bradycardia appeared to be the result of increased vagal discharge. When ischemia reached the pons, the mean arterial pressure rose to a maximum of 245 mm Hg (+/- 45) but then fell progressively when the ischemia reached the spinal cord. The decrease in cardiac output persisted throughout the CR and was associated with decreased flow in most extracerebral organs. Exceptions were the heart muscle and the adrenal medulla in which blood flow increased considerably. Changes in regional vascular resistance reciprocated the changes in flow. These results suggest that the vasomotor component of the CR is brought about entirely by peripheral vasoconstriction.