Influence of Plasma and Cerebrospinal Fluid Levels of Endothelin-1 and No in Reducing Cerebral Vasospasm after Subarachnoid Hemorrhage During Treatment with Mild Hypothermia, in a Dog Model

Abstract

Using vascular heat-exchange controller implemented mild hypothermia treatment, the authors established the cerebral vasospasm model in which blood was injected twice into dog's foramen magnum; and it was discussed the influence of the concentration of endothelin-1 and NO in blood plasma and cerebrospinal fluid through continuing treatment of mild hypothermia at different times in secondary brain vasospasm model after subarachnoid hemorrhage. Thirty healthy mongrel dogs were randomly divided into five groups; artificial cerebrospinal fluid group (group A), normal temperature control group (group C), mild hypothermia 8 h group (group H1), mild hypothermia 16 h group (group H2), and mild hypothermia 32 h group (group H3). The authors injected the artificial CSF into dog's foramen magnum in group A while the other four groups were injected with autologous arterial blood. The normal group's temperature maintained 38.5°C. The authors set the temperature at 33.5°C in mild hypothermia groups and this was maintained for 8, 16, and 32 h, respectively. ET-1 and NO levels in the cerebrospinal fluid and plasma were assayed in each group on days 0, 7, 14, and 21. Then the changes of the diameter of blood vessels of cerebral basilar artery and overall performance categories score in each group through application of CT angiography were recorded. In the cerebral vasospasm model which was constructed by injecting the blood to dog twice, mild hypothermia treatment, through the application of vascular heat-exchange controller, could reduce cerebral vasospasm. It was observed that the duration of the mild hypothermia is directly proportional to the longer duration of the relieving of cerebral vasospasm. The reciprocal changes observed in the levels of ET-1 and NO in cerebrospinal fluid and plasma revealed that it might be possible to reduce the cerebral vasospasm by regulating the rising amplitude of ET-1 and the decrease in NO in CSF and plasma.

Is Hypothermia Helpful in Severe Subarachnoid Hemorrhage? An Exploratory Study on Macro Vascular Spasm, Delayed Cerebral Infarction and Functional Outcome after Prolonged Hypothermia

“…TH was related to significant reductions of MCA and peak spastic velocities, which may resemble a decreased degree of macrovascular spasm [23] . As previously suggested, TH mediates its neuroprotective effects by modulations of molecular, metabolic and inflammatory processes, possibly supporting associations with cerebral blood flow velocities [6,12,[28][29][30] . Such a mechanistic association of TH seems likely, yet its influence on actual peak spasm and its clinical significance warrant further investigations [31] .…”

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

“…Cerebral vasospasm is considered an important cause of DCI and can partly be explained by the mismatch between vasodilatatory and -constrictor substances as well as detrimental effects of SAHrelated inflammatory reactions [44]. Animal studies have shown the potentially beneficial effects of hypothermia on cerebral vasospasm [3,4,7]. Further-more, we previously demonstrated the attenuation of inflammatory reactions during combined hypothermia and barbiturate coma in patients with severe SAH [45].…”

Correlation between the hematocrit and slow coronary flow

“…Studies have shown an imbalance between the release of nitric oxide (vasodilator) and endothelin-1 (vasoconstrictor) and higher baseline levels of endothelin-1 in the plasma of subjects with SCF [6,19,20,27]. The correlation of a high hematocrit with SCF might be because increased blood viscosity impairs the endothelial release of vasoactive substances, and the imbalance between the release of nitric oxide and endothelin-1 may have a pathophysiologic role in SCF.…”