Related Experiment Video
Updated: Oct 3, 2026
A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
Effect of hemorrhagic hypotension on cerebrovascular reactivity and ultrastructure in the cat
A G Kovách1, C Szabó, M Faragó
1Experimental Research Department, Semmelweis University Medical School, Budapest, Hungary.
Insights
Hemorrhagic hypotension altered feline middle cerebral artery responses, enhancing some relaxations while impairing others. Nerve terminals showed fewer transmitter vesicles, suggesting potential for cerebral vasoconstriction.
Area of Science:
- Neuroscience
- Vascular Biology
- Physiology
Background:
- Hemorrhagic hypotension can significantly impact cerebrovascular function.
- Understanding these effects is crucial for managing neurological complications.
Purpose of the Study:
- To investigate changes in contractile and dilatory responses of the feline middle cerebral artery after hemorrhagic hypotension.
- To examine the ultrastructural alterations in this artery following hemorrhagic hypotension.
Main Methods:
- Anesthetized cats were subjected to induced hemorrhagic hypotension (50 mm Hg for 2 hours).
- Isometric tension recordings were used to assess arterial ring responses to contractile and relaxant agents.
- Vascular ultrastructure was analyzed using electron microscopy.
Main Results:
- Endothelium-dependent relaxations to acetylcholine showed biphasic effects (enhanced at low, inhibited at high concentrations).
- Relaxations to adenosine triphosphate and adenosine were impaired.
- Contractions to norepinephrine and prostaglandin F2 alpha were unchanged, but 5-hydroxytryptamine-induced contractions were enhanced.
- No morphological changes were observed in endothelium or smooth muscle, but perivascular nerve terminals had fewer transmitter vesicles.
Conclusions:
- Hemorrhagic hypotension induces significant alterations in cerebrovascular reactivity and adventitial ultrastructure.
- These changes may contribute to cerebral vasoconstriction during and after hemorrhagic states.
Background And Purpose:
The goal of this study was to determine the alterations in contractile and dilatory responses and ultrastructure of the feline middle cerebral artery after hemorrhagic hypotension.
Methods:
In the sodium pentobarbital anesthetized cats, a steady 50 mm Hg level of hypotension was reached by bleeding into a reservoir and maintained at this level by further bleeding or autotransfusion for 2 hours. Rings of the arteries, from control animals and from animals after hypotension, were suspended for isometric tension recording in organ chambers filled with modified Krebs-Henseleit solution, aerated with 95% O2-5% CO2 at 37 degrees C, and their reactions to contractile and relaxant agents were tested. Vascular ultrastructure was studied by electron microscope.
Results:
Endothelium-dependent relaxations induced by 10(-8) M acetylcholine were enhanced, whereas there was a marked inhibition of the relaxation at 10(-6) M. Relaxations induced by adenosine triphosphate and adenosine showed an impairment. Contractions induced by norepinephrine and prostaglandin F2 alpha remained unchanged, whereas 5-hydroxytryptamine caused a more pronounced contraction after hypotension. No alterations in the morphology of endothelium or smooth muscle were found after hemorrhage. There was, however, a marked decrease in the number of transmitter vesicles in the perivascular nerve terminals.
Conclusions:
The present results show marked alterations in cerebrovascular reactivity and ultrastructure of the adventitia after hypotension. These alterations might play an important role in the development of cerebral vasoconstriction during and after this hemorrhagic state.
