ORIGINAL RESEARCH article
Front. Neurol.
Sec. Stroke
Volume 16 - 2025 | doi: 10.3389/fneur.2025.1649577
Posterior Communicating Artery Vasospasm Impairs Cerebral Pulsatility in an Experimental Subarachnoid Hemorrhage Model
Provisionally accepted
- 1A life hospital, Ankara, Türkiye
- 2Department of Neurosurgery, Alife Hospital, Ankara, Türkiye
- 32Department of Neurosurgery, Faculty of Medicine, Trabzon University, Trabzon, Türkiye
- 4Recep Tayyip Erdogan University, Medical Faculty, Department of Neurosurgery, Rize, Türkiye
- 5Department of Neurosurgery, Faculty of Medicine, Atatürk University, Erzurum, Türkiye
- 6Department of Neurology, Medicana Interantional Ankara Hospital, Ankara, Türkiye
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Background: Subarachnoid hemorrhage (SAH) commonly causes cerebral vasospasm and delayed ischemia. Spasm of the posterior communicating artery (PCoA) can disrupt cerebral hemodynamics. We assessed its effect on cerebral pulsatility in a rabbit SAH model, focusing on intracranial pressure pulse amplitude as an early, sensitive marker of vasospasm-driven change, whereas global CBF or neurological outcomes generally require larger or longer studies. Methods: Rabbits were randomly assigned to three groups: control (no injection), sham-controlled (saline injection), and SAH (0.75 mL autologous blood injection into the basal subarachnoid space near the PCoA under anesthesia). Heart rate and cerebral pulsation amplitude (measured via intracranial pressure transducer) were recorded on day 1 and day 7. On day 7, animals were euthanized, and histological analysis of the PCoA was performed. Vasospasm index (VSI) was calculated as the ratio of arterial wall area to lumen area. Group comparisons and temporal changes were assessed statistically. Results: Twenty-three rabbits completed the study (5 control, 5 sham-controlled, 13 SAH; 2 SAH animals excluded due to early mortality). On day 1, the SAH group showed a significantly reduced pulsation amplitude compared to controls and sham-controlled groups. By day 7, pulsation amplitude partially recovered in the SAH group but remained lower than in controls. Control and sham-controlled groups exhibited a slight, non-significant decline in pulsation. The VSI was highest in the SAH group, moderate in sham-controlled, and lowest in the control groups. Heart rate declined over time across all groups, with significant bradycardia in the SAH group by day 7. Conclusion: PCoA vasospasm following experimental SAH results in a sustained reduction in cerebral pulsatility. These findings suggest that localized vasospasm disrupts pulsatile intracranial dynamics, potentially contributing to SAH-related pathophysiology.
Keywords: Subarachnoid Hemorrhage, cerebral vasospasm, Posterior Cerebral Artery, Intracranial Pressure, Animal Experimentation
Received: 18 Jun 2025; Accepted: 12 Sep 2025.
Copyright: © 2025 Daltaban, Gel, Kanat, Aydin and Turğut. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: İskender Samet Daltaban, A life hospital, Ankara, Türkiye
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