Page 9 - ITPS-7-2

INNOSC Theranostics and
Pharmacological Sciences Novel pharmacologic therapies for SAH

Figure 1. Pathophysiology and symptoms of subarachnoid hemorrhage.

the persistence of headaches following aneurysmal heme, which generates reactive oxygen species (ROS).
SAH, shedding light on the long-term consequences of These ROS induce oxidative stress, damaging neuronal
aneurysmal rupture. Collectively, these sources underscore and vascular structures. Oxidative stress is associated
the critical role of intracranial aneurysm rupture in the with cerebral vasospasm, delayed cerebral ischemia
pathophysiology of SAH. This highlights the need for (DCI), and brain injury following SAH. Sorrentino
early diagnosis and intervention to mitigate the potentially et al. discuss the persistence of headaches after
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severe consequences associated with this event. SAH, attributing them, in part, to the oxidative stress
and inflammation resulting from toxic hemoglobin
2.2. Toxic hemoglobin products products.
The breakdown of hemoglobin results in the production of (ii) Inflammation: Toxic hemoglobin products can trigger
toxic substances, leading to the following adverse effects: an inflammatory response within the subarachnoid
(i) Oxidative stress: Hemoglobin breakdown releases space and brain parenchyma. This inflammation,

Volume 7 Issue 2 (2024) 3 doi: 10.36922/itps.2019