# Bleeding pattern in the early phase after experimental rotational acceleration induced traumatic brain injury

## TL;DR

This study investigates bleeding patterns in the brain immediately after rotational acceleration injury in rats, finding that hemorrhages appear immediately and remain stable for the first hour.

## Contribution

The study introduces a validated model to investigate immediate hemorrhage patterns after rotational traumatic brain injury in rats.

## Key findings

- Hemorrhages appear immediately after rotational injury and remain unchanged for the first hour.
- Subarachnoid hemorrhages are widespread, while intracerebral hemorrhages are few and small.
- Amyloid precursor protein beta staining did not show axonal accumulation, but fibrinogen and P-selectin indicated hemostasis.

## Abstract

Lethal rotational acceleration induced injury to the brain may leave few detectable intracerebral injuries if the survival time is short. Eighty-two Sprague Dawley rats were utilized in a validated model for standardized rotational acceleration traumatic brain injury to investigate the number and area of subarachnoid and intracerebral hemorrhages. The rats were divided into groups with survival times of 0, 5, 10, 20 and 60 min with equal amounts of experimental and sham operated rats in each group. In addition, a “postmortem” group of rats were euthanizied 5 min before the trauma and samples collected 5 min after the trauma. From all rats, hemispheres were collected, cut and double stained with immunohistochemistry with anti-collagen IV and anti-hemoglobin. Brains from the 20- and 60-minutes groups were stained with immunohistochemistry for amyloid precursor protein beta. The 2 rats with the most and 2 rats with the least intracerebral hemorrhages from all time points were stained for fibrinogen and P-selectin. The group that sustained trauma postmortem and all sham operated rats showed either no bleedings or only a few, minimal, isolated hemorrhages. All other experimental groups showed widespread subarachnoid hemorrhages and few and small intracerebral hemorrhages. The hemorrhages were observed immediately after the rotational brain injury and did not change in number or size during the first hour. Amyloid precursor protein beta staining did not show any convincing axonal accumulation. Fibrinogen and P-selectin showed signs of hemostasis in all antemortem trauma groups. Our conclusion is that hemorrhages from rotatory traumatic brain injury develops immediately upon trauma and do not change during the first hour.