Wed. Jun 19th, 2024

Researchers learn how to use the body’s innate signal to fight blood loss

Researchers at the University of Virginia School of Medicine have identified a group of brainstem cells that regulate the body's reaction to significant blood loss. This finding may aid efforts to create novel treatments for traumatic injuries.

The latest findings by Stephen Abbott, Ph.D., of UVA and colleagues provide insight on a critical procedure the body utilises to keep blood pressure in check.

The finding identifies a group of neurons that triggers a response that keeps blood pressure steady during blood loss. The new findings provide insight into why excessive blood loss finally culminates in circulatory collapse, a disease known as “decompensated haemorrhage” that is characterised by a rapid and hazardous drop in blood pressure.

The “adrenergic C1 neurons” that Abbott and his team describe monitor blood pressure and react when there is blood loss. When neurons notice blood loss, they intensify nerve activity, which narrows blood vessels and keeps blood pressure within normal range. Via cutting-edge imaging and a method called optogenetics, which enables the remote regulation of neurons using light, the researchers were able to come to this conclusion.

According to the study, when blood is lost, the C1 neurons become hyperactive, which helps to keep blood pressure stable. However, with significant blood loss, these neurons become dormant, leading to cardiovascular collapse. Hemorrhagic shock, in which the body starts to shut down, is preceded by decompensated bleeding. The C1 neurons in lab rats, however, were shown to be activated again, restoring both blood pressure and heart rate.

According to the study, reactivating the brain’s blood pressure-regulating mechanisms following a decompensated bleed can successfully prevent cardiovascular collapse.

The researchers concluded that this suggested neuromodulation of the study’s disclosed pathways would be an effective supplementary treatment for low blood pressure following blood loss.

The researchers point out that the C1 neurons’ activity may have decreased for a variety of reasons at the start of a decompensated haemorrhage. On that front, more study is required. However, the team’s findings point to significant new directions for that ongoing investigation.

The results shed light on the significance of brain-body connections during blood loss and offer a fresh viewpoint on what is really causing the cardiovascular collapse.

By Editor

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