When the brain is briefly starved of blood, the body does not simply recover and move on — the disruption echoes through distant vessels, quietly remaking them. Researchers at the Universitat Autònoma de Barcelona have found that a stroke-like event in hypertensive rats triggers lasting structural damage in abdominal arteries far removed from the brain, suggesting that stroke is as much a systemic vascular event as a neurological one. Into this picture steps SAHA, a drug already approved for cancer treatment, which showed early promise in preventing these downstream arterial changes and protec
Drug SAHA shows promise in protecting blood vessels after stroke-like events in hypertensive rats
A stroke in the brain triggers vascular changes throughout the body
Mark
So the stroke happens in the brain, but the damage shows up in the arteries of the abdomen? How does that work?
Mimi
The researchers induced a temporary loss of blood flow to the brain—essentially a stroke-like event. When blood flow was restored, they found that small arteries in the mesenteric system, which supplies the intestines, had undergone structural changes. The walls thickened, the arteries enlarged, and they lost the ability to contract properly.
Luke
But this is in rats with high blood pressure. We don't know yet if the same cascade happens in humans, or if it happens the same way.
Mimi
That's exactly right. The researchers were careful about that. They're saying this opens a door to further research, not that it's proven in people.
Mark
And SAHA prevented these changes?
Mimi
It prevented some of the early arterial changes and reduced long-term brain damage in the rats. The doses used were equivalent to what humans receive for cancer treatment.
Luke
So SAHA is already approved for human use, which is why this matters—the safety profile is known. But we're still talking about rat studies. The leap to clinical trials is significant.
Mark
What would the next step actually be?
Mimi
The researchers say more studies are needed to understand SAHA's long-term effects on blood vessels and whether those effects would translate to humans. They're being cautious about claiming this could prevent stroke complications in hypertensive patients.
Luke
And we don't know yet whether preventing these arterial changes in rats would actually improve outcomes for stroke patients. That's a separate question.
Mark
So this is promising, but early.
Mimi
Very early. It's a mechanism study that suggests a possible intervention. But the clinical path is still ahead.
Der Puls
- A brief interruption of blood flow to the brain sets off a chain reaction in arteries throughout the abdomen, thickening their walls and stripping them of flexibility — damage that does not resolve on its own within the critical first week.
- The finding reframes stroke as a whole-body vascular crisis, not merely a brain injury, raising urgent questions about how much silent damage accumulates in patients who survive the initial event.
- SAHA, administered during the window when blood flow returns to the brain, interrupted the early cascade of arterial changes and delivered measurable long-term protection against brain damage in hypertensive rats.
- Because SAHA is already cleared for human use in oncology, researchers believe the road to stroke trials could be shorter than usual — but animal-to-human translation remains an open and cautious question.
- The study, a collaboration across multiple Spanish institutions, calls explicitly for further research into SAHA's long-term vascular effects before any clinical application can be responsibly pursued.
When the brain is briefly starved of blood, the body does not simply recover and move on — the disruption echoes through distant vessels, quietly remaking them. Researchers at the Universitat Autònoma de Barcelona have found that a stroke-like event in hypertensive rats triggers lasting structural damage in abdominal arteries far removed from the brain, suggesting that stroke is as much a systemic vascular event as a neurological one. Into this picture steps SAHA, a drug already approved for cancer treatment, which showed early promise in preventing these downstream arterial changes and protecting the brain itself — offering a potential shortcut toward clinical application, even as the distance between animal studies and human medicine remains humbling.
When blood flow to the brain is cut off and then restored, the damage does not stay contained to the skull. A research team led by Dr. Francesc Jiménez-Altayó at the Institut de Neurociències of the Universitat Autònoma de Barcelona induced a brief stroke-like event in hypertensive rats and then watched what happened to their mesenteric arteries — the small vessels supplying the intestines. What they found, published in Life Sciences, was a cascade of structural changes in vessels that had no direct connection to the original injury.
The abdominal arteries lost their ability to contract and relax properly, and this dysfunction persisted across the eight days of observation. Their walls thickened, the vessels enlarged, and collagen accumulated at elevated rates — all signs of lasting vascular remodeling triggered by an event in a distant organ. Hypertension, already the leading risk factor for stroke, appeared to make these vessels especially vulnerable to the ripple effects.
The team then tested SAHA — suberoylanilide hydroxamic acid — administering it during the reperfusion window at doses equivalent to those used in human cancer treatment. The drug prevented some of the early arterial changes and, crucially, offered long-term protection against brain damage from the ischemic event itself. Lead author Andrea Díaz-Pérez noted that SAHA's existing regulatory approval could accelerate the path to stroke trials.
Dr. Jiménez-Altayó was measured in his conclusions: the findings open a door, but further studies are needed to understand SAHA's long-term vascular effects and whether the results would hold in humans. The collaboration, spanning several Spanish biomedical institutions, leaves the field with a sharper picture of stroke as a systemic vascular event — and a credible, if still distant, candidate for addressing the damage it leaves behind.
When blood stops flowing to the brain, even briefly, the damage spreads far beyond the skull. A study led by Dr. Francesc Jiménez-Altayó at the Institut de Neurociències of the Universitat Autònoma de Barcelona found that a temporary stroke-like event in hypertensive rats caused lasting structural changes in small arteries throughout the abdomen—arteries that had nothing to do with the initial injury. The research, published in Life Sciences, also tested whether a drug called SAHA could reverse or prevent these downstream effects.
Hypertension is the single largest risk factor for stroke. To understand what happens when blood flow to the brain is cut off and then restored, the researchers induced a brief interruption of blood supply in rats with high blood pressure and then tracked what happened to their mesenteric arteries—the small vessels that feed the intestines. They measured how well these arteries could contract and relax, and they examined structural changes: wall thickness, the number of cells, collagen deposits, and markers of oxidative stress. They took measurements at one day and again at eight days after blood flow was restored to the brain.
The results were striking. The arteries had lost their ability to contract properly, and this impairment did not improve over the week that followed. The vessel walls had thickened and the arteries themselves had enlarged, apparently because collagen was being deposited at higher rates. The stroke-like event, in other words, had triggered a cascade of changes in blood vessels far from the site of the original injury.
The team then tested whether suberoylanilide hydroxamic acid—SAHA—could intervene. They administered the drug during the period when blood flow was being restored to the brain. SAHA is already approved by regulators for treating a type of cancer, and the researchers used doses equivalent to what humans receive. The drug worked. It prevented some of the early arterial changes and, more importantly, it provided long-term protection against brain damage caused by the temporary ischemia.
Andrea Díaz-Pérez, the lead author, noted that because SAHA is already in clinical use, the pathway to testing it in stroke patients might be shorter than it would be for a completely novel compound. But Dr. Jiménez-Altayó, a professor in the Department of Pharmacology, Therapeutics and Toxicology at the university, was careful about what the findings actually showed. The work opens a door to further research into whether SAHA could reduce stroke-related brain damage in hypertensive patients, he said, but more studies are needed to understand its long-term effects on blood vessels and whether those effects would hold in humans.
The research involved collaboration across multiple institutions in Spain, including the Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares, the Biomedical Research Institute of Barcelona, and several others. What emerges from their work is a clearer picture of how a stroke in one part of the body can trigger vascular changes throughout it—and a hint that a drug already known to be safe in humans might offer some protection. But the path from rat studies to clinical use remains long, and the researchers are explicit that further work is needed to develop strategies that can fully prevent the persistent vascular damage that spreads through the body after a stroke.
Bemerkenswerte Zitate
This opens the door to further research into whether it could also reduce stroke-related brain damage in hypertensive patients. However, more studies are needed to fully understand its long-term effects on blood vessels.— Dr. Francesc Jiménez-Altayó, Institut de Neurociències, UAB
Möchten Sie die ganze Geschichte?
Das Original lesen bei News-Medical.net ↗
Science & Space