Blocking the action of kallikrein improves outcomes after haemorrhage in mice and could work form the basis of a treatment, the researchers believe.
Dr Edward Feener, from Harvard Medical School, and colleagues induced brain haemorrhages in a group of diabetic and non-diabetic mice. They found that the diabetic animals bled over a much greater area of the brain than those without diabetes.
The researchers examined the impact on these haemorrhages of inhibiting kallikrein, which interferes with clotting and is involved in the development of vascular disease in diabetes.
When diabetic mice were injected with kallikrein they showed increased levels of damage following haemorrhage, but the non-diabetic mice showed little difference.
In addition, when the diabetic mice were pre-treated with the compound mannitol, which inhibits the effects of kallikrein, the level of damage following haemorrhage was similar to that in non-diabetic animals.
Reducing glucose levels in diabetic mice blocked the effect of kallikrein and raising glucose levels in non-diabetic animals replicated the effects seen in diabetic mice.
‘Here we have shown that hyperglycemia increases the magnitude of hematoma expansion during experimental intracerebral haemorrhage and that this effect is mediated by plasma kallikrein,’ the researchers said.
‘We suggest that plasma kallikrein represents a target for interfering with hematoma expansion under conditions of hyperglycemia,’ they added.