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Absent recruitment of capillaries in brain tissue recovering from stroke
1Positron Imaging Laboratories, McConnell Brain Imaging Unit, Montreal, Quebec, Canada.
Insights
Stroke reduces glucose transport in brain capillaries, impacting metabolism and blood flow. Even after blood flow recovery, capillary density remains low, hindering nutrient vessel recruitment.
Area of Science:
- Neuroscience
- Cerebrovascular Medicine
- Medical Imaging
Background:
- Stroke significantly impacts brain function and metabolism.
- Understanding capillary dynamics is crucial for stroke recovery.
- Positron emission tomography (PET) offers insights into brain hemodynamics.
Purpose of the Study:
- To quantify changes in capillary hemodynamics and glucose metabolism in stroke patients.
- To compare ischemic regions with contralateral healthy regions.
- To assess the recovery of capillary function post-stroke.
Main Methods:
- In vivo assessment of brain hemodynamics using positron tomography.
- Calculation of capillary density (dCAP), volume fraction (fCAP), and transit time (tCAP).
- Determination of cerebral metabolic rate for glucose (CMRglc) and oxygen (CMRO2).
Main Results:
- Infarct regions showed reduced CMRglc, CMRO2, cerebral blood flow (CBF), and capillary diffusion capacity (K1).
- Capillary volume fraction (fCAP) decreased, while transit time (tCAP) doubled in ischemic areas.
- One week post-stroke, CBF normalized, but capillary density and diffusion capacity remained depressed.
Conclusions:
- Stroke causes significant deactivation and reduced perfusion in affected brain regions.
- Capillary function, specifically density and diffusion capacity, remains impaired even after blood flow normalization.
- There is a lack of recruitment of essential nutrition vessels following stroke.
Abstract:
The density of perfused capillaries (dCAP), defined as capillaries that transport glucose, as well as the volume fraction of these capillaries in the vascular bed (fCAP), and the mean transit time of blood through the capillaries (tCAP), were calculated from hemodynamic variables obtained in vivo by positron tomography of brains of six patients affected by stroke. Each patient was studied twice, within 38 hrs of the insult, and one week later. 38 ischemic and 38 contralateral mirror regions were compared. The metabolic rate for glucose (CMRglc) was determined on the basis of regional calculations of the lumped constant. No significant change of the lumped constant was observed in any region. In normal regions, no significant differences of any variables existed between the first and second studies. In the infarct regions of the first study, CMRglc and CMRO2 (cerebral metabolic rate for oxygen) were 30-50% of control (deactivation) and CBF (cerebral blood flow), capillary density, and the capillary diffusion capacity for fluorodeoxyglucose (K1) were similarly reduced, although the oxygen/glucose ratio was only 3.75 in the ischemic regions. While fCAP decreased, tCAP doubled. One week after the first study, blood flow returned to normal in the infarct regions despite continued depression of metabolism. Capillary density and diffusion capacity remained low, indicating absent recruitment of nutrition vessels (perfusion capillaries).