Normal perfusion pressure breakthrough: the role of capillaries

Abstract

Excision of human cerebral arteriovenous malformations (AVMs) can be complicated by postoperative edema and hemorrhage in adjacent brain tissue, despite the complete excision of the malformation. Various theories have purported to explain the hemodynamic basis for this predisposition, including disordered autoregulation causing "normal perfusion pressure breakthrough" and obstruction of venous drainage leading to "occlusive hyperemia." This study did not evaluate the arterial or venous circulations in this scenario, but rather examined the capillaries in adjacent brain parenchyma for any structural deficiencies that would predispose the brain to the postoperative formation of edema and hemorrhage. Arteriovenous fistulas (AVFs) were created surgically in the necks of 10 male Sprague-Dawley rats, which caused chronic cerebral hypoperfusion with a reduction in cerebral blood flow of between 25% and 50%. Ten age-matched animals were used as controls. Twenty-six weeks after AVF formation the animals were killed and perfusion fixed. Their brain tissue was prepared for light microscopic studies by staining for glial fibrillary acidic protein or for transmission electron microscopy. In the CA1 pyramidal cell region of the hippocampus, it was found that in the animals with AVFs there was increased capillary density and absent astrocytic foot processes in some of these vessels. It was concluded that these vessels had developed as a result of neovascularization in response to chronic cerebral ischemia and that their anatomical configuration made them prone to mechanical weakness and instability following the increase in perfusion pressure that occurs in adjacent brain parenchyma after AVM excision. The authors believe that this study pinpoints a structural accompaniment to the hemodynamic changes that occur in brain tissue in the vicinity of cerebral AVMs that predispose these areas to the formation of edema and hemorrhage after AVM excision.

Postcarotid Endarterectomy Hyperperfusion or Reperfusion Syndrome

“…18 The "normal perfusion pressure breakthrough" hypothesis 19 could explain the development of a bilateral (PLES) or unilateral (HS) "hypertensive encephalopathy" in the absence of severe hypertension. In a rat model of chronic cerebral hypoperfusion, 20 it has been documented a Ͼ100% increase in capillary density, with some of these capillaries becoming structurally defective in their walls. These capillaries are mechanically weaker and consequently more vulnerable to breakthrough by the distending forces that occur on reperfusion.…”

Distributions of Local Oxygen Saturation and Its Response to Changes of Mean Arterial Blood Pressure in the Cerebral Cortex Adjacent to Arteriovenous Malformations

“…35 A third mechanism to compensate for a low CPP is a reduced glucose and oxygen metabolism without increased oxygen extraction in the perilesional brain tissue, which has been found in studies with either positron emission tomography 36,37 or PtO 2 electrodes. 38 Accordingly, our results did not point to a higher than normal oxygen consumption.…”

Reducing Delay of Carotid Endarterectomy in Acute Ischemic Stroke Patients

“…Furthermore, there is uncertainty about the optimal timing for CEA in patients with medium or large acute infarcts because of fear of perioperative and postoperative complications, 9 in particular the risk of cerebral hyperperfusion syndrome and hemorrhagic transformation. [10][11][12] The aim of this study was to examine the effect of a multidisciplinary nationwide initiative aimed at reducing time to CEA after acute ischemic stroke (AIS) in Denmark. This initiative included the introduction of time limits for ultrasound examination of the carotids (USC) in the acute stroke setting and for operation after referral to vascular surgery.…”