Impact of Cerebral Microcirculatory Changes on Cerebral Blood Flow During Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Abstract

Background and Purpose-Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) are still controversial and uncertain. The aim of this study was to investigate the changes of cerebral microcirculation during cerebral vasospasm and to clarify the roles of microcirculatory disturbances in cerebral ischemia by measuring cerebral circulation time (CCT) and regional cerebral blood flow (rCBF). Methods-In 24 cases with aneurysmal SAH, rCBF studies by single-photon emission CT and digital subtraction angiography (DSA) were performed on the same day between 5 and 7 days after SAH and/or within 4 hours after the onset of delayed ischemic neurological deficits. CCT was obtained by analyzing the time-density curve of the contrast media on DSA images and was divided into proximal CCT, which was the circulation time through the extraparenchymal large arteries, and peripheral CCT, which was the circulation time through the intraparenchymal small vessels. They were analyzed in association with rCBF and angiographic vasospasm. Results-Severe angiographic vasospasm statistically decreased rCBF, and correlation between the degree of angiographic vasospasm and rCBF was seen (rϭ0.429, Pϭ0.0006). Peripheral CCT showed strong inverse correlation with rCBF (rϭϪ0.767, PϽ0.0001). Even in none/mild or moderate angiographic vasospasm, prolonged peripheral CCT was clearly associated with decreased rCBF. Conclusions-In addition to the marked luminal narrowing of large arteries detected as severe angiographic vasospasm, microcirculatory changes detected as prolonged peripheral CCT affected cerebral ischemia during cerebral vasospasm. These results suggested that impaired autoregulatory vasodilation or decreased luminal caliber in intraparenchymal vessels may take part in cerebral ischemia during cerebral vasospasm.

Cerebral Vasospasm Affects Arterial Critical Closing Pressure

“…This preliminary inference would be in agreement with previous studies demonstrating dilated parenchymal small arteries and arterioles in the low perfusion area distal to spasm, [11][12][13][14]34 attributed to a possible autoregulatory response. 35,36 The behavior of the microvasculature during CVS has previously attracted considerable interest, although both clinical and experimental studies have produced conflicting results.…”

Reduced Ca2+ Spark Activity after Subarachnoid Hemorrhage Disables BK Channel Control of Cerebral Artery Tone

“…Additional factors contributing to the deleterious consequences of aneurysmal SAH may include global transient ischemia, early brain injury, disruption of the bloodbrain barrier, and activation of inflammatory pathways (Ostrowski et al, 2006;Prunell et al, 2005). It has now been realized that SAH may also impact small-diameter arteries and arterioles, i.e., those involved in the autoregulation of cerebral blood flow (Hattingen et al, 2008;Ishiguro et al, 2002;Ohkuma et al, 2000).…”

“…Additional factors contributing to the deleterious consequences of aneurysmal SAH may include global transient ischemia, early brain injury, disruption of the bloodbrain barrier, and activation of inflammatory pathways (Ostrowski et al, 2006;Prunell et al, 2005). It has now been realized that SAH may also impact small-diameter arteries and arterioles, i.e., those involved in the autoregulation of cerebral blood flow (Hattingen et al, 2008;Ishiguro et al, 2002;Ohkuma et al, 2000).In resistance arteries from healthy animals, vasoconstrictor stimuli such as physiologic increases in intravascular pressure lead to smooth muscle membrane potential depolarization, increased voltage-dependent Ca 2+ channel (VDCC) activity, and elevated global cytosolic calcium (Knot and Nelson, 1998 , the NIH (R01 HL078983, R01 HL078983-05S1, R01 HL44455, R37 DK053832, R01 DK065947, R01 HL098243, R01 HL077378, NCRR P20 RR16435, and P01 HL095488), and the American Heart Association (0725837T, 0725841T, 0815736D). Blood Flow & Metabolism (2011) (Jahromi et al, 2008b).…”

Isoflurane does not further impair microvascular vasomotion in a rat model of subarachnoid hemorrhage

“…Cerebral microvascular vasospasm may actually be more important in producing cerebral ischemia than conduit vessel vasospasm. 4 In our previous study using a rat model of SAH, 5 we demonstrated that cerebral arterioles after SAH have endothelial dysfunction that could contribute to vasospasm. As a result, cerebral arterioles after SAH demonstrated attenuated response to the endothelium-dependent dilator adenosine diphosphate (ADP) and accentuated constriction to endothelin-1 (ET-1).…”