Acetazolamide reactivity on cerebral blood flow in patients with subarachnoid haemorrhage

Abstract

Cerebral vasodilatory capacity was evaluated by acetazolamide-activated N-isopropyl-p-[123I]iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) in 42 patients with subarachnoid haemorrhage (SAH). A low perfusion area was present in the corresponding region of haematoma seen on the CT and continued to be noted throughout the time courses. Deteriorated acetazolamide reactivity affected by surgical intervention was seen in 100% of the patients who underwent aneurysm repair in the 1st postoperative week, 92% in the second week, 73% in the third week, and 47% in the fourth week. Three patients with acute diffuse brain swelling seen on CT showed intracranial non-filling of 123I-IMP on SPECTs performed on Day 6, and all three died by Day 10. Some low perfusion areas, due to probable vasospasm, were present in 77% of Hunt and Hess grades I and II patients and in 100% of grades III, IV, and V patients throughout their time courses. Overall, low perfusion areas, due to probable vasospasm, were seen in 10 patients (31%) of 32 who underwent SPECT between Day 4 and 8,23 (77%) of 30 between Day 9 and 14, 21 (72%) of 29 between Day 15 and 21, and 11 (48%) of 23 between Day 22 and 28. The results suggest acetazolamide-activated 123I-IMP study is of value in evaluating changes in vasodilatory capacity in SAH patients in the acute and subacute stages.

Intro-arterial Administration of Fasudil Hydrochloride for Vasospasm Following Subarachnoid Hemorrhage-Analysis of Time-Density Curve With Digital Subtraction Angiography-

“…1,2,11,16) This weak autoregulatory response has been attributed to maximal dilation of the peripheral arterioles to maintain sufficient cerebral blood flow in the presence of decreased cerebral perfusion pressure due to vasospasm. However, a recent histological study revealed that intraparenchymal small arteries or arterioles show luminal narrowing rather than dilation during cerebral vasospasm after experimental SAH.…”

The Role of Arterioles and the Microcirculation in the Development of Vasospasm after Aneurysmal SAH

“…They suggested that cerebral vasospasm of large arteries is accompanied by a massive dilation of the intraparenchymal vessels [28]. A CBF study using single photon emission computed tomography showed that CBF did not increase by administering acetazolamide in SAH patients [29]. Furthermore, a transcranial Doppler sonography (TCD) study revealed that hypercapnia does not decrease flow velocities in the middle cerebral arteries or the internal carotid arteries of patients with cerebral vasospasm [30].…”

“…Furthermore, a transcranial Doppler sonography (TCD) study revealed that hypercapnia does not decrease flow velocities in the middle cerebral arteries or the internal carotid arteries of patients with cerebral vasospasm [30]. These decreased reactivities to vasodilating stimuli were thought to be due to a lack of response by small vessels because of their maximal dilation in an attempt to maintain sufficient CBF in the face of severe vasospasm [29, 30]. Studies using several imaging techniques in patients with SAH [31–34] and in animal models of SAH [35–37] have suggested the existence of microvessel constriction and microthrombi formation after SAH.…”

Acetazolamide as a vasodilatory stimulus in cerebrovascular diseases and in conditions affecting the cerebral vasculature

“…Therefore, AZ tests may help in timing surgery and in the follow‐up of patients after the operation (Mourier et al. , 1991; Shinoda et al. , 1991; George et al.…”