The coagulation hemostasis dynamics in rats in the post-ischemic time

Introduction. Ischemic injury to the endothelium influences on a coagulation hemostasis, worsening hemodynamics of cerebral microcirculation as a result of rheological occlusion. The long-term post-ischemic blood clotting system changes are not studied well by now.The work purpose – to study a coagulation hemostasis and endothelial prostacyclin – synthetic activity of pial vessels within 21 days after single short-term transient cerebral ischemia in rat.Material and Methods. Ischemia was reproduced by means of 12-minute time occlusion of both carotids with the simultaneous arterial hypotension. Post-ischemic changes were investigated in 4 groups of rats: on the 3rd, 7th, 14th and 21st day after ischemia. The state of blood clotting system was estimated on time of clot formation in the blood plasma by an automatic optical method with use of screening tests of definition of prothrombin and thrombin clotting time and concentration of fibrinogen. Endothelial prostacyclin – synthetic activity was estimated by pial vessel reaction to indometacin.Results. On the 3rd day after ischemia the increase in prothrombin time was observed. Level of fibrinogen increased on the 3rd and the 14th days of the post-ischemic time. On the 21st day after ischemia thrombin time decreased. The inverse correlation of pial vessel endothelial prostacyclin – synthetic activity with the fibrinogen level and direct correlation with vessel cross-sectional area of these vessels is established.Conclusions. Short-time global cerebral ischemia causes changes of blood clotting system mechanisms lasting for 21 days of the post-ischemic time. Post-ischemic abnormalities in hemostasis system are connected with changes in endothelial prostacyclin – synthetic activity of cerebral vessels that, along with decreased anti-aggregation ability of vascular system, is also the reason of narrowing of the lumen in pial vessels.

Safety and Feasibility of Balloon-Assisted Embolization with Onyx of Brain Arteriovenous Malformations Revisited: Personal Experience with the Scepter XC Balloon Microcatheter

Background/Objective: Compliant dual-lumen balloon microcatheters have been used to perform balloon-assisted embolization (BAE) of brain arteriovenous malformations (AVMs) with ethylene vinyl alcohol copolymer (Onyx). However, vessel rupture and microcatheter retention have been reported from BAE using these microcatheters. Using an extra-compliant balloon microcatheter (Scepter XC; Microvention, Tustin, CA, USA) could help avoid pial vessel rupture during BAE. We herein report our experience using this balloon microcatheter for BAE. Methods: This retrospective study included patients who underwent BAE of brain AVMs at our institution between June 2012 and March 2017. Results: The extra-compliant Scepter XC balloon microcatheter was used for BAE of brain AVMs in 23 patients aged 44.3 ± 16.7 years (range 0–65 years). A total of 40 intracranial vessels (39 pial arteries and 1 pial vein) were catheterized and embolized during 30 separate sessions. In all instances, the balloon microcatheter could be successfully advanced to the AVM nidus. A mean volume of 2.4 ± 1.7 mL (range 0.65–4.6 mL) of Onyx was injected per session. There were no instances of vessel rupture, microcatheter retention, or stroke. Conclusion: Utilization of the extra-compliant balloon microcatheter results in safe and effective BAE, which adds to the growing experience with BAE for AVM treatment.

Abstract WMP23: Regional Assessment of Multi-phase CTA and CT Perfusion are Equivalent in Predicting Tissue Fate in Ischemic Stroke

Introduction: The use of CT Perfusion (CTP) in acute ischemic stroke (AIS) to determine patients with large ischemic core is still hampered by slow processing time, among other technical/standardization issues. Multi-phase CTA (mCTA) may be quicker and more practical in this regard. We sought to determine i) the performance of mCTA and CTP to predict regional infarction and ii) which mCTA construct(s) corresponds to which CTP parameter . Methods: mCTA and CTP was performed less than 12hrs from ictus in 77 patients with MCA-M1 occlusions. Regional analysis was performed within M2-M6 ASPECTS-regions. mCTA: regional pial vessels were assessed according to three constructs: i) Delay in maximal pial vessel enhancement compared to contralateral hemisphere; ii) Washout of contrast within pial vessels; iii) Extent of maximal pial vessel enhancement compared to contralateral hemisphere (Figure 1). CTP-CBF, CBV, MTT, IRF-T0, and Tmax values were determined. 24-hour MR-DWI or NCCT was used for final infarction. Results: There was a negligible difference in the predictive accuracy of mCTA and CTP in discriminating infarction (i.e., 84.59% and 83.04%, respectively). mCTA-Extent had the largest discriminatory power, while CTP-Tmax had the largest discriminatory power. Conclusion: Herein we show that mCTA assessments, even within small brain regions can help determine tissue fate when adjusted for recanalization, and is as good as CTP. mCTA may be a more practical modality to obtain similar prognostic information for radiological and clinical outcomes in AIS, informing acute treatment and tertiary centre triaging.

Dynamics of pial vessels reactivity after brief cerebral ischemia

Cerebral blood vessel reactivity is one of the main determinants of final outcome of brain ischemia. Most of studies on the vascular mechanisms of ischemic brain injury, however, focus on the acute changes within ischemic period or several hours after it. Dilatatory capacity of cerebral arterioles (perfusion reservoir) is considered as an important factor of brain perfusion elevation in critical situations.The aim of the present study was to examine the pial vessel reactivity in response to hypercapnia in rats, subjected to transient global cerebral ischemia, at 7, 14 and 21 days after ischemia. Materials and methods. Transient global cerebral ischemia was induced in anesthetized Wistar rats by bilateral common carotid artery occlusion for 12 min with simultaneous controlled hypotension to 45±3 mm Hg, followed by blood reinfusion and recovery from anesthesia. Three different groups of rats were re-anesthetized at 7, 14 or 21 days after ischemia and subjected to microvascular reactivity studies using in vivo video microscopy. Hypercapnia was caused by i.v. injection of acetazolamide. The changes in diameter of pial arteries and veins in response to hypercapnia were measured. Results and discussion. Global cerebral ischemia led to marked decrease in pial vessels (both arteries and veins) reactivity in response to hypercapnia, caused by i.v. injection of acetazolamide. In intact rats, i.v. injection of acetazolamide led to pial arteries dilation and pial veins constriction; in animals subjected to ischemia-reperfuion. the numbers of dilated large arteries and constricted small veins were much less, as well as the extent of arterial dilation. Reactivity changes were observed in all time points studied. Conclusions. Thus, transient global cerebral ischemia cause marked and long lasting (3 weeks) decrease in pial vessel reactivity in response to hypercapnia.

Estrogen restores postischemic pial microvascular dilation

Estrogen protects the brain from experimental cerebral ischemia, likely through both vascular and neuronal cellular mechanisms. The purpose of this study was to determine whether chronic estrogen treatment in males and repletion in ovariectomized (Ovx) females reverses abnormalities in pial arteriolar reactivity during reperfusion from global forebrain ischemia (4-vessel occlusion, 15 min) and whether the site of protection is vascular endothelium. Male and Ovx female rats were implanted with either placebo or a 25-μg 17β-estradiol pellet 10 days before ischemia. With the use of intravital microscopy, pial vessel dilation to ACh (10 μM) and S-nitroso- N-acetyl-penicillamine (SNAP; 1 μM) and vasoconstriction to serotonin (10 μM) was examined in situ at 30–60 min of reperfusion. Postischemic changes in vessel diameter were compared with preischemic values for each agent. Postischemic response to both ACh and SNAP was lost in males and Ovx females, but not in estrogen pellet-implanted males and estrogen-implanted Ovx females, suggesting that estrogen protects both endothelial and smooth muscle-mediated vasodilation. Ischemia blunted vessel constriction to serotonin regardless of treatment. These data demonstrate that estrogen acts as a vasoprotective agent within the cerebral circulation and can improve microvascular function under conditions of an acutely evolving ischemic pathology.