scholarly journals In vivo observation of cerebral microcirculation after experimental subarachnoid hemorrhage in mice

2018 ◽  
Vol 13 (3) ◽  
pp. 456 ◽  
Author(s):  
Jing-yan Han ◽  
Chun-hua Chen ◽  
Xiao-mei Yang ◽  
Xu-hao Chen ◽  
Jian-fei Lu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Microcirculation ◽  
Experimental Subarachnoid Hemorrhage

Hypothalamic neuropeptide release after experimental subarachnoid hemorrhage: in vivo microdialysis study

2004 ◽  
Vol 109 (5) ◽  
pp. 361-368 ◽  
Author(s):  
A. Kleindienst ◽  
G. Hildebrandt ◽  
S. A. Kroemer ◽  
G. Franke ◽  
M. R. Gaab ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
In Vivo Microdialysis ◽  
Neuropeptide Release ◽  
Experimental Subarachnoid Hemorrhage ◽  
Microdialysis Study

scholarly journals Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

2011 ◽  
Vol 32 (3) ◽  
pp. 447-455 ◽  
Author(s):  
Benjamin Friedrich ◽  
Frank Müller ◽  
Sergej Feiler ◽  
Karsten Schöller ◽  
Nikolaus Plesnila
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Perfusion Pressure ◽  
Early Brain Injury ◽  
Microscopy Study ◽  
Cerebral Microvessels ◽  
Experimental Subarachnoid Hemorrhage ◽  
Pial Arterioles

Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a severe, cerebral perfusion pressure (CPP)-independent reduction in cerebral blood flow suggesting alterations on the level of cerebral microvessels. Therefore, we aimed to use in-vivo imaging to investigate the cerebral microcirculation after experimental SAH. Subarachnoid hemorrhage was induced in C57/BL6 mice by endovascular perforation. Pial arterioles and venules (10 to 80 μm diameter) were examined using in-vivo fluorescence microscopy, 3, 6, and 72 hours after SAH. Venular diameter or flow was not affected by SAH, while >70% of arterioles constricted by 22% to 33% up to 3 days after hemorrhage ( P<0.05 versus sham). The smaller the investigated arterioles, the more pronounced the constriction ( r2=0.92, P<0.04). Approximately 30% of constricted arterioles were occluded by microthrombi and the frequency of arteriolar microthrombosis correlated with the degree of constriction ( r2=0.93, P<0.03). The current study demonstrates that SAH induces microarterial constrictions and microthrombosis in vivo. These findings may explain the early CPP-independent decrease in cerebral blood flow after SAH and may therefore serve as novel targets for the treatment of early perfusion deficits after SAH.

scholarly journals Angiotensin IV Reverses the Acute Cerebral Blood Flow Reduction after Experimental Subarachnoid Hemorrhage in the Rat

1994 ◽  
Vol 14 (6) ◽  
pp. 1096-1099 ◽  
Author(s):  
Liisa Näveri ◽  
Christer Strömberg ◽  
Juan M. Saavedra
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Saline Group ◽  
Ang Ii ◽  
Doppler Flowmetry ◽  
Blood Flow Reduction ◽  
Experimental Subarachnoid Hemorrhage ◽  
Ang Iv ◽  
Oxide Synthase

The effect of angiotensin (ANG) IV on CBF after experimental subarachnoid hemorrhage (SAH) was studied in rats using laser–Doppler flowmetry. ANG IV (1 μg/kg/min i.v.) or saline treatments were started 20 min after SAH. ANG IV increased CBF (from 45 to 84% of baseline) by 60 min. In the saline group, CBF remained low (51%). Pretreatment with the specific ANG II antagonist Sar1, Ile8-ANG II did not antagonize ANG IV. Determination of nitric oxide synthase (NOS) activity in vitro or inhibition of NOS in vivo did not support a role for NO in the action of ANG IV.

Reintroduction of the Rat for Experimental Subarachnoid Hemorrhage with Accelerated Clot Formation: A Low Mortality Model with Persistent Clots as a Precondition for Studies in Vasospasm

2018 ◽  
Vol 79 (05) ◽  
pp. 424-433 ◽  
Author(s):  
Ulrich Budde ◽  
Ralf Middendorff ◽  
Gerd Manthei ◽  
Andre Kemmling ◽  
Bastian Tiemann ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Tissue Factor ◽  
Rat Model ◽  
Animal Studies ◽  
Clot Formation ◽  
Delayed Effects ◽  
In Vivo Testing ◽  
Experimental Subarachnoid Hemorrhage

Background Cerebral vasospasm as a delayed, possibly treatable sequel of subarachnoid hemorrhage (SAH) is a focus of experimental animal research. For this purpose, the rat is not a good model because of the difficulty creating a stable subarachnoid clot that persists > 1 to 2 days and could induce vasospasm. Only in rat models with a high mortality of ∼ 50% or more can SAH and its effects be investigated. Therefore, other animals than rodents are used for investigating the delayed effects of SAH. Only animal studies addressing the acute effects of SAH use rats. Objective We designed a model that allows intensive clot formation combined with low mortality to facilitate studies on the delayed effects of experimental SAH, for example, delayed vasospasm or other alterations of vessels. Methods After in vitro acceleration of the clotting process in the rats' blood by tissue factor and preliminary in vivo testing, we induced a SAH by injecting blood together with tissue factor in 22 rats. We analyzed clot expansion, length of clot persistence, chronic alterations, and histologic changes. Results The injection of blood supplemented by tissue factor led to persistent voluminous blood clots in the subarachnoid space close to the large arteries. Despite the pronounced SAH, all animals survived, allowing investigation of delayed SAH effects. All animals killed within the first 7 days after surgery had extensive clots; in some animals, the clots remained until postoperative day 12. During further clot degradation connective tissue appeared, possibly as a precursor of SAH-related late hydrocephalus. Conclusion The injection of blood together with tissue factor significantly improves SAH induction in the rat model. This rat model allows studying delayed SAH effects as found in humans.

scholarly journals Long-term impairment of neurovascular coupling following experimental subarachnoid hemorrhage

2019 ◽  
Vol 40 (6) ◽  
pp. 1193-1202 ◽  
Author(s):  
Matilde Balbi ◽  
Max Jativa Vega ◽  
Athanasios Lourbopoulos ◽  
Nicole A Terpolilli ◽  
Nikolaus Plesnila
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Neurovascular Coupling ◽  
Early Brain Injury ◽  
Vessel Diameter ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Experimental Subarachnoid Hemorrhage

CO2-reactivity and neurovascular coupling are sequentially lost within the first 24 h after subarachnoid hemorrhage (SAH). Whether and when these impairments recover is not known. Therefore, we investigated the reactivity of pial and intraparenchymal vessels by in vivo two-photon microscopy one month after experimental SAH. C57BL/6 mice were subjected to either sham surgery or SAH by filament perforation. One month later, cerebral blood flow following CO2-challenge and forepaw stimulation was assessed by laser Doppler fluxmetry. Diameters of pial and intraparenchymal arterioles were quantified by in vivo two-photon microscopy. One month after SAH, pial and parenchymal vessels dilated in response to CO2. Neurovascular coupling was almost completely absent after SAH: vessel diameter did not change upon forepaw stimulation compared to a 20% increase in sham-operated mice. The current results demonstrate that neurovascular function differentially recovers after SAH: while CO2-reactivity normalizes within one month after SAH, neurovascular coupling is still absent. These findings show an acute and persistent loss of neurovascular coupling after SAH that may serve as a link between early brain injury and delayed cerebral ischemia, two distinct pathophysiological phenomena after SAH that were so far believed not to be directly related.

Scavenging Free Iron Reduces Arteriolar Microvasospasms After Experimental Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Author(s):  
Hanhan Liu ◽  
Julian Schwarting ◽  
Nicole Angela Terpolilli ◽  
Kathrin Nehrkorn ◽  
Nikolaus Plesnila
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Free Iron ◽  
Acute Cerebral Ischemia ◽  
Experimental Subarachnoid Hemorrhage ◽  
Underlying Mechanisms ◽  
Novel Therapeutic Strategies

Background and Purpose: Subarachnoid hemorrhage (SAH) is associated with acute and delayed cerebral ischemia resulting in high acute mortality and severe chronic neurological deficits. Spasms of the pial and intraparenchymal microcirculation (microvasospasms) contribute to acute cerebral ischemia after SAH; however, the underlying mechanisms remain unknown. We hypothesize that free iron (Fe 3+ ) released from hemolytic red blood cells into the subarachnoid space may be involved in microvasospasms formation. Methods: Male C57BL/6 mice (n=8/group) received 200 mg/kg of the iron scavenger deferoxamine or vehicle intravenously and were then subjected to SAH by filament perforation. Microvasospasms of pial and intraparenchymal vessels were imaged three hours after SAH by in vivo 2-photon microscopy. Results: Microvasospasms occurred in all investigated vessel categories down to the capillary level. Deferoxamine significantly reduced the number of microvasospasms after experimental SAH. The effect was almost exclusively observed in larger pial arterioles (>30 µm) covered with blood. Conclusions: These results provide proof-of-principle evidence that Fe 3+ is involved in the formation of arteriolar microvasospasms after SAH and that arteriolar and capillary microvasospasms are triggered by different mechanisms. Deciphering the mechanisms of Fe 3+ -induced microvasospasms may result in novel therapeutic strategies for SAH patients.

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