Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

10.3791/62567 ◽  
2021 ◽  
Author(s):  
Jesper Peter Bömers ◽  
Sara Ellinor Johansson ◽  
Lars Edvinsson ◽  
Tiit Illimar Mathiesen ◽  
Kristian Agmund Haanes
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Rat Model ◽  
Single Injection ◽  
Autologous Blood ◽  
Experimental Subarachnoid Hemorrhage

Experimental Subarachnoid Hemorrhage in Rats 

1997 ◽  
Vol 87 (6) ◽  
pp. 1486-1493 ◽  
Author(s):  
Daniel J. Cole ◽  
Jeffrey C. Nary ◽  
Lowell W. Reynolds ◽  
Piyush M. Patel ◽  
John C. Drummond
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Death ◽  
Autologous Blood ◽  
The Other ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Experimental Subarachnoid Hemorrhage ◽  
Hematoxylin And Eosin

Background Hemodilution with diaspirin crosslinked hemoglobin (DCLHb) ameliorates occlusive cerebral ischemia. However, subarachnoid hemoglobin has been implicated as a cause of cerebral hypoperfusion. The effect of intravenous DCLHb on cerebral perfusion and neuronal death after experimental subarachnoid hemorrhage was evaluated. Methods Rats (n = 48) were anesthetized with isoflurane and subarachnoid hemorrhage was induced by injecting 0.3 ml of autologous blood into the cistema magna. Each animal received one of the following regimens: Control, no hematocrit manipulation; DCLHb, hematocrit concentration decreased to 30% with DCLHb; or Alb, hematocrit concentration decreased to 30% with human serum albumin. The experiments had two parts, A and B. In part A, after 20 min, cerebral blood flow (CBF) was assessed with 14C-iodoantipyrine autoradiography. In part B, after 96 h, in separate animals, the number of dead neurons was determined in predetermined coronal sections by hematoxylin and eosin staining. Results Cerebral blood flow was greater for the DCLHb group than for the control group; and CBF was greater for the Alb group than the other two groups (P < 0.05). In one section, CBF was 45.5 +/- 10.9 ml x 100 g(-1) x min(-1) (mean +/- SD) for the control group, 95.3 +/- 16.6 ml x 100 g(-1) x min(-1) for the DCLHb group, and 138.1 +/- 18.7 ml x 100 g(-1) x min(-1) for the Alb group. The number of dead neurons was less in the Alb group (611 +/- 84) than in the control group (1,097 +/- 211), and was less in the DCLHb group (305 +/- 38) than in the other two groups (P < 0.05). Conclusions These data support a hypothesis that hemodilution decreases hypoperfusion and neuronal death after subarachnoid hemorrhage. The data do not support the notion that intravascular molecular hemoglobin has an adverse effect on brain injury after subarachnoid hemorrhage.

The role of p53 in brain edema after 24 h of experimental subarachnoid hemorrhage in a rat model

2008 ◽  
Vol 214 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Junhao Yan ◽  
Chunhua Chen ◽  
Qing Hu ◽  
Xiaomei Yang ◽  
Jiliang Lei ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Edema ◽  
Rat Model ◽  
Experimental Subarachnoid Hemorrhage

Effect of intrathecal fibrinolysis on cerebrospinal fluid absorption after experimental subarachnoid hemorrhage

1991 ◽  
Vol 74 (5) ◽  
pp. 789-793 ◽  
Author(s):  
Thomas Brinker ◽  
Volker Seifert ◽  
Dietmar Stolke
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Autologous Blood ◽  
Recombinant Tissue Plasminogen Activator ◽  
Outflow Resistance ◽  
Content Type ◽  
Experimental Subarachnoid Hemorrhage ◽  
Logarithmic Relationship ◽  
Subarachnoid Blood ◽  
Csf Absorption

✓ The effect of intrathecal fibrinolysis on cerebrospinal fluid (CSF) absorption was investigated after experimental subarachnoid hemorrhage (SAH). In 11 cats, SAH was induced by intracisternal application of 1 to 4 ml of fresh autologous blood. Thirty minutes after the experimental SAH, the CSF outflow resistance was found to be elevated from a median of 77 mm Hg/ml/min (range 41.3 to 109 mm Hg/ml/min) to a median of 580 mm Hg/ml/min (range 104 to 7000 mm Hg/ml/min). A logarithmic relationship could be demonstrated between the volume of subarachnoid blood and the elevation of the CSF outflow resistance. The intrathecal application of 2 mg of recombinant tissue plasminogen activator (rt-PA), which is a fibrinolytic substance suitable for lysis of subarachnoid blood clots in man, resulted in an almost total restoration of CSF absorption after experimental SAH. The CSF outflow resistance after SAH was lowered by application of rt-PA from a median of 1028.05 mm Hg/ml/min (range 394 to 7000 mm Hg/ml/min) to 79 mm Hg/ml/min (range 56.7 to 223 mm Hg/ml/min). It is concluded that the impairment of CSF absorption after SAH may play an important role in the pathogenesis of post-hemorrhagic vasospasm.

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.

Resolvin D1 Attenuates Innate Immune Reactions in Experimental Subarachnoid Hemorrhage Rat Model

2021 ◽  
Author(s):  
Guang-Jie Liu ◽  
Tao Tao ◽  
Xiang-Sheng Zhang ◽  
Yue Lu ◽  
Ling-Yun Wu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Rat Model ◽  
Innate Immune ◽  
Resolvin D1 ◽  
Immune Reactions ◽  
Experimental Subarachnoid Hemorrhage

scholarly journals Roflumilast Reduces Cerebral Inflammation in a Rat Model of Experimental Subarachnoid Hemorrhage

Inflammation ◽  
2017 ◽  
Vol 40 (4) ◽  
pp. 1245-1253 ◽  
Author(s):  
Qingjian Wu ◽  
Lifeng Qi ◽  
Hanxia Li ◽  
Leilei Mao ◽  
Mingfeng Yang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Rat Model ◽  
Experimental Subarachnoid Hemorrhage ◽  
Cerebral Inflammation

Effect of experimental subarachnoid hemorrhage on the adrenergic innervation of cerebral arteries

1980 ◽  
Vol 53 (4) ◽  
pp. 477-479 ◽  
Author(s):  
Ramiro D. Lobato ◽  
Jesús Marín ◽  
Mercedes Salaices ◽  
Javier Burgos ◽  
Fernando Rivilla ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Autologous Blood ◽  
Cerebral Arteries ◽  
Adrenergic Innervation ◽  
Noradrenaline Content ◽  
Content Type ◽  
Perivascular Nerves ◽  
Experimental Subarachnoid Hemorrhage ◽  
6 Hydroxydopamine ◽  
Chronic Cerebral Vasospasm

✓ The effect of subarachnoid hemorrhage (SAH) on the adrenergic innervation of cat cerebral arteries was analyzed. Intracisternal injections of autologous blood reduced the noradrenaline content from the perivascular nerves. Dopamine beta-hydroxylase and the uptake of 3H-noradrenaline were also decreased. These changes returned to normal in a period of 2 to 3 weeks after the SAH. Superior cervical ganglionectomy and intracisternal injections of 6-hydroxydopamine also reduced these three parameters. It is suggested that SAH induces a transient adrenergic denervation of the cerebral arteries that might be involved in the production of the chronic cerebral vasospasm.

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