Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study

2019 ◽  
Vol 80 (06) ◽  
pp. 430-440 ◽  
Author(s):  
Huseyin Findik ◽  
Ayhan Kanat ◽  
Mehmet Dumlu Aydin ◽  
Murteza Cakir ◽  
Sevilay Akalp Ozmen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Retinal Detachment ◽  
Sham Group ◽  
Autologous Blood ◽  
Control Group ◽  
Neuron Density ◽  
Before And After ◽  
Facial Nerves ◽  
Pterygopalatine Ganglion ◽  
Retinal Examination

Abstract Background The pterygopalatine ganglion (PPG) and ophthalmic arteries (OpAs) have important roles in ocular autoregulation and retinal and visual functions. The relationship between PPG neuron density, OpA vasospasm, and retinal detachment in subarachnoid hemorrhage (SAH) has never been studied. Methods This study was conducted on 25 rabbits. Five animals were in the control group (GI; n = 5), five in the sham group (GII; n = 5), and 15 in the study group (GIII; n = 15). After injection of 1 cc serum saline into the cisterna magna in the sham group, and autologous blood in the SAH group, the animals were followed for 3 weeks. All animals underwent a retinal examination five times a week for 3 weeks before and after the experiment. After the experiment, the neuron density of PPGs of the facial nerves, vasospasm index (VSI) of OpAs, and total basal surface values of the detached retinal parts (DRPs) were calculated. Results In the funduscopic examination, intravitreous hemorrhage ( Terson's syndrome) was detected in four animals in the SAH group. In the control groups, neuron density was 12,000 ± 1,240/mm3, VSI = 0.345 ± 0.076, and DRP = 0 to 1.5 mm2. Mean neuron density was 9,450 ± 940/mm3, VSI = 1.645 ± 0.940, and DRP = 6.23 ± 1.61 mm2 in the sham group (p < 0.05). Neuron density was 6,890 ± 932/mm3, VSI = 2.92 ± 0.97, and DRP = 9.43 ± 2.54 mm2 in SAH group. Conclusion Mean neuron density, VSI of OpAs, and DRP values differed statistically significant between the SAH group and other groups (p < 0.005). There is an inverse relationship between PPG neurons and DRP. However, a direct relationship was observed between the mean VSI and DRP values.

How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study

2017 ◽  
Vol 79 (04) ◽  
pp. 302-308 ◽  
Author(s):  
Cengiz Ozturk ◽  
Nuriye Ozdemir ◽  
Mehmet Aydin ◽  
Huseyin Findik ◽  
Nazan Aydin ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Sham Group ◽  
Posterior Communicating Artery ◽  
Nerve Degeneration ◽  
Control Group ◽  
Pupillary Diameter ◽  
Cisterna Magna ◽  
Neuron Density ◽  
Axon Density ◽  
The Mean

Background and Study Aim  Basic neurophysiologic principles of the light reflex are well known. However, the effects of degenerated axon densities of oculomotor nerves (OMNs) secondary to posterior communicating artery (PComA) vasospasm following subarachnoid hemorrhage (SAH) have not been investigated. Our aim was to study this subject. Methods This study was conducted on 19 rabbits. There was a control group of five animals, a sham group of five animals in which saline was injected into the cisterna magna and a study group of nine animals in which homologous blood was injected into the cisterna magna. Pupillary diameters were measured for 1 week, then the animals were decapitated. The normal and degenerated axon densities of the OMNs were examined by stereological methods. Vasospasm indexes (VSIs) of posterior communicating arteries (PComAs) supplying OMNs were estimated and analyzed statistically. Results The pupillary diameter was 5.439 ± 368 µm, and the mean axon density of the OMNs was 0.924 ± 324/mm3 in the control group. The pupillary diameter and degenerated axon density of the OMNs in animals of the sham group were 6.980 ± 0.370 µm and 36 ± 8/mm3, respectively. The pupillary diameter was 9.942 ± 653 µm, and degenerated axon density of the OMNs was 265 ± 57/mm3 in animals with SAH. The mean VSI values of PComAs were 0.927 ± 0.224 in the control group, 1.542 ± 0.257 in the sham group, and 2.321 ± 0.324 in the SAH group. Conclusion We found a linear relationship between the axon density of the OMNs and pupillary diameters. High degenerated neuron density in the OMNs may be responsible for an unresponsive pupillary that has not been mentioned in the literature.

Effects of the Ca++-permeable nonselective cation channel blocker LOE 908 on subarachnoid hemorrhage—induced vasospasm in the basilar artery in rabbits

2003 ◽  
Vol 98 (3) ◽  
pp. 561-564 ◽  
Author(s):  
Yoshifumi Kawanabe ◽  
Tomoh Masaki ◽  
Nobuo Hashimoto
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intravenous Administration ◽  
Basilar Artery ◽  
Channel Blocker ◽  
Autologous Blood ◽  
Content Type ◽  
Dependent Part ◽  
Before And After ◽  
Fine Print

Object. The Ca++ influx into vascular smooth-muscle cells (VSMCs) plays a fundamental role in the development and chronic effects of vasospasm after subarachnoid hemorrhage (SAH). The Ca++-permeable nonselective cation channels (NSCCs) are activated by several endothelium-derived constricting factors such as endothelin 1 (ET-1) and thromboxane A2. Moreover, the receptor-operated Ca++ channel blocker LOE 908 inhibits ET-1—induced extracellular Ca++ influx via NSCCs in the VSMCs of the basilar artery (BA) and the NSCC-dependent part of ET-1—induced vasoconstriction of BA rings. The purpose of the present study was to evaluate the in vivo role of LOE 908 on SAH-induced vasospasm. Methods. Forty-two Japanese white rabbits were assigned to seven groups. Treatment groups consisted of the following: 1) control rabbits without SAH that received a cisternal injection of saline; 2) rabbits with SAH that were subjected to the intravenous administration of saline; 3 through 6) rabbits with SAH that underwent the intravenous administration of 0.01, 0.1, 1, or 10 mg/kg LOE 908, respectively; and 7) rabbits without SAH that underwent the intravenous administration of 10 mg/kg LOE 908. Autologous blood was injected into the cisterna magna. The caliber of the BA was measured on angiographic studies before and after the cisternal injection of autologous blood. The intravenous injection of LOE 908 inhibited the magnitude of an SAH-induced vasosapsm. In addition, the concentration of LOE 908 required to relax vasospasm (1 mg/kg) correlated with that required to block Ca++ influx into VSMCs. Conclusions. The Ca++ channel blocker LOE 908 may inhibit the magnitude of an SAH-induced vasospasm by blocking the influx of Ca++ through NSCCs in rabbit BAs. Blocking the NSCCs may represent a new treatment for cerebral vasospasm after SAH.

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 &lt; 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 &lt; 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.

Alterations of mechanical properties in canine basilar arteries after subarachnoid hemorrhage

1989 ◽  
Vol 71 (3) ◽  
pp. 430-436 ◽  
Author(s):  
Phyo Kim ◽  
Thoralf M. Sundt ◽  
Paul M. Vanhoutte
Keyword(s):  
Mechanical Properties ◽  
Subarachnoid Hemorrhage ◽  
Autologous Blood ◽  
Myogenic Tone ◽  
Control Group ◽  
Resting Tension ◽  
Length Contraction ◽  
Basilar Arteries ◽  
Chronic Vasospasm

✓ The purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic vasospasm were induced in dogs by two cisternal injections of autologous blood (on Day 0 and Day 2). Vasospasm was confirmed by angiography performed on Day 0 and Day 7. Animals in the control group underwent angiography only. On Day 8, the mechanical properties of the basilar arteries were studied in vitro. Passive compliance, measured under total inhibition of spontaneous myogenic tone with diltiazem (10−4 M) plus papaverine (10−4 M) was smaller in the SAH group. The length-contraction curve was shifted to the left and the optimum length for maximum contraction (Lmax) was significantly shorter in the spastic blood vessels. The spontaneous myogenic tone was augmented in the SAH group, resulting in an increase in resting tension at each length. By contrast, the maximum contractions in response to KCl and uridine 5′-triphosphate were markedly reduced in the SAH group, without changes in sensitivity to these agents. These differences in mechanical properties were observed in rings both with and without endothelium. The results indicate that, in chronic vasospasm, stiffening of the noncontractile component of the vasculature takes place as well as alterations in the contractile component, both of which presumably contribute to the shift in resting length-tension relationship and length-contraction relationship of the artery. The decreased distensibility, the increase in resting tension, and the shortening of the Lmax all favor a smaller diameter of the artery after SAH, possibly contributing to vasospasm.

Role of ferrous iron chelator 2,2′-dipyridyl in preventing delayed vasospasm in a primate model of subarachnoid hemorrhage

1998 ◽  
Vol 88 (2) ◽  
pp. 298-303 ◽  
Author(s):  
Laura L. Horky ◽  
Ryszard M. Pluta ◽  
Robert J. Boock ◽  
Edward H. Oldfield
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Clot ◽  
Autologous Blood ◽  
Iron Chelator ◽  
Preventive Therapy ◽  
Control Group ◽  
Primate Model ◽  
Content Type ◽  
Fine Print

Object. Oxyhemoglobin (HbO2) causes vasospasm after subarachnoid hemorrhage (SAH). The most likely spasmogenic component of HbO2 is iron. Various iron chelators, such as deferoxamine, have prevented vasospasm in vivo with limited success. However, only chelators of iron in the ferric state have been studied in animal models of vasospasm after SAH. Because free radical formation requires the ferrous (Fe++) moiety and Fe++ is a potent binder of the vasodilator nitric oxide, the authors hypothesized that iron in the ferrous state causes vasospasm and that chelators of Fe++, such as 2,2′-dipyridyl, may prevent vasospasm. This study was undertaken to investigate the influence of 2,2′-dipyridyl on vasospasm after induction of SAH in a primate model. Methods. Twelve cynomolgus monkeys were randomly divided into two groups and then both groups underwent placement of an arterial autologous blood clot in the subarachnoid space around the right middle cerebral artery (MCA). The five animals in the control group received intravenously administered saline and the seven treated animals received intravenously administered chelator (2,2′-dipyridyl) for 14 days. Sequential arteriography for assessment of MCA diameter was performed before and on the 7th day after SAH. Conclusions. Prevention of cerebral vasospasm by means of treatment with continuous intravenous administration of 2,2′-dipyridyl is reported in a primate model of SAH. This result provides insight into the possible mechanism of delayed vasospasm after aneurysmal SAH and provides a potential preventive therapy for it.

scholarly journals Effect of N-acetylcysteine on vasospasm in subarachnoid hemorrhage

2010 ◽  
Vol 68 (6) ◽  
pp. 918-922 ◽  
Author(s):  
Nelson de Azambuja Pereira Filho ◽  
Arthur de Azambuja Pereira Filho ◽  
Fabiano Pasqualotto Soares ◽  
Ligia Maria Barbosa Coutinho
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Experimental Model ◽  
Basilar Artery ◽  
Intracranial Aneurysms ◽  
Wistar Rats ◽  
Autologous Blood ◽  
Control Group ◽  
Arterial Vasospasm ◽  
Significant Difference ◽  
Ruptured Intracranial Aneurysms

Vasospasm remains an extremely serious complication that affects patients presenting with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms. The current therapeutic armamentarium is still insufficient in many cases, and the search for new therapies is necessary. In this study, we evaluated the effect of N-acetylcysteine (NAC) on cerebral arterial vasospasm using an experimental model. Twenty-four wistar rats were divided into 4 groups: [1] Control, [2] SAH, [3] SAH+NAC and [4] SAH+Placebo. The experimental model employed double subarachnoid injections of autologous blood. The proposed dose of NAC was 250 mg/kg intraperitoneally per day. We analyzed the inner area of the basilar artery to assess the action of NAC. The experimental model proved to be very adequate, with a mortality rate of 4%. The inner area of the basilar artery in the SAH group showed significant difference to the control group (p=0.009). The use of NAC significantly reduced vasospasm as compared to the untreated group (p=0.048) and established no significant difference to the control group (p=0.098). There was no significant improvement with the administration of placebo (p=0.97). The model of the dual hemorrhage proved to be very useful for vasospasm simulation, with overall low mortality. The administration of NAC significantly reduced vasospasm resulting from SAH, and may represent a new therapeutic alternative.

scholarly journals Acupuncture Anxiolytic Effects on Physiological and Psychological Assessments for a Clinical Trial

Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Monir Shayestehfar ◽  
Tohid Seif-Barghi ◽  
Sahar Zarei ◽  
Amir Mehran
Keyword(s):  
Skin Conductance ◽  
Sham Group ◽  
Acupuncture Group ◽  
Control Group ◽  
Wait List ◽  
Wait List Control Group ◽  
Wait List Control ◽  
Somatic Anxiety ◽  
Cognitive Anxiety ◽  
Before And After

In a randomized controlled trial we examined the effect of acupuncture on anxiety of the adolescent football players prior to the competition using psychological and physiological markers. A total of 45 athletes were equally allocated to either acupuncture group, sham group, or wait-list control group. Thereafter, all participants were asked to complete an anxiety questionnaire before and after the intervention. Their heart rate and skin conductance were also examined before and after the intervention. The results of ANOVA on posttest scores showed that acupuncture had a significant effect on cognitive anxiety (p=0.001) and somatic anxiety (p<0.001) but not on self-confidence (p>0.05). Furthermore, the results showed that acupuncture significantly decreased the skin conductance in acupuncture group compared to sham group (p=0.006) and wait-list control group (p<0.001). In conclusion, the results suggested that acupuncture has the capacity to decrease cognitive anxiety and somatic anxiety prior to competition in adolescent athletes, while this was accompanied by significant physiological changes. This trial is registered withIRCT138904074264N1(IRCT is a Primary Registry in the WHO Registry Network).

Prevention of vasospasm by anti-CD11/CD18 monoclonal antibody therapy following subarachnoid hemorrhage in rabbits

2004 ◽  
Vol 101 (1) ◽  
pp. 88-92 ◽  
Author(s):  
Gustavo Pradilla ◽  
Paul P. Wang ◽  
Federico G. Legnani ◽  
Lynn Ogata ◽  
Gregory N. Dietsch ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cells ◽  
Subarachnoid Hemorrhage ◽  
Autologous Blood ◽  
Rabbit Model ◽  
Control Group ◽  
Lymphocyte Function ◽  
Content Type ◽  
Basilar Arteries ◽  
Fine Print

Object. Adhesion of leukocytes and their migration into the periadventitial space may be critical in the pathophysiology of vasospasm following subarachnoid hemorrhage (SAH). The cell adhesion molecules involved in this process are lymphocyte function—associated antigen—1 (CD11a/CD18) and macrophage antigen—1 (CD11b/CD18), which are present on neutrophils/macrophages, and intercellular adhesion molecule—1 (CD54), which is present in endothelial cells. A humanized monoclonal antibody (mAb), Hu23F2G, targets CD11/CD18 and prevents leukocyte adhesion to endothelial cells. In this study, systemic administration of Hu23F2G prevented vasospasm in the rabbit model of SAH. Methods. Twenty-six New Zealand White rabbits were injected with autologous blood into the cisterna magna to induce SAH, after which they were randomized to receive injections of either Hu23F2G (10 animals) or a placebo at 30 minutes and 24 and 48 hours after SAH (six animals). Control animals underwent sham operations (four animals) or SAH alone (six animals). The animals were killed 72 hours after SAH, their bodies perfused and fixed, and their basilar arteries processed for morphometric analysis. Peripheral white blood cells (WBCs) were counted at 72 hours. The percentages of lumen patency were compared using the Student t-test. The presence of neutrophils and macrophages was confirmed by immunohistochemical analysis in which a rat anti—rabbit anti-CD18 mAb and cresyl violet were used. Treatment with Hu23F2G resulted in the significant prevention of vasospasm. Animals treated with Hu23F2G had 90 ± 7% lumen patency compared with 65 ± 7% in the placebo group (p = 0.025). The percentage of lumen patency in the SAH-only group was 59 ± 10%. The mean WBC count was 16,300 ± 2710/µl in the treatment group, compared with 7000 ± 386/µl in the control group (p = 0.02). Administration of Hu23F2G produced increased numbers of WBCs in 70% of the animals treated. Conclusions. This study supports the concept that leukocyte—endothelial cell interactions play an important role in the pathophysiology of chronic vasospasm after SAH. Systemic therapy with an anti-CD11/CD18 mAb prevents vasospasm after SAH by inhibiting adhesion of neutrophils and macrophages and their migration into the periadventitial space.

Immunology, Treatment and Public Health Aspects of Subarachnoid Hemorrhage

2020 ◽  
Author(s):  
Junjing ZHAO ◽  
Jianping ZHANG ◽  
Yongxia BU ◽  
Wei LU ◽  
Gejin ZHAO
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Hospital Stay ◽  
Length Of Hospital Stay ◽  
Effective Rate ◽  
Control Group ◽  
Observation Group ◽  
Before And After ◽  
Immune Globulins ◽  
The Impact ◽  
Ig G

Background: We aimed to explore the treatment and safety of subarachnoid hemorrhage. Methods: A retrospective analysis was applied on 137 patients with subarachnoid hemorrhage treated in Binzhou Central Hospital, Bingzhou, China from March 2015 to October 2018. Seventy cases with interventional embolization of intracranial aneurysms were divided as the observation group, and 67 cases with craniotomy for aneurysm clipping were divided as the control group. The changes of immune globulins before and after surgery, CD4+, CD8+, NIHSS scores, BI scores, the total effective rate of subarachnoid hemorrhage, the total length of postoperative hospital stay and conditions of postoperative complications as well as 30-day survival were compared between the two groups. Results: The levels of Ig G, Ig M, Ig A, and CD4+ after surgery in the observation group were significantly lower than those before surgery (P<0.05), but significantly higher than those in the control group (P<0.05); the total time of postoperative hospitalization in the observation group was shorter than that in the control group (P<0.05). The incidence of intracranial infection and cerebral vasospasm in the observation group was significantly lower than that in the control group (P<0.05). The NIHSS score of the observation group was significantly lower than that of the control group (P<0.05), and the BI score was significantly higher than that of the control group (P<0.05). Conclusion: Patients with subarachnoid hemorrhage undergoing interventional embolization of aneurysms can reduce the impact on immune function, decrease the adverse reactions caused by treatments, shorten the length of hospital stay and fully improve the efficacy.

scholarly journals Vagosympathetic imbalance induced thyroiditis following subarachnoid hemorrhage: a preliminary study

2020 ◽  
Vol 8 (1) ◽  
pp. 17-17
Author(s):  
Ozgur Caglar ◽  
Erdem Karadeniz ◽  
Irem Ates ◽  
Sevilay Ozmen ◽  
Mehmet Dumlu Aydin
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Thyroid Hormone ◽  
Sham Group ◽  
Study Group ◽  
Superior Cervical Ganglia ◽  
Neuron Density ◽  
Thyroid Glands ◽  
Preliminary Study ◽  
Thyroid Hormone Levels ◽  
Cervical Ganglia

Introduction: This preliminary study evaluates the possible responsibility of ischemia-induced vagosympathetic imbalances following subarachnoid hemorrhage (SAH), for the onset of autoimmune thyroiditis. Methods: Twenty-two rabbits were chosen from our former experimental animals, five of which were picked from healthy rabbits as control (nG-I=5). Sham group (nG-II=5) and animals with thyroid pathologies (nG-III=12) were also included after a one-month-long experimental SAH follow-up. Thyroid hormone levels were measured weekly, and animals were decapitated. Thyroid glands, superior cervical ganglia, and intracranial parts of vagal nerve sections obtained from our tissue archives were reexamined with routine/immunohistochemical methods. Thyroid hormone levels, hormone-filled total follicle volumes (TFVs) per cubic millimeter, degenerated neuron density (DND) of vagal nuclei and neuron density of superior cervical ganglia were measured and statistically compared. Results: The mean neuron density of both superior cervical ganglia was estimated as 8230±983/ mm3 in study group animals with severe thyroiditis, 7496±787/mm3 in the sham group and 6416±510/mm3 in animals with normal thyroid glands. In control group (group I), T3 was 107±11 μg/dL, T4: 1,43±0.32 μg/dL and TSH <0.5, while mean TFV was 43%/mm3 and DND of vagal nuclei was 3±1/mm3. In sham group (group II), T3 was 96±11 μg/dL, T4: 1.21±0.9 μg/ dL and TSH>0.5 while TFV was 38%/mm3 and DND of vagal nuclei was 13±4. In study group, T3 was 54±8 μg/dL, T4: 1,07±0.3 μg/dL and TSH >0.5, while TFV was 27%/mm3 and DND of vagal nuclei was 42±9/mm3. Conclusion: Sympathovagal imbalance characterized by relative sympathetic hyperactivity based on vagal insufficiency should be considered as a new causative agent for hypothyroidism.

Sign in / Sign up

Export Citation Format

Share Document