Combined effect of L-arginine and superoxide dismutase on the spastic basilar artery after subarachnoid hemorrhage in dogs

1994 ◽  
Vol 80 (3) ◽  
pp. 476-483 ◽  
Author(s):  
Yasukazu Kajita ◽  
Yoshio Suzuki ◽  
Hirofumi Oyama ◽  
Toshihiko Tanazawa ◽  
Masakazu Takayasu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Superoxide Anion ◽  
Content Type ◽  
Vasodilator Effect ◽  
Intracisternal Injection ◽  
Dose Dependent ◽  
Fine Print

✓ To investigate the function of nitric oxide (a major endothelium-derived relaxing factor) in cerebral arteries after subarachnoid hemorrhage (SAH) in vivo, several nitric oxide-related substances were administered to dogs that had undergone double SAH. These included L-arginine (a substrate for the formation of nitric oxide), NG-monomethyl-L-arginine (L-NMMA, an analog of L-arginine that inhibits the formation of nitric oxide from L-arginine), and superoxide dismutase (SOD, which protects nitric oxide from oxidation by superoxide anion), which were given via intracisternal injection. The diameter of the basilar artery was assessed angiographically. In intact dogs, intracisternal bolus injections of L-arginine (1, 10, or 100 µmol) produced a dose-dependent increase in the internal diameter of the basilar artery; conversely, L-NMMA reduced the diameter of the basilar artery from baseline in a dose-dependent manner. On Days 4 and 7, after two intracisternal injections of autologous blood, L-arginine produced transient vasodilation of the spastic basilar artery, whereas L-NMMA produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on Day 4 than on Day 7, but less than in intact dogs. Intracisternal injection of SOD, which caused no effect per se, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on Day 4 and both the magnitude and duration of that effect on Day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. The finding that the simultaneous injection of SOD enhanced and prolonged the vasodilation induced by sufficient exogenous L-arginine suggests that the inactivation of nitric oxide by superoxide anion contributes to the development of vasospasm.

Selective hemoglobin inhibition of endothelium-dependent vasodilation of rabbit basilar artery

1986 ◽  
Vol 64 (3) ◽  
pp. 445-452 ◽  
Author(s):  
Shigeru Fujiwara ◽  
Neal F. Kassell ◽  
Tomio Sasaki ◽  
Tadayoshi Nakagomi ◽  
Richard M. Lehman
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Degradation Products ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Isometric Tension ◽  
Content Type ◽  
Adenosine Antagonist ◽  
Dose Dependent ◽  
Fine Print

✓ The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10−7−10−4 M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10−6 M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10−7-10−5 M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10−7-10−4 M) also relaxed isolated rabbit basilar artery already contracted by 10−6 M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.

Significance of a small bulge on the basilar artery in patients with perimesencephalic nonaneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (2) ◽  
pp. 426-429 ◽  
Author(s):  
Yuji Matsumaru ◽  
Kiyoyuki Yanaka ◽  
Ai Muroi ◽  
Hiroaki Sato ◽  
Takao Kamezaki ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Three Dimensional ◽  
Distinct Type ◽  
Rotational Angiography ◽  
Bleeding Pattern ◽  
Content Type ◽  
Nonaneurysmal Subarachnoid Hemorrhage ◽  
Excellent Clinical Outcome ◽  
Fine Print

✓ Perimesencephalic nonaneurysmal subarachnoid hemorrhage (SAH) is a distinct type of hemorrhage with a characteristic bleeding pattern and an excellent clinical outcome. The cause of this benign form of SAH remains unknown. The authors report on two cases of perimesencephalic nonaneurysmal SAH in which a small bulge on the basilar artery (BA) was demonstrated on three-dimensional rotational angiography studies. Based on data from these cases, one may infer that the lesion on the BA is responsible for the SAH. The possible pathogenesis is discussed.

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.

Upregulation of rho A and rho kinase messenger RNAs in the basilar artery of a rat model of subarachnoid hemorrhage

2000 ◽  
Vol 93 (3) ◽  
pp. 471-476 ◽  
Author(s):  
Yasushi Miyagi ◽  
Robin C. Carpenter ◽  
Toshinari Meguro ◽  
Andrew D. Parent ◽  
John H. Zhang
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Rho Kinase ◽  
Rt Pcr ◽  
Content Type ◽  
Blood Injection ◽  
Rho A ◽  
Rho Kinases ◽  
Fine Print

Object. Rho A, a small guanosine triphosphate—binding protein, and rho kinases have been suggested to play an important role in the agonist-induced myofilament Ca++ sensitization and cytoskeletal organization of smooth-muscle cells. To discover their possible roles in the prolonged contraction seen in cerebral vasospasm, the authors investigated the messenger (m)RNA expressions of rho A and rho-associated kinases α and β in the basilar artery (BA) of a rat double cisternal blood—injection model.Methods. An experimental subarachnoid hemorrhage (SAH) was achieved in rats by twice injecting autologous arterial blood into the cisterna magna of each animal. The mRNAs for rho A and rho-associated kinases α and β of the rat BA were analyzed using reverse transcription—polymerase chain reaction (RT-PCR). The cisternal blood injection induced a marked corrugation of elastic lamina and contraction of smooth-muscle cells observed with the aid of light and transmission electron microscopy in the rat BA on Days 3, 5, and 7. Results of the RT-PCR revealed that mRNAs for rho A and rho kinases α and β were expressed in the rat BA and that they were significantly upregulated and reached their peaks on Day 5.Conclusions. The mRNA upregulation of these proteins indicates that activation of rho A/rho kinase—related signal transduction pathways is involved in the development of long-lasting contraction of cerebral arteries after SAH.

A true mycotic (Aspergillus) aneurysm leading to fatal subarachnoid hemorrhage in a patient with hereditary hemorrhagic telangiectasia

1971 ◽  
Vol 35 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Peter Davidson ◽  
David M. Robertson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Hereditary Hemorrhagic Telangiectasia ◽  
Artery Aneurysm ◽  
Content Type ◽  
Intracranial Involvement ◽  
Basilar Artery Aneurysm ◽  
Fine Print

✓ A mycotic basilar artery aneurysm, in which Aspergillus was identified histologically, was found to be the cause of a massive subarachnoid hemorrhage in a 75-year-old man who suffered from hereditary hemorrhagic telangiectasia; there was no evidence of intracranial involvement by the latter disorder.

Intentional body clipping of wide-necked basilar artery bifurcation aneurysms

2000 ◽  
Vol 93 (2) ◽  
pp. 169-174 ◽  
Author(s):  
Yuichiro Tanaka ◽  
Shigeaki Kobayashi ◽  
Kazuhiro Hongo ◽  
Tsuyoshi Tada ◽  
Hisashi Nagashima ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Unfavorable Outcome ◽  
Content Type ◽  
Aneurysm Neck ◽  
Term Efficacy ◽  
Major Vessel ◽  
Perforating Arteries ◽  
Fine Print

Object. Neck clipping or coil embolization cannot always achieve complete neck obstruction in wide-necked basilar artery (BA) bifurcation aneurysms. Clipping of the aneurysm body, leaving a small aneurysm rest, is one clipping method used for this kind of aneurysm to maintain the patency of the posterior cerebral arteries and perforating vessels. However, the long-term efficacy of intentional body clipping has not been well investigated. The authors reviewed their experience with intentional body clipping of wide-necked BA bifurcation aneurysms to determine suitable clipping techniques and the long-term efficacy of the procedure.Methods. Complete neck occlusion was abandoned and body clipping intentionally performed in 17 patients with BA bifurcation aneurysms; wrapping of the aneurysm rest was made in seven cases. There were 10 ruptured aneurysms (58.8%), and the size of the aneurysm was larger than 10 mm in 11 patients (64.7%). The width between the clip blades and the base of the aneurysm neck was 1 mm in 11 cases, 2 mm in four, and 3 mm in two. Favorable outcome (Glasgow Outcome Scale [GOS] Score 4 or 5) was obtained in 13 cases (76.5%) and unfavorable outcome (GOS Scores 1–3) in four cases (23.5%). Major causes of unfavorable outcome included injury to perforating arteries and major vessel occlusion following surgical manipulation, in addition to the primary damage caused by subarachnoid hemorrhage. Subarachnoid hemorrhage did not occur during a mean follow-up period of 7.4 ± 5.6 years (range 0.7–18.1 years) after treatment.Conclusions. Intentional body clipping of wide-necked BA aneurysms proved to be effective to prevent subarachnoid hemorrhage, although injury to perforating arteries remains problematic. The choice of complete neck clipping or body clipping should be established early during the microsurgical procedure to reduce the risk of injury to perforating vessels.

The blood-brain barrier following experimental subarachnoid hemorrhage

1983 ◽  
Vol 58 (3) ◽  
pp. 338-344 ◽  
Author(s):  
Eric W. Peterson ◽  
Erico R. Cardoso
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Arterial Hypertension ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Hemodynamic Variable ◽  
Content Type ◽  
Blood Brain ◽  
Intracisternal Injection ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓ In three groups of cats, the authors studied the effect of subarachnoid hemorrhage (SAH) on the permeability of the blood-brain barrier (BBB) to the penetration of Evans blue-protein complex. One group received arterial hypertension alone, one group SAH alone, and one group SAH followed by arterial hypertension. Animals subjected to arterial hypertension alone showed areas of BBB breakdown. However, when cats were rendered hypertensive after SAH, there were no demonstrable BBB lesions. The SAH was produced by intracisternal injection of whole blood and hypertension by the intravenous injection of metaraminol. The preservation of the BBB after SAH is discussed. Vasospasm is considered as a possible hemodynamic variable responsible for the protection of the BBB from hypertensive damage. The need for a new model is proposed to further investigate the state of the BBB after SAH.

An in vitro comparative study of conducting vessels and penetrating arterioles after experimental subarachnoid hemorrhage in the rabbit

1992 ◽  
Vol 77 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Dennis G. Vollmer ◽  
Masakazu Takayasu ◽  
Ralph G. Dacey
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Cerebral Microvessels ◽  
Content Type ◽  
Large Arteries ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓ The reactivity of rabbit basilar artery and penetrating arteriolar microvessels was studied in vitro using an isometric-tension measurement technique and an isolated perfused arteriole preparation, respectively. Comparisons were made between reactivities of normal vessels and those obtained from animals subjected to experimental subarachnoid hemorrhage (SAH) 3 days prior to examination. Subarachnoid hemorrhage produced significant increases in basilar artery contraction in response to increasing concentrations of serotonin (5-hydroxytryptamine) (10−9 to 10−5 M) and prostaglandin F2α (10−9 to 10−5 M) when compared to normal arteries. In addition, SAH attenuated the relaxing effect of acetylcholine following serotonin-induced contraction and of adenosine triphosphate after KCl-induced basilar artery contractions. In contrast to the changes observed in large arteries, cerebral microvessels did not demonstrate significant differences in spontaneous tone or in reactivity to a number of vasoactive stimuli including application of calcium, serotonin, and acetylcholine. On the other hand, small but significant changes in arteriolar responsiveness to changes in extraluminal pH and to application of KCl were noted. Findings from this study suggest that intracerebral resistance vessels of the cerebral microcirculation are not greatly affected by the presence of subarachnoid clot, in contrast to the large arteries in the basal subarachnoid space. The small changes that do occur are qualitatively different from those observed for large arteries. These findings are consistent with the observation of significant therapeutic benefit with the use of calcium channel blockers without changes in angiographically visible vasospasm in large vessels. It is likely, therefore, that calcium antagonists may act to decrease total cerebrovascular resistance at the level of the relatively unaffected microcirculation after SAH without changing large vessel diameter.

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage

1995 ◽  
Vol 83 (1) ◽  
pp. 118-122 ◽  
Author(s):  
John K. B. Afshar ◽  
Ryszard M. Pluta ◽  
Robert J. Boock ◽  
B. Gregory Thompson ◽  
Edward H. Oldfield
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Content Type ◽  
Continuous Release ◽  
Blood Flow Velocities ◽  
The Right ◽  
Fine Print

✓ The continuous release of nitric oxide (NO) is required to maintain basal cerebrovascular tone. Oxyhemoglobin, a putative spasmogen, rapidly binds NO, implicating loss of NO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). If vasospasm is mediated by depletion of NO in the vessel wall, it should be reversible by replacement with NO. To investigate this hypothesis, the authors placed blood clots around the right middle cerebral artery (RMCA) of four cynomolgus monkeys; four unoperated animals served as controls. Arteriography was performed before and 7 days after surgery to assess the presence and degree of vasospasm, which was quantified in the anteroposterior (AP) projection by computerized image analysis. On Day 7, cortical cerebral blood flow (CBF) in the distribution of the right MCA was measured during four to six runs in the right internal carotid artery (ICA) of brief infusions of saline followed by NO solution. Arteriography was performed immediately after completing the final NO infusion in three of the four animals with vasospasm. Right MCA blood flow velocities were obtained using transcranial Doppler before, during, and after NO infusion in two vasospastic animals. After ICA NO infusion, arteriographic vasospasm resolved (mean percent of preoperative AP area, 55.9%); that is, the AP areas of the proximal portion of the right MCA returned to their preoperative values (mean 91.4%; range 88%–96%). Compared to ICA saline, during ICA NO infusion CBF increased 7% in control animals and 19% in vasospastic animals (p < 0.002) without significant changes in other physiological parameters. During NO infusion, peak systolic right MCA CBF velocity decreased (130 to 109 cm/sec and 116 to 76 cm/sec) in two vasospastic animals. The effects of ICA NO on CBF and CBF velocity disappeared shortly after terminating NO infusion. Intracarotid infusion of NO in a primate model of vasospasm 1) increases CBF, 2) decreases cerebral vascular resistance, 3) reverses arteriographic vasospasm, and 4) decreases CBF velocity in the vasospastic artery without producing systemic hypotension. These findings indicate the potential for the development of targeted therapy to reverse cerebral vasospasm after SAH.

Subarachnoid hemorrhage inhibition of endothelium-derived relaxing factor in rabbit basilar artery

1988 ◽  
Vol 69 (2) ◽  
pp. 247-253 ◽  
Author(s):  
Kazuhiro Hongo ◽  
Neal F. Kassell ◽  
Tadayoshi Nakagomi ◽  
Tomio Sasaki ◽  
Tetsuya Tsukahara ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Selective Inhibitor ◽  
Isometric Tension ◽  
The Other ◽  
Content Type ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Fine Print

✓ Vascular contractions in response to KCl and serotonin (5-hydroxytryptamine, 5-HT) in rabbit basilar artery were studied in vitro using an isometric tension-measurement technique. Hemoglobin ( 10−5 M) markedly augmented contractions induced by 5-HT (10−9 to 10−6 M) and slightly augmented those induced by KCl (20 to 80 mM) in arteries with intact endothelium. On the other hand, the augmentation induced by hemoglobin was almost abolished in arteries that were chemically denuded of endothelial cells by pretreatment with saponin. Since hemoglobin is known to be a selective inhibitor of endothelium-derived relaxing factor (EDRF), it is possible that the augmentation of contraction by hemoglobin in endothelium-intact arteries was mediated via an inhibition of spontaneously released EDRF. The effect of subarachnoid hemorrhage (SAH) on spontaneously released EDRF was investigated by injecting 5 ml of blood into the cisterna magna and sacrificing the rabbits 2 days later. Arteries after SAH showed a significant reduction in hemoglobin-induced augmentation compared to that seen in control arteries with intact endothelium. This result suggests that spontaneously released EDRF is significantly reduced after SAH. It is concluded that EDRF is released spontaneously in the rabbit basilar artery and that inhibition of its release might be involved in pathogenesis of cerebral vasospasm.

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