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.

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.

Cerebral arterial spasm

1974 ◽  
Vol 40 (4) ◽  
pp. 442-450 ◽  
Author(s):  
George S. Allen ◽  
Lavell M. Henderson ◽  
Shelley N. Chou ◽  
Lyle A. French
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Human Serum ◽  
Basilar Artery ◽  
Contractile Activity ◽  
Arterial Spasm ◽  
Content Type ◽  
Canine Basilar Artery ◽  
Fine Print

✓ In vitro experiments were performed to determine the contractile activity of human serum and cerebrospinal fluid on the canine basilar artery. The majority of contractile activity in these CSF samples, which were collected 2 to 7 days following a subarachnoid hemorrhage, was proven to be due to serotonin. Serotonin was capable of producing a prolonged contraction of the artery depending on its activity. Methylsergide reversibly blocked the artery's response to serotonin and caused a contraction of the basilar artery. Phenoxybenzamine irreversibly blocked the basilar artery's response to serotonin, serum, and CSF.

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.

Effect of subarachnoid hemorrhage on endothelium-dependent vasodilation

1987 ◽  
Vol 66 (6) ◽  
pp. 915-923 ◽  
Author(s):  
Tadayoshi Nakagomi ◽  
Neal F. Kassell ◽  
Tomio Sasaki ◽  
Shigeru Fujiwara ◽  
R. Michael Lehman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
The Other ◽  
Response Curves ◽  
Content Type ◽  
Arterial Blood ◽  
Vasodilatory Response ◽  
Dose Dependent ◽  
Fine Print

✓ The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. The SAH was induced by injecting 5 ml of fresh arterial blood into the cisterna magna. Sixty-two rabbits were separated into four groups according to the timing of sacrifice: control rabbits, and operated rabbits sacrificed on Days 2, 4, and 6 after SAH. Acetylcholine (ACh) (10−7 M to 10−4 M) and adenosine triphosphate (ATP) (10−7 M to 10−4 M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10−6 M serotonin (5-HT). There were no significant differences in the vasodilatory response to ACh among these four groups. Relaxation to approximately 84% of the initial contractile tone occurred with 10−4 M ACh. On the other hand, the vasodilatory response to ATP was suppressed in the animals sacrificed 2 days after SAH; the relaxation of this group was approximately 52% at 10−4 M ATP, compared to a relaxation of 87% observed in the other groups of animals. One of the major causes of the impairment of endothelium-dependent vasodilation seems to be an inhibition of the production of endothelium-derived relaxing factor by endothelial cells. After the relaxation studies, the dose-response curves for 5-HT were obtained. Serotonin caused significantly more contraction in the animals sacrificed 2 days after SAH than in the other groups. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH, together with the potentiation of the contractile response to vasoactive agents in cerebral arteries, may play an important role in the pathogenesis of vasospasm.

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.

scholarly journals Triphasic Response of Rat Intracerebral Arterioles to Increasing Concentrations of Vasopressin in vitro

1993 ◽  
Vol 13 (2) ◽  
pp. 304-309 ◽  
Author(s):  
Masakazu Takayasu ◽  
Yasukazu Kajita ◽  
Yoshio Suzuki ◽  
Masato Shibuya ◽  
Kenichiro Sugita ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Vascular Tone ◽  
Cerebral Arteries ◽  
Specific Inhibitor ◽  
In Vitro Study ◽  
Relaxing Factor ◽  
Pathological Conditions ◽  
Cerebral Arterioles ◽  
Endothelium Derived Relaxing Factor

To determine how vasopressin affects the vascular tone of the smaller cerebral arterioles, we carried out an in vitro study of isolated and cannulated intracerebral arterioles of rats. We found that increasing concentrations of vasopressin induced a triphasic response of vasodilation (10−12–10−11 M), vasoconstriction (10−10–10−8 M), and vasodilation stabilizing to control diameter (10−7–10−6 M) and that the maximum constriction was twice the maximum dilation in these smaller arterioles [21.2 ± 13.1% (mean ± SD) decrease in diameter vs. 11.2 ± 5.7% increase]. Pretreatment of the arterioles with NG-monomethyl-l-arginine (10−4 M), a specific inhibitor of endothelium-derived relaxing factor, abolished the vasopressin-induced vasodilation and significantly increased the vasoconstriction. These results suggest that these arterioles were maintained in a dilated state by an endothelium-derived relaxing factor activated by vasopressin. Both vasodilation and vasoconstriction were found to be mediated through vasopressin V1 receptors in a study of arterioles pretreated with d(CH2)5Tyr(Me)arginine vasopressin (10−6 M), a vasopressin V1 receptor antagonist. These results support the hypothesis that vasopressin may constrict smaller cerebral arterioles while simultaneously dilating larger cerebral arteries. Our results also suggest that vasopressin may aggravate cerebral ischemia in pathological conditions, such as subarachnoid hemorrhage, when the arteriolar response to vasopressin shifts from vasodilation to vasoconstriction due to increased vasopressin levels in plasma and CSF and impaired endothelium-derived relaxation.

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.

Does dexamethasone inhibit the growth of human gliomas?

1977 ◽  
Vol 47 (6) ◽  
pp. 864-870 ◽  
Author(s):  
Gajanan V. Sherbet ◽  
M. S. Lakshmi ◽  
Salim K. Haddad
Keyword(s):  
Generation Time ◽  
Deoxyribonucleic Acid ◽  
The Other ◽  
Human Gliomas ◽  
Content Type ◽  
Other Hand ◽  
Fine Print

✓ Dexamethasone (104M) was shown to inhibit the growth of human gliomas in culture. This was indicated by the inhibition of incorporation of radioactively labeled thymidine into the deoxyribonucleic acid (DNA) of the cells, and by the increase in the generation time of cells exposed to the drug in vitro. On the other hand, tumors obtained from patients who had received dexamethasone before craniotomy grew considerably faster in vitro than tumors from patients who had not been given the drug before operation.

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.

Cigarette smoke extract contracts isolated porcine coronary arteries by superoxide anion-mediated degradation of EDRF

1994 ◽  
Vol 266 (3) ◽  
pp. H874-H880 ◽  
Author(s):  
T. Murohara ◽  
K. Kugiyama ◽  
M. Ohgushi ◽  
S. Sugiyama ◽  
H. Yasue
Keyword(s):  
Methylene Blue ◽  
Cigarette Smoke ◽  
Coronary Arteries ◽  
Cigarette Smoke Extract ◽  
Isometric Tension ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Endothelium Derived Relaxing Factor ◽  
Pig Coronary Arteries

To test whether cigarette smoke extract (CSE) influences the endothelial regulation of vascular tone in vitro, pig coronary arterial rings were incubated in organ chambers and isometric tension changes were examined. CSE was prepared by bubbling mainstream smoke of one filter cigarette into phosphate-buffered saline (2 ml). Fresh CSE (3.3, 10, and 30 microliters/ml) elicited initial contraction and subsequent relaxation during stable contraction to prostaglandin F2 alpha (PGF2 alpha). Initial contraction to CSE was dependent on the presence of endothelium, whereas subsequent relaxation was endothelium independent. Initial contraction was significantly attenuated by superoxide dismutase (SOD), methylene blue, but not by catalase. Prior inhibition of the basal release of endothelium-derived relaxing factor by NG-monomethyl-L-arginine also inhibited the initial contraction, and this inhibition was reversed by coincubation with L-arginine but not D-arginine. Subsequent relaxation was significantly potentiated by SOD but was markedly attenuated by methylene blue. CSE reduced ferricytochrome c, and this reduction was significantly inhibited by SOD. In conclusion, CSE induced biphasic tension change, initial contraction, and subsequent relaxation during stable contraction to PGF2 alpha in isolated pig coronary arteries. The initial contraction may be, at least in part, mediated through the degradation of basally released endothelium-derived relaxing factor (nitric oxide) by superoxide anions derived from CSE.

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