Altered reactivity of human cerebral arteries after subarachnoid hemorrhage

1995 ◽  
Vol 83 (3) ◽  
pp. 510-515 ◽  
Author(s):  
Hisashi Onoue ◽  
Nobuyoshi Kaito ◽  
Masahiko Akiyama ◽  
Masato Tomii ◽  
Shogo Tokudome ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Vasoactive Agents ◽  
Content Type ◽  
Vasoactive Substances ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F ◽  
Human Cadavers ◽  
Endothelium Dependent Relaxation

✓ To investigate the effects of subarachnoid hemorrhage (SAH) on the responsiveness of human cerebral arteries to vasoactive substances, the authors measured the isometric tension generated in helical strips of basilar and middle cerebral arteries isolated from human cadavers Contractions caused by KCl, prostaglandin F2α, noradrenaline, and serotonin were reduced in arteries obtained from cadavers with aneurysmal SAH damage and compared to those obtained from cadavers with no indication of intracranial diseases. Endothelium-dependent relaxation elicited by substance P and bradykinin, and endothelium-independent relaxation induced by prostaglandin I2 and nitroglycerin were also markedly decreased in arteries affected by SAH. However, the reduction in relaxation response to prostaglandin I2 was significantly less than that to the other vasodilator agents. These results indicate that human cerebral artery functions are severely impaired after SAH and that poor responses to vasoactive agents may result primarily from dysfunction of smooth-muscle cells.

Cerebrovascular sensitivity to vasoconstricting agents induced by subarachnoid hemorrhage and vasospasm in dogs

1977 ◽  
Vol 46 (3) ◽  
pp. 296-303 ◽  
Author(s):  
Noboru Toda ◽  
Takashi Ozaki ◽  
Tomio Ohta
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Internal Carotid ◽  
Cerebral Arteries ◽  
Sham Operation ◽  
Vasoactive Agents ◽  
Content Type ◽  
Middle Cerebral Arteries ◽  
Anesthetized Dogs ◽  
Endogenous Substances ◽  
Mechanical Rupture

✓ In anesthetized dogs, subarachnoid hemorrhage (SAH) was induced by the mechanical rupture of the unilateral intracranial internal carotid artery. Vasospasm was angiographically determined 24 hours and 7 days after SAH. Contractile responses to serotonin, norepinephrine, histamine, and K+ were compared in control and bleeding sides of the middle cerebral arteries removed from dogs with SAH, and from sham-operated dogs. Under sham operation and 2 hours after SAH, responses in the arteries of both sides did not appreciably differ but response was significantly less in arteries from the bleeding side as compared with the control side 24 hours and 7 days after hemorrhage. However, median effective concentrations of serotonin, histamine, and K+ were approximately the same in the arteries from both sides. Vasospasm and decreased sensitivity to the vasoactive agents of middle cerebral arteries were reversed 42 days after SAH. It is thus quite likely that initiation and maintenance of post-hemorrhage vasospasm is not associated with an increase in the sensitivity of cerebral arteries to vasoconstricting endogenous substances, rather the state of decreased sensitivity of cerebral arteries in contact with SAH may be instrumental in relieving prolonged vasospasm.

Pharmacological studies on relaxation of spastic primate cerebral arteries in subarachnoid hemorrhage

1989 ◽  
Vol 71 (6) ◽  
pp. 909-915 ◽  
Author(s):  
Kenji Kanamaru ◽  
Bryce K. A. Weir ◽  
J. Max Findlay ◽  
Christel A. Krueger ◽  
David A. Cook
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Receptor Antagonist ◽  
Autologous Blood ◽  
Cerebral Arteries ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Small Component ◽  
Content Type ◽  
Prostaglandin F

✓ Chronic cerebral vasospasm was induced in 16 monkeys by direct placement of a clot of autologous blood over the arteries of the circle of Willis on the right side. The middle cerebral arteries (MCA's) on the clot side all showed angiographic vasospasm, which was maximal 7 days after subarachnoid hemorrhage. Animals were sacrificed at this time and vascular responses to acetylcholine (ACh), histamine, and the calcium ionophore A23187 were studied in MCA rings from the clot (spastic) side and the non-clot (control) side. In control preparations with an intact endothelium, which had been precontracted by prostaglandin F2agr; (PGF2agr;), histamine and A23187 produced significant relaxation. The same concentrations of histamine and A23187 did not relax vascular tissues in which the endothelium had been mechanically removed. Acetylcholine did not produce a significant endothelium-dependent relaxation of primate MCA rings, but did relax rings of primate common carotid artery. Pretreatment with chlorpheniramine (an H1-receptor antagonist) prevented histamine-induced relaxation; however, cimetidine (an H2-receptor antagonist) had no inhibitory action. It thus seems that histamine mediates relaxation of intact MCA's mostly by an H1-receptor-mediated release of endothelium-derived relaxing factor (EDRF). Relaxations induced by histamine and A23187 in MCA's from the clot side were substantially reduced. Moreover, the small component of ACh-induced relaxation was also abolished. Endothelium-independent relaxation induced by glyceryl trinitrate (GTN) occurred in arteries from both the control and the clot sides. Constrictions induced by KCl and PGF2agr; were reduced on the clot side of the MCA's. These results suggest that subarachnoid hemorrhage influences both the generation of EDRF and the constriction of affected arteries. The small contraction which was elicited in spastic arteries was fully relaxed by GTN.

Cerebral arterial spasm

1974 ◽  
Vol 40 (4) ◽  
pp. 433-441 ◽  
Author(s):  
George S. Allen ◽  
Lavell M. Henderson ◽  
Shelly N. Chou ◽  
Lyle A. French
Keyword(s):  
Small Volume ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Arterial Spasm ◽  
Vasoactive Agents ◽  
Response Curves ◽  
Content Type ◽  
Middle Cerebral Arteries ◽  
Fine Print

✓ In vitro experiments were performed using a small volume chamber to determine the contractile activity of various vasoactive agents on the canine basilar and middle cerebral arteries. Cumulative dose-response curves were obtained for most of the agents tested including serotonin and three different prostaglandins; many of these curves were found to be similar for segments from both arteries. It was concluded from these curves, and the known concentrations in blood, that serotonin is probably the agent in blood responsible for the cerebral arterial spasm that often follows a subarachnoid hemorrhage. This in vitro method is capable of detecting serotonin concentrations as low as 10−12 gm/ml and may prove useful as a quantitative and well-controlled method for studying the etiology of spasm and the receptor mechanisms present in the cerebral arteries.

Cerebral vasospasm evaluated by transcranial ultrasound correlated with clinical grade and CT-visualized subarachnoid hemorrhage

1986 ◽  
Vol 64 (4) ◽  
pp. 594-600 ◽  
Author(s):  
Rolf W. Seiler ◽  
Peter Grolimund ◽  
Rune Aaslid ◽  
Peter Huber ◽  
Helge Nornes
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Infarction ◽  
Cerebral Arteries ◽  
Clinical Status ◽  
Transcranial Doppler Sonography ◽  
Transcranial Ultrasound ◽  
Unaffected Side ◽  
Content Type ◽  
Middle Cerebral Arteries ◽  
Subarachnoid Blood

✓ In 39 patients with a proven subarachnoid hemorrhage (SAH), the clinical status, the amount of subarachnoid blood on a computerized tomography scan obtained within 5 days after SAH, and the flow velocities (FV's) in both middle cerebral arteries (MCA's) measured by transcranial Doppler sonography were recorded daily and correlated. All patients had pathological FV's over 80 cm/sec between Day 4 and Day 10 after SAH. The side of the ruptured aneurysm showed higher FV's than did the unaffected side in cases of laterally localized aneurysms. Increase in FV preceded clinical manifestation of ischemia. A steep early increase of FV's portended severe ischemia and impending infarction. Maximum FV's in the range of 120 to 140 cm/sec were not critical and in no case led to brain infarction. Maximum FV's over 200 cm/sec were associated with a tendency for ischemia, but the patients may remain clinically asymptomatic. In cases of no or only a little blood in the basal cisterns, mean FV's in both MCA's increased only moderately whereas, with thick clots of subarachnoid blood, there was a steeper and higher increase of mean FV's.

Pharmacological comparison of endothelium-dependent relaxation in isolated cerebral and extracerebral arteries

1988 ◽  
Vol 69 (4) ◽  
pp. 580-587 ◽  
Author(s):  
Tadayoshi Nakagomi ◽  
Kazuhiro Hongo ◽  
Neal F. Kassell ◽  
Tomio Sasaki ◽  
R. Michael Lehman ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Content Type ◽  
Wide Range ◽  
Basilar Arteries ◽  
The Common ◽  
The Difference ◽  
Endothelium Dependent Relaxation ◽  
Fine Print

✓ Endothelium-dependent relaxation was induced by acetylcholine (ACh), adenosine triphosphate (ATP), and thrombin in isolated cerebral and extracerebral arteries obtained from rabbits and dogs. Using an isometric tension-recording method, the authors then examined the difference in the extent of relaxation between the cerebral and extracerebral arteries. In rabbits, the dose-response curve of the basilar artery for ACh was significantly different (p < 0.05) from curves of the femoral and common carotid arteries. The IC50 value (the concentration inducing a one-half inhibition of the initial contractile tone) for the basilar artery in ACh-induced relaxation was significantly higher (p < 0.05) than for the common carotid artery, although the mean maximum relaxation of the basilar artery to ACh was not significantly different from that seen in extracerebral arteries. The relaxing effect of ACh in dogs was much less in the middle cerebral and basilar arteries than in the common carotid, vertebral, and femoral arteries. On the other hand, both ATP (in rabbits and dogs) and thrombin (in dogs) induced significantly more (p < 0.05) relaxation in the cerebral arteries than in the extracerebral arteries. Endothelium-dependent relaxation induced by ACh or ATP has been demonstrated in a wide range of arteries from a variety of animals. The present results suggest that ATP has a more important role than ACh in the regulation of the vascular tone of the major cerebral arteries in these two species.

Cytoskeletal and extracellular matrix proteins in cerebral arteries following subarachnoid hemorrhage in monkeys

1992 ◽  
Vol 76 (1) ◽  
pp. 81-90 ◽  
Author(s):  
R. Loch Macdonald ◽  
Bryce K. A. Weir ◽  
James D. Young ◽  
Michael G. A. Grace
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Smooth Muscle Contraction ◽  
Intimal Thickening ◽  
Content Type ◽  
Tunica Media ◽  
Middle Cerebral Arteries ◽  
Fine Print

✓ It is unclear if vasospasm after subarachnoid hemorrhage (SAH) is predominantly due to smooth-muscle contraction, proliferative vasculopathy, or other changes within the arterial wall such as fibrosis or change in smooth-muscle phenotype. In this study, immunohistochemistry was used to examine changes in extracellular and cytoskeletal proteins in cerebral arteries after SAH that might support one of these mechanisms. Following baseline cerebral angiography, bilateral SAH was created in nine monkeys. Three animals each were killed 7, 14, or 28 days after SAH. Cerebral angiography was repeated on Day 7 in all animals and immediately prior to sacrifice in animals killed on Days 14 and 28. Both middle cerebral arteries and four control basilar arteries were examined using fluorescent antibody techniques with antisera to α-actin, myosin, fibronectin, fibrinogen, vimentin, desmin, laminin, and collagens (types I, III, IV, and V). Angiography showed that vasospasm was most severe on Day 7, present but resolving on Day 14, and completely resolved by Day 28. Microscopic study of arterial sections and blinded review of microphotographs of arterial sections by five independent observers did not reveal changes in intensity of density of staining for collagens, desmin, myosin, laminin, or α-actin in the tunica media of tunica adventitia. Fibronectin immunoreactivity increased 14 days after SAH. Seven days after SAH, occasional areas of tunica media showed immunoreactivity to fibrinogen. On Day 28, intimal thickening was observed in four of six middle cerebral arteries and this tissue demonstrated immunoreactivity to α-actin, myosin, vimentin, desmin, fibronectin, laminin, and each type of collagen. No significant increases in the number of intimal cells showing immunoreactivity to α-actin were seen and no significant changes in the hydroxyproline content of cerebral arteries developed at any time after SAH. These results suggest that rigidity and lumen narrowing of vasospasm are not due to increased arterial collagen, although other proteins in the arterial wall or an alteration in cross-linking of existing proteins could produce these changes. There is no indication that smooth-muscle contractile proteins change during vasospasm or that increases in the number of α-actin-containing myointimal cells contribute to vasospasm. The occurrence of intimal thickening and increased tunica media fibronectin after vasospasm suggests that vasospasm damages smooth muscle, possibly as a result of intense prolonged smooth-muscle contraction.

The effect of hemoglobin on vasodilatory effect of calcium antagonists in the isolated rabbit basilar artery

1992 ◽  
Vol 76 (4) ◽  
pp. 670-678 ◽  
Author(s):  
Masahiko Toshima ◽  
Neal F. Kassem ◽  
Tomio Sasaki ◽  
Yuichiro Tanaka ◽  
Takao Machi
Keyword(s):  
Calcium Antagonists ◽  
Inhibitory Effect ◽  
Isometric Tension ◽  
Content Type ◽  
Vasoactive Substances ◽  
Vasodilatory Effect ◽  
High K ◽  
Prostaglandin F ◽  
Basilar Arteries ◽  
Tonic Phase

✓The effect of hemoglobin on the vasodilatory effect of calcium antagonists was studied in isolated rabbit basilar arteries using an isometric tension measurement method. The ability of nimodipine to relax or inhibit contractions elicited by high K+ depolarization or serotonin (5-hydroxytryptamine, 5-HT) was investigated in control arterial rings and rings pretreated by hemoglobin. Hemoglobin (10−6 and 10−5 M) reduced the relaxation induced by nimodipine (10−10 to 10−8 M) in the rings contracted by 40 mM KCl. This reduction in relaxation was also observed with 3 × 10−10 to 3 × 10−9 M nicardipine, 3 × 10−8 to 3 × 10−7 M verapamil, and 10−7 to 10−6 M diltiazem. On the other hand, the effect of nimodipine was not influenced by endothelial removal or by pretreatment with 10−5 M albumin or 10−6 M prostaglandin F2α Hemoglobin restored the 10−10 and 10−9 M nimodipine-induced inhibition of the contraction elicited by CaCl2 (0.3 to 20 mM) in a K+-rich, Ca++-free solution. This restoration was greater at higher concentrations of CaCl2. Hemoglobin enhanced both the nimodipine-sensitive tonic phase and the less sensitive phasic phase of contractions produced by 10−6 M of 5-HT. It abolished the inhibitory effect of 10−8 and 10−7 M nimodipine on the phasic contraction. Endothelial removal also enhanced both phases of the contraction, but did not abolish the effect of nimodipine. This study showed that the vasodilatory effect of calcium antagonists, especially nimodipine, on the vasoconstriction induced by other vasoactive substances decreased in the presence of hemoglobin.

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.

Human basilar and middle cerebral arteries exhibit endothelium-dependent responses to peptides

1994 ◽  
Vol 267 (3) ◽  
pp. H880-H886 ◽  
Author(s):  
H. Onoue ◽  
N. Kaito ◽  
M. Tomii ◽  
S. Tokudome ◽  
M. Nakajima ◽  
...  
Keyword(s):  
Substance P ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Middle Cerebral Arteries ◽  
Vasopressin Receptors ◽  
Basilar Arteries ◽  
Human Cadavers ◽  
Endothelium Derived Relaxing Factor

We examined the activities of bradykinin, substance P, and vasopressin in isolated human cerebral arteries to better understand humoral control of cerebrovascular tone. Basilar and middle cerebral arteries were isolated from human cadavers during autopsy, and isometric tension was measured in helical strips of the arteries. Both bradykinin and substance P relaxed strips of both arteries precontracted with prostaglandin F2 alpha to similar extents. The relaxations induced by both peptides were abolished by removal of the vascular endothelium and were markedly reduced by pretreatment with NG-nitro-L-arginine, an inhibitor of endothelium-derived relaxing factor. Treatment with indomethacin, a cyclooxygenase inhibitor, did not attenuate the relaxations. These results indicate that the responses of human cerebral arteries to bradykinin and substance P are mediated by endothelium-derived relaxing factor. In contrast, vasopressin primarily produced endothelium-independent contractions in human cerebral arteries. Contractions of basilar arteries induced by vasopressin were much less than those of middle cerebral arteries. Two of eighteen basilar arteries, but none of the middle cerebral arteries, responded to vasopressin with endothelium-dependent relaxation. This suggests that the function of vasopressin receptors differs in basilar and middle cerebral arteries.

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