Experimental cerebral vasospasm: Resolution by chlorpromazine

Blaumanis, Otis R.; Grady, Patricia A.

doi:10.1016/0090-3019(82)90118-5

Cited by 13 publications

(5 citation statements)

References 53 publications

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“…In a previous study of cerebral vessels,5' 19 20 spasm was induced in the basilar artery of the cat by either mechanical stroking with a blunt probe, by stimulation with bipolar electrodes or by introduction of autologous blood into the adjacent subarachnoid space. As confirmed by SEM, the response to these spasmogenic stimuli was also close to a 50% reduction in transluminal diameter which is equivalent to that achieved by design in the present study.…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell damage and thrombus formation after partial arterial constriction: relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction.

Gertz¹,

Uretsky²,

Wajnberg³

et al. 1981

Circulation

166

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SUMMARY The left anterior descending coronary artery of four dogs and the right common carotid artery of 15 rabbits were subjected to 40-60% reduction in transluminal diameter for 1 hour by partial ligation with suture thread. Scanning electron microscopic examination of the luminal surface of these vessels revealed endothelial craters and balloons, fragmentation and desquamation on the proximal slope of the constriction. Platelet attachment to exposed subendothelial tissues was clearly evident, and microthrombi were seen at the point of maximum constriction. Blood flow, as measured by electromagnetic flow probe, was virtually unchanged upon partial ligation. In control studies, where a second ligature was placed proximal to and before the first to reduce blood flow to the distal constriction site substantially or totally, endothelial desquamation was found in only one of 14 animals, and the number of craters and balloons was significantly reduced. We suggest that endothelial damage and thrombus formation may occur at the site of focal arterial constriction even when the reduction in transluminal diameter is insufficient to alter substantially the rate of flow.THE THREAT posed by coronary vasospasm for the initiation of myocardial ischemia or infarction is assumed to depend on the degree to which the reduction in transluminal diameter results in the interference with coronary blood flow. Further, it is thought that the thrombosis that may accompany vasospasm is a result of the grossly reduced blood flow secondary to a critical vascular constriction and that the interaction of platelets with a damaged vascular wall, with the ensuing release reaction, may further potentiate the coronary spasm." 2 In the present report we present evidence from scanning electron microscopic (SEM) studies that indicates that marked endothelial damage, extensive platelet deposition and thrombus formation may occur at the site of a focal arterial constriction even when the reduction in transluminal diameter is insufficient to alter flow substantially. MethodsFifteen New Zealand white rabbits (3.1 ± 0.4 kg, mean ± SD) were anesthetized with sodium pentobar- The RCCA of five rabbits and the LAD of two dogs were focally constricted 1 cm proximal to the probe by partial ligation with suture thread (0-cotton) to achieve a 50% reduction in transluminal diameter ( fig. 1). The desired degree of luminal constriction was achieved by the apposition of two points on the suture thread; the distance between these points was calculated from the vascular circumference, with the wall thickness (0.1 mm) considered negligible. The diameters were confirmed during SEM examination and varied from 40-60% luminal reduction. Group 2In a second group of five rabbits and two dogs, a second ligature was placed 1 cm proximal and immediately before the first ( fig. 1)

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Section: Discussionmentioning

confidence: 99%

Endothelial cell damage and thrombus formation after partial arterial constriction: relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction.

Gertz¹,

Uretsky²,

Wajnberg³

et al. 1981

Circulation

166

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“…In the beginning of experimental CVS research mechanical stimulation was used to induce arterial narrowing [46,47]. Other authors with a similar setting of continuous intracisternal drug infusion to attenuate SAH induced CVS do not report a control group of saline infusion and therefore the possibility to compare our findings lacks [48].…”

Section: Discussionmentioning

confidence: 99%

“…The remarkable vasospasms in the control group (no SAH/NaCl) may have occurred due to aseptic inflammatory response to mechanical disruption [46]. In the beginning of experimental CVS research mechanical stimulation was used to induce arterial narrowing [46,47].…”

Section: Discussionmentioning

confidence: 99%

Prevention of delayed cerebral vasospasm by continuous intrathecal infusion of glyceroltrinitrate and nimodipine in the rabbit model in vivo

Marbacher¹,

Neuschmelting²,

Graupner³

et al. 2008

Intensive Care Med

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Objective: Intrathecal bolus administration of nitric oxide donors and calcium channel antagonists has been proposed to reduce cerebral vasospasm (CVS) in animal subarachnoid hemorrhage (SAH) models. Intrathecal continuous administration of these substances for CVS prevention has not been extensively evaluated. This study compared the efficacy of continuous intrathecal infusions of the NO donor glyceroltrinitrate and nimodipine in preventing delayed CVS associated with SAH in an animal model in vivo. Methods: New Zealand White rabbits were randomly assigned to six groups: no SAH/NaCl, no SAH/NO, no SAH/nimodipine, SAH/NaCl, SAH/NO, or SAH/nimodipine. Glyceroltrinitrate (GTN) at 0.5 µg/µl (0.5 µl/h) or nimodipine at 0.2 µg/µl (10 µl/h) or NaCl was continuously infused into the cisterna magna via an Alzet osmotic pump from day 0 to day 5 after injection of 1.0 ml autologous blood. The magnitude of spasm in the basilar artery was determined by comparison of pre-and posttreatment angiography and was calculated as proportional change in intraluminal diameter based on automatic measurements. Results: A total of 55 experiments and 110 angiograms were performed. SAH was associated with vasoconstriction of the basilar artery (SAH/NaCl group 19.85 ± 2.94%). Continuous intrathecal injection of GTN and nimodipine prevented SAH-induced CVS. There was significant prevention of CVS in animals treated with GTN (SAH/NO group 5.93 ± 5.2%, n = 11) and nimodipine (SAH/nimodipine group: 0.55 ± 2.66%, n = 9). There was no significant difference between the treatment groups and controls in prevention of CVS. Conclusions: This study demonstrates that prophylactic continuous intrathecal administration of either GTN or nimodipine equally prevents SAH-associated CVS in an animal model.

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“…Blaumanis and Grady 34 reported that a topical application of 10" 7 to 10" 4 M chlorpromazine led to a prompt relaxation of the spastic cerebral artery segment induced by electrical, mechanical, or chemical stimuli or by subarachnoid hemorrhage. The sustained contraction of the canine basilar artery induced by PGF^, PGEj, Hb, or serum in the present study was relaxed in a dose-dependent manner by chlorpromazine or amitriptyline.…”

Section: Discussionmentioning

confidence: 99%

Responses of isolated canine basilar artery and human platelet to chlorpromazine and amitriptyline.

Sukenaga¹,

Tani²,

Fukumori³

et al. 1984

Stroke

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SUMMARY Sustained contraction of isolated canine basilar artery was induced by addition of prostaglandin F^, prostaglandin E 2 , hemoglobin-containing solution, or serum. Human platelet aggregation was induced by 1.0 /iM adenosine diphosphate. The sustained contraction of basilar artery and the aggregation of platelet, particularly its secondary aggregation, were inhibited in a dose-dependent manner by addition of chlorpromazine or amitriptyline; calmodulin antagonist. The molar concentrations at 50% inhibition by chlorpromazine or amitriptyline were 5.9 to 7.7 /xM or 28 to 39 /xM for the contraction of basilar artery and 57 fiM or 111 fiM for the secondary aggregation of platelet. The results were discussed mainly on the basis of interaction of psychotropic drugs and Ca 2+ , calmodulin-dependent enzymes, particularly rayosin light chain phosphorylation.

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Experimental cerebral vasospasm: Resolution by chlorpromazine

Cited by 13 publications

References 53 publications

Endothelial cell damage and thrombus formation after partial arterial constriction: relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction.

Endothelial cell damage and thrombus formation after partial arterial constriction: relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction.

Prevention of delayed cerebral vasospasm by continuous intrathecal infusion of glyceroltrinitrate and nimodipine in the rabbit model in vivo

Responses of isolated canine basilar artery and human platelet to chlorpromazine and amitriptyline.

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