Treatment of vasospasm with a 480-nm pulsed-dye laser

1991 ◽  
Vol 75 (4) ◽  
pp. 613-622 ◽  
Author(s):  
Robert Macfarlane ◽  
Atsushi Teramura ◽  
Christopher J. Owen ◽  
Scott Chase ◽  
Ralph de la Torre ◽  
...  
Keyword(s):  
Laser Treatment ◽  
Basilar Artery ◽  
Laser Energy ◽  
Autologous Blood ◽  
Dye Laser ◽  
Pulsed Dye Laser ◽  
Laser Application ◽  
Morphological Examination ◽  
Content Type ◽  
Fine Print

✓ Laser energy at a wavelength of 480 nm was applied in 1-µsec pulses of 3 to 10 mJ to two models of vasospasm. Rabbit common carotid arteries (CCA's) were constricted chronically by the application of human blood within a silicone sheath. Peak vasospasm developed 24 to 48 hours later, and persisted for up to 6 days. Endovascular laser treatment was delivered to 40 CCA's via a 200-µm diameter silica quartz fiber introduced through the femoral artery. The CCA caliber increased from 60% of the pre-vasospasm control diameter to a minimum post-laser diameter of 83% of control. No instances of laser-induced perforation or of arterial thrombosis were observed for up to 60 days after treatment. Prophylactic laser application to nine normal vessels was able to attenuate the development of vasospasm if blood was applied immediately thereafter (88% vs. 59% of control diameter, p < 0.02), but not if blood was applied 7 days later. Studies in 16 normal CCA's established that there was a considerable margin between the laser energy required to induce dilatation and that which caused perforation, providing that the fiber remained relatively central within the artery. Morphological examination demonstrated focal loss of endothelial cells immediately after laser application, followed approximately 7 days later by the development of areas of intimal hyperplasia. Only minimal changes were observed in the medial or adventitial layers. In a second study, the basilar artery of seven dogs was constricted chronically by two intracisternal injections of autologous blood 3 days apart. Five dogs received endovascular laser treatment 7 or 10 days after the first injection, when basilar artery diameter was reduced to a mean of 61% and 77% of control, respectively. Immediately following treatment, basilar artery diameter increased to 104% and 102% of resting diameter, respectively. Both untreated and laser-treated arteries were smaller than the control diameter at 30 days (80% and 82%, respectively), but in each group the vasodilatory response to hypercapnia was preserved. These findings indicate that 1-µsec laser pulses are well tolerated by systemic and cerebral arteries in two different animal models, and suggest that the 480-nm pulsed-dye laser may have an application for the treatment or prophylaxis of cerebral vasospasm.

scholarly journals Application of the 1-µsec pulsed-dye laser to the treatment of experimental cerebral vasospasm

1991 ◽  
Vol 75 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Atsushi Teramura ◽  
Robert Macfarlane ◽  
Christopher J. Owen ◽  
Ralph de la Torre ◽  
Kenton W. Gregory ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Laser Energy ◽  
Autologous Blood ◽  
Preliminary Investigation ◽  
Dye Laser ◽  
Pulsed Dye Laser ◽  
Content Type

✓ Laser energy of 480 nm was applied in 1-µsec pulses varying between 2.2 and 10 mJ to in vitro and in vivo models of cerebral vasospasm. First, the pulsed-dye laser was applied intravascularly via a 320-µm fiber to basilar artery segments from six dogs. The segments were mounted in a vessel-perfusion apparatus and constricted to, on average, 70% of resting diameter by superfusion with dog hemolysate. Immediate increase in basilar artery diameter occurred to a mean of 83% of control. In a second model, the basilar artery was exposed transclivally in the rabbit. In three normal animals, superfusion of the artery with rabbit hemolysate resulted in a reduction of mean vessel diameter to 81% of control. Following extravascular application of the laser, vessels returned to an average of 106% of the resting state. In six rabbits, the basilar artery was constricted by two intracisternal injections of autologous blood, 3 days apart. Two to 4 days after the second injection, the basilar artery was exposed. Extravascular laser treatment from a quartz fiber placed perpendicular to the vessel adventitia resulted in an immediate 53% average increase in caliber to an estimated 107% of control. No reconstriction was observed over a period of up to 5 hours. Morphologically, damage to the arterial wall was slight. This preliminary investigation suggests that the 1-µsec pulsed-dye laser may be of benefit in the treatment of cerebral vasospasm.

Basic mechanism of in vitro pulsed-dye laser-induced vasodilation

1995 ◽  
Vol 82 (2) ◽  
pp. 256-261 ◽  
Author(s):  
Marios C. Kaoutzanis ◽  
John W. Peterson ◽  
R. Rox Anderson ◽  
Daniel J. McAuliffe ◽  
Robert F. Sibilia ◽  
...  
Keyword(s):  
Laser Energy ◽  
Bubble Formation ◽  
Basic Mechanism ◽  
Underlying Mechanism ◽  
Dye Laser ◽  
Pulsed Dye Laser ◽  
Content Type ◽  
Vasodilatory Response ◽  
Fine Print

✓ Vasodilation of rabbit carotid arteries induced by a pulsed-eye laser was studied in vitro to clarify the underlying mechanism. Artery segments were double cannulated in a pressure-perfusion apparatus which, under physiological conditions, allows for differential application of various solutions, pharmacological agents, and pulsed-dye laser light. Vaso-constriction was activated using both pharmacological and nonpharmacological agonists. Laser energy at a wavelength of either 480 or 575 nm was applied intraluminally in 1-µsec pulses, which caused dilation of the arteries if hemoglobin was present in the lumen at sufficient concentration. Induced vasodilation did not specifically require the presence of hemoglobin; the same phenomenon could be repeated using an inert dye such as Evans blue as an optical absorber of laser energy. The optical density of the absorber, the number of applied laser pulses, and total amount of applied energy directly influenced the vasodilatory response. Laser-induced vasodilation was possible in both normal vessels and vessels denuded of endothelium. Pulsed-dye laser-induced vasodilation is therefore not a phenomenon mediated through chemical processes, but is rather a purely physical process initiated by the optical absorption of laser energy by the intraluminal medium, which probably induces cavitation bubble formation and collapse, resulting in the vasodilatory response of the vessel.

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.

Pulsed dye laser treatment of telangiectasia after radiotherapy for breast carcinoma

1999 ◽  
Vol 52 (3) ◽  
pp. 236-237 ◽  
Author(s):  
M. Ahmad ◽  
S. Mirza ◽  
I.T.H. Foo
Keyword(s):  
Breast Carcinoma ◽  
Laser Treatment ◽  
Dye Laser ◽  
Pulsed Dye Laser

Evaluation of prostaglandin biosynthetic activity in canine basilar artery following subarachnoid injection of blood

1981 ◽  
Vol 55 (5) ◽  
pp. 771-778 ◽  
Author(s):  
Tomio Sasaki ◽  
Sei-itsu Murota ◽  
Susumu Wakai ◽  
Takao Asano ◽  
Keiji Sano
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Biosynthetic Activity ◽  
Content Type ◽  
Blood Injection ◽  
Canine Basilar Artery ◽  
Subarachnoid Blood ◽  
Fine Print

✓ Transformation of arachidonic acid into prostaglandins was investigated in the basilar artery by incubating sections of artery with carbon-14-labeled arachidonic acid. Thin-layer radiochromatography revealed that, in normal canine basilar arteries, 14C-arachidonic acid was transformed mainly to 6-ketoprostaglandin (PG)F1α, a spontaneous metabolite of prostacyclin (PGI2). Among other prostaglandins, only a small amount of PGF2α was detected, whereas PGD2, PGE2, and thromboxane B2 were not. Arteries removed on Days 3 and 8 after subarachnoid blood injection showed a prostaglandin synthesis profile similar to that in the normal cerebral artery. In borate-buffered saline (0.1M borate buffer, pH 9.0/0.15M NaCl = 1:9, vol/vol), canine basilar artery produced a PGI2-like substance that inhibited adenosine diphosphate (ADP)-induced platelet aggregation. Its anti-aggregatory activity was completely abolished by acidification. Aspirin likewise inhibited production of the anti-aggregatory substance. From these results, it was concluded that the anti-aggregatory activity was due solely to the production of PGI2 by the arterial specimen. Based on the above results, PGI2 biosynthetic activity in the cerebral artery exposed to subarachnoid blood injection was bioassayed by measuring the inhibitory activity of the incubation product upon ADP-induced platelet aggregation following incubation of the arteries in borate-buffered saline for 5 to 30 minutes at 20°C, using synthetic PGI2-Na as a standard. The synthetic activity of PGI2 in the artery exposed to subarachnoid blood injection had diminished remarkably by Days 3 and 8. This diminution of PGI2 synthesis in the cerebral artery may be involved in the pathogenesis of cerebral vasospasm.

A fatal, chronically growing basilar artery: a new type of dissecting aneurysm

1996 ◽  
Vol 84 (6) ◽  
pp. 962-971 ◽  
Author(s):  
Tohru Mizutani
Keyword(s):  
Mr Imaging ◽  
Basilar Artery ◽  
Dissecting Aneurysm ◽  
Neurological Deficits ◽  
Vertebrobasilar Insufficiency ◽  
Content Type ◽  
Asymptomatic Patients ◽  
Basilar Arteries ◽  
Fine Print

✓ A long-term follow-up study (minimum duration 2 years) was made of 13 patients with tortuous dilated basilar arteries. Of these, five patients had symptoms related to the presence of such arteries. Symptoms present at a very early stage included vertebrobasilar insufficiency in two patients, brainstem infarction in two patients, and left hemifacial spasm in one patient. Initial magnetic resonance (MR) imaging in serial slices of basilar arteries obtained from the five symptomatic patients showed an intimal flap or a subadventitial hematoma, both of which are characteristic of a dissecting aneurysm. In contrast, the basilar arteries in the eight asymptomatic patients did not show particular findings and they remained clinically and radiologically silent during the follow-up period. All of the lesions in the five symptomatic patients gradually grew to fantastic sizes, with progressive deterioration of the related clinical symptoms. Dilation of the basilar artery was consistent with hemorrhage into the “pseudolumen” within the laminated thrombus, which was confirmed by MR imaging studies. Of the five symptomatic patients studied, two died of fatal subarachnoid hemorrhage (SAH) and two of brainstem compression; the fifth patient remains alive without neurological deficits. In the three patients who underwent autopsy, a definite macroscopic double lumen was observed in both the proximal and distal ends of the aneurysms within the layer of the thickening intima. Microscopically, multiple mural dissections, fragmentation of internal elastic lamina (IEL), and degeneration of media were diffusely observed in the remarkably extended wall of the aneurysms. The substantial mechanism of pathogenesis and enlargement in the symptomatic, highly tortuous dilated artery might initially be macroscopic dissection within a thickening intima and subsequent repetitive hemorrhaging within a laminated thrombus in the pseudolumen combined with microscopic multiple mural dissections on the basis of a weakened IEL. The authors note and caution that symptomatic, tortuous dilated basilar arteries cannot be overlooked because they include a group of malignant arteries that may grow rapidly, resulting in a fatal course.

Transluminal angioplasty for atherosclerotic disease of the vertebral and basilar arteries

1993 ◽  
Vol 78 (2) ◽  
pp. 192-198 ◽  
Author(s):  
Randall T. Higashida ◽  
Fong Y. Tsai ◽  
Van V. Halbach ◽  
Christopher F. Dowd ◽  
Tony Smith ◽  
...  
Keyword(s):  
Vertebral Artery ◽  
Basilar Artery ◽  
Cerebral Circulation ◽  
Transluminal Angioplasty ◽  
Content Type ◽  
Atherosclerotic Stenosis ◽  
Basilar Arteries ◽  
Posterior Cerebral Circulation ◽  
Fine Print

✓ Transluminal angioplasty for hemodynamically significant stenosis (> 70%) involving the posterior cerebral circulation is now being performed by the authors in selected cases. A total of 42 lesions affecting the vertebral or basilar artery have been successfully treated by percutaneous transluminal angioplasty techniques in 41 patients. The lesions involved the proximal vertebral artery in 34 cases, the distal vertebral artery in five, and the basilar artery in three. Patients were examined clinically at 1 to 3 and 6 to 12 months after angioplasty. Three (7.1%) permanent complications occurred, consisting of stroke in two cases and vessel rupture in one. There were four (9.5%) transient complications (< 30 minutes): two cases of vessel spasm and two of cerebral ischemia. Clinical follow-up examination demonstrated improvement of symptoms in 39 cases (92.9%). Radiographic follow-up studies demonstrated three cases (7.1 %) of restenosis involving the proximal vertebral artery; two were treated by repeat angioplasty without complication, and the third is being followed clinically while the patient remains asymptomatic. In patients with significant atherosclerotic stenosis involving the vertebral or basilar artery territories, transluminal angioplasty may be of significant benefit in alleviating symptoms and improving blood flow to the posterior cerebral circulation.

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