Stasis of 111In-DTPA in the posterior fossa in patients with cerebellar degeneration.
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Prolonged stasis of 111In-DTPA was noted in the poterior fossa in two patients during cisternography. Both patients had clinical signs of cerebellar dysfunction and pneumoencephalographic evidence of marked cerebellar degeneration. Cisternography may be a useful adjunct in evaluation patients with suspected cerebellar atrophy. (+info)
Centrally mediated cardiovascular responses to intracisternal injections of sympathomimetic amines in anesthetized rats.
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The cardiovascular effects resulting from intracisternal (i.c.) injections of sympathomimetic amines were studied in alpha-chloralose-urethanized rats. Norepinephrine (0.5-5 mug i.c.) caused a typical rise in blood pressure with no significant change in heart rate and a fall in blood pressure with a bradycardia, which were completely blocked after treatment with phentolamine (10-50 mug i.c.) L-isoproterenol (0.05-0.5 mug i.c.) and trimetoquinol (0.5-3 mug i.c.), a beta-sympathomimetic agent, usually caused a fall in blood pressure with a tachycardia, which was reduced after treatment with propranolol (10-50 mug i.c.), but trimetoquinol was inclined to cause a rise in blood pressure with a tachycardia. Epinephrine (5 mug i.c.) showed both centrally mediated alpha- and beta-sympathomimetic effects. Tyramine (0.5-1 mg i.c.) caused mixed blood pressure responses presumably due to a release of norepinephrine and epinephrine, and these responses were partially blocked after treatment with phentolamine (100 mug i.c.) or propranolol (50 mug i.c.). These observations suggest that both alpha- and beta-sensitive adrenergic zones may exist on the vasomotor center of the pons and medulla in rats, and both norepinephrine and epinephrine might centrally play a physiological role as the neurotransmitters controlling blood pressure in rats. (+info)
Contribution of 5-hydroxytryptamine1B receptors and 20-hydroxyeiscosatetraenoic acid to fall in cerebral blood flow after subarachnoid hemorrhage.
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BACKGROUND AND PURPOSE: This study examined the interaction between 5-hydroxytryptamine1B (5-HT1B) receptors and 20-hydroxyeiscosatetraenoic acid (20-HETE) in contributing to the acute fall in regional cerebral blood flow (rCBF) after subarachnoid hemorrhage (SAH) in rats. METHODS: The effects of intracisternal injection of 0.3 mL of arterial blood, artificial cerebrospinal fluid, and 5-HT on rCBF and the levels of 20-HETE and 5-HT in cerebrospinal fluid were measured in rats pretreated with vehicle, a 5-HT1B receptor antagonist (isamoltane hemifumarate), or an inhibitor of the synthesis of 20-HETE (HET0016). The effects of HET0016 and isamoltane on the vasoconstrictor response and changes in [Ca2+]i to 5-HT were also studied in middle cerebral arteries and vascular smooth muscle cells isolated from these vessels. RESULTS: 20-HETE and 5-HT levels in cerebrospinal fluid rose from 172+/-10 to 629+/-44 ng/mL and from 6+/-4 to 1163+/-200 nmol/mL, respectively, after SAH. rCBF fell by 30% 10 minutes after SAH, and it remained at this level for the next 2 hours. Blockade of 5-HT1B receptors prevented the sustained fall in rCBF seen after SAH. Intracisternal injection of 5-HT mimicked SAH by increasing 20-HETE levels in cerebrospinal fluid to 475+/-94 ng/mL and reducing rCBF by 30%. Blockade of the synthesis of 20-HETE with HET0016 prevented the fall in rCBF produced by 5-HT. Isamoltane and HET0016 reduced the vasoconstrictor response of isolated MCA to 5-HT by >60% and diminished the rise in [Ca2+]i produced by 5-HT in vascular smooth muscle cells isolated from these arteries. CONCLUSIONS: These results suggest that the release of 5-HT after SAH activates 5-HT1B receptors and the synthesis of 20-HETE and that 20-HETE contributes to the acute fall in rCBF by potentiating the vasoconstrictor response of cerebral vessels to 5-HT. (+info)
Single blood injection into the ventral cisterna magna through a microcatheter for the production of delayed cerebral vasospasm: experimental study in dogs.
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BACKGROUND AND PURPOSE: We developed an experimental canine subarachnoid hemorrhage (SAH) model in which one-time blood injection by means of a microcatheter into the ventral cisterna magna (CM) is performed without direct CM puncture. We assessed the severity and duration of the vasospasm produced in this model. METHODS: Fresh autologous blood (0.25 or 0.5 ml/kg) or saline (0.5 ml/kg) was injected into the ventral CM of dogs through a microcatheter inserted at the lumbar region. Serial angiograms were obtained on days 3, 7, 10, and 14, and chronologic changes in the mean diameter of the basilar artery (BA) were recorded. The BA was examined histologically on day 7 after injection. RESULTS: A remarkable amount of clot was present in front of the brain stem at 24 hours after SAH induction. The clot was smaller in the 0.25 ml/kg SAH than in the 0.5 ml/kg SAH group. On day 3, narrowing of the BA was apparent in both SAH groups compared with the control (P <.05). The BA gradually returned to nearly normal on day 14 in the 0.25 ml/kg SAH group. Arterial narrowing was more severe and persistent in the 0.5 ml/kg SAH than in the 0.25 ml/kg SAH group (P <.05). Histologic examination of the BA on the 7th postinjection day confirmed narrowing of the lumen, indicative of arterial spasm, in both SAH groups. CONCLUSION: Our method of SAH induction by means of a single injection of blood directly into the ventral CM through a microcatheter induced severe, prolonged spasms in the canine BA. Because our model facilitates the induction of different-sized clots, we could control of the severity and duration of the induced vasospasms. (+info)
Intrathecal urokinase infusion through a microcatheter into the cisterna magna to prevent cerebral vasospasm: experimental study in dogs.
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BACKGROUND AND PURPOSE: Our preliminary report on intrathecal urokinase (UK) infusion into the cisterna magna (CM) with a microcatheter showed good results in terms of vasospasm prevention in humans. In this study, we evaluated the relationship between different urokinase (UK) infusion sites and their effect on vasospasm prevention by using our canine subarachnoid hemorrhage (SAH) model. METHODS: At 24 hours after SAH induction, we injected 1000 IU/kg UK into the cisterna magna (CM) or lumbar sac (LS) of dogs by using a microcatheter inserted at the lumbar region. We then obtained serial angiograms and chronologically examined the changes in the mean diameter of the basilar artery (BA) during a 14-day period to determine the effect of the different injection sites on vasospasm prevention. At 24 hours after UK injection, one dog from each group was killed for gross inspection of the subarachnoid clot. To measure its concentration in the CM and sylvian fissure, UK (1000 IU/kg) was injected into the CM or LS of dogs without SAH; measurements were taken at 15-minute intervals until 4 hours after injection. RESULTS: At 24 hours after UK injection, subarachnoid clot in front of the brain stem persisted strongly in the LS group; it had almost disappeared in the CM group. In the LS group, there was severe and persistent BA constriction during the 14-day observation period. In the CM group, the BA was constricted on day 3; however, gradual dilatation occurred over time. The mean diameter of the BA on days 7, 10, and 14 was 48.2%, 53.9%, and 58.9% in the LS group and 62.6%, 70.5%, and 82.3% in the CM group. The difference between the two groups was significant on days 7, 10, and 14 (P <.05). In dogs without SAH, the average maximum UK concentration in the CM and the sylvian fissure was 2.5 and 6.7 times higher, respectively, in the CM group than in the LS group. CONCLUSIONS: In our canine SAH model, the administration of UK into the CM was significantly more effective in preventing cerebral vasospasms than was administration into the LS. (+info)
Focally increased activity on scinticisternography: report of two cases.
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Two cases where focally increased activity was noted on scinticisternography are reported. One case involves a documented arteriovenous malformation, and the other, documented embolic vascular disease. After a review of the pertient literature, various other pathologic entities associated with similar scan findings are described. Possible causative mechanisms are discussed. (+info)
Enhanced depressor response to endothelial nitric oxide synthase gene transfer into the nucleus tractus solitarii of spontaneously hypertensive rats.
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Previously, we demonstrated that endothelial nitric oxide synthase (eNOS) gene transfer into the nucleus tractus solitarii (NTS) decreased blood pressure, heart rate and sympathetic nerve activity in conscious normotensive Wistar-Kyoto rats (WKY). In order to determine whether overexpression of eNOS in the NTS causes different effects on blood pressure and heart rate between spontaneously hypertensive rats (SHR) and WKY, we transfected adenovirus vectors encoding either eNOS (AdeNOS) or beta-galactosidase (Ad beta gal) into the NTS of SHR and WKY in vivo. The local expression of eNOS in the NTS was confirmed by Western blot analysis for eNOS protein, and the magnitude of expression did not differ between SHR and WKY. Blood pressure and heart rate were monitored by the use of a radio-telemetry system in a conscious state before and 7 days after the gene transfer. Systolic blood pressure (SBP) and heart rate decreased on day 7 in both AdeNOS-transfected SHR and WKY. However, the magnitude of decreases in SBP of AdeNOS-transfected SHR was greater than that of AdeNOS-transfected WKY (-24.1 +/- 2.9 vs. -15.9 +/- 2.1 mmHg, p < 0.05). Transfection of Ad beta gal into the NTS did not alter SBP in either group. A depressor response evoked by microinjection of L-glutamate into the NTS did not differ between the two strains. These results suggest that overexpression of eNOS in the NTS causes a greater depressor response in SHR than in WKY in a conscious state. An abnormality of the L-arginine-NO pathway in the NTS may be related to the hypertensive mechanism(s) of SHR. (+info)
Safety of chronic intrathecal morphine infusion in a sheep model.
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BACKGROUND: The safety of chronically administered intrathecal morphine has been questioned. Therefore, the authors examined the behavioral and neurologic effects and neurotoxicity of continuous intrathecal morphine administration in sheep. METHODS: Groups of three sheep were implanted with intrathecal infusion systems for the continuous administration of morphine (3, 6, 9, 12, or 18 mg/day) or saline at a fixed infusion rate of 1.92 ml/day beginning approximately 7 days after implantation. Sheep were examined daily for any changes in behavior or neurologic function. After 28-30 days, the animals were humanely killed. Cerebrospinal fluid samples were collected and analyzed for protein, erythrocytes and leukocytes, and morphine content. The spinal cord and meninges with the catheter in situ was removed en bloc and fixed in formalin for histologic analysis. RESULTS: Unilateral hind-leg gait deficits were observed in two of three animals in each of the 12- and 18-mg/day dose groups. Gross and microscopic evaluation of spinal cord tissue from these animals revealed intradural-extramedullary inflammatory masses that compressed the spinal cord at the catheter-tip and mid-catheter areas. This inflammation was ipsilateral to extremities that exhibited gait deficits and had acute and chronic cellular components. CONCLUSIONS: The toxicity of intrathecal morphine seems to be dependent on the amount of morphine infused, although the effects of dose versus concentration cannot be clearly distinguished in this study. Intrathecal morphine doses of 12- 18 mg/day produced inflammatory masses extending from the catheter tip down the length of the catheter within the subarachnoid space. Doses of 6-9 mg/day produced mild-to-moderate inflammation 5 cm cranial to the catheter tip. A dose of 3 mg/day produced no neurotoxicity and spinal histopathologic changes that were equivalent to those observed in the saline-treated animals. (+info)