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M Zuccarello

Publications and source records attributed to M Zuccarello.

At least 19 recordsLinked to original sources
PubMed2006

Evidence for the improved exposure of the ophthalmic segment of the internal carotid artery after anterior clinoidectomy: morphometric analysis.

BACKGROUND: Although resection of the anterior clinoid process (ACP) is valuable in the surgical treatment of aneurysms of the ophthalmic (C6) segment of the internal carotid artery (ICA), quantitative assessment of this adjunct is incomplete. Our morphometric study assesses the effectiveness of the anterior clinoidectomy for exposure of the C6 segment of the ICA. METHODS: Ten formalin-fixed adult cadaveric heads were dissected bilaterally and pterional craniotomies were performed bilaterally. Measurements before and after resection of the ACP included the length of C6 segment of the ICA on its lateral aspect; C6 segment length on its medial aspect; and medial length of the optic nerve from the optic chiasm to falciform ligament (before ACP resection) then to the annulus of Zinn (after ACP resection). FINDINGS: Height and width of the intradural ACP were 8.67 +/- 2.63 and 6.57 +/- 1.68 mm, respectively. After clinoidectomy, mean length of the lateral C6 segment of the ICA increased 60% and mean exposure of the medial C6 segment of the ICA increased 113% (p < 0.001). Exposure of the optic nerve increased 150% (p < 0.001) after clinoidectomy and sectioning of the falciform ligament. No correlations were found between the lengths of the ACP and entire C6 segment, or the ACP size and amount of the C6 segment covered by the clinoid. CONCLUSIONS: Exposure of the C6 segment of the ICA is markedly increased by increase of the mobility of the optic nerve with clinoidectomy and section of the falciform ligament.

Cadaver↗
PubMed2006

Delayed profound local brain hypothermia markedly reduces interleukin-1beta gene expression and vasogenic edema development in a porcine model of intracerebral hemorrhage.

White matter (lobar) intracerebral hemorrhage (ICH) can cause edema-related deaths and life-long morbidity. In our porcine model, ICH induces oxidative stress, acute interstitial and delayed vasogenic edema, and up-regulates interleukin-1beta (IL-1beta), a proinflammatory cytokine-linked to blood-brain barrier (BBB) opening. In brain injury models, hypothermia reduces inflammatory cytokine production and protects the BBB. Clinically, however, hypothermia for stroke treatment using surface and systemic approaches can be challenging. We tested the hypothesis that an alternative approach, i.e., local brain cooling using the ChillerPad System, would reduce IL-1beta gene expression and vasogenic edema development even if initiated several hours after ICH. We infused autologous whole blood (3.0 mL) into the frontal hemispheric white matter of 20 kg pentobarbital-anesthetized pigs. At 3 hours post-ICH, we performed a craniotomy for epidural placement of the ChillerPad. Chilled saline was then circulated through the pad for 12 hours to induce profound local hypothermia (14 degrees C brain surface temperature). We froze brains in situ at 16 hours after ICH induction, sampled perihematomal white matter, extracted RNA, and performed real-time RT-PCR. Local brain cooling markedly reduced both IL-1beta RNA levels and vasogenic edema. These robust results support the potential for local brain cooling to protect the BBB and reduce injury after ICH.

Animals↗
PubMed2005

Multiple, peripheral aneurysms of the anterior inferior cerebellar artery.

In this case report, a 49-year-old woman developed subarachnoid hemorrhage in the right cerebellopontine angle cistern and blood into the fourth ventricle from a ruptured peripheral aneurysm of the anterior inferior cerebellar artery (AICA) located at the meatal loop. Concomitantly, a contralateral peripheral aneurysm was found in the posterior inferior cerebellar artery (PICA). A second peripheral aneurysm, not identified by previous angiography, was found in the caudomedial branch of AICA. We describe this diagnostic dilemma, management, and review the clinical presentation and location of 84 other peripheral AICA aneurysms reported in the literature.

Angiography, Digital Subtraction↗
PubMed2004

Evidence-based surgical treatment of carotid stenosis. Literature review.

Carotid stenosis is an important cause of transient ischemic attacks and stroke. The cause of carotid stenosis is most often atherosclerosis, which accounts for 10% to 20% of brain infarction cases. Despite the introduction of tissue-plasminogen activator and other promising experimental therapies for select patients with acute ischemic stroke prevention remains the best approach to reduce its impact. Stroke-prone patients can be identified and targeted for specific interventions. At this juncture, treatment of carotid stenosis is a well-established therapeutic target and a pillar of stroke prevention. Two main strategies exist for the treatment of carotid stenosis. The 1st is stabilization or halting the progression of the carotid plaque formation with medications and modifications of risk factors (e.g., hypertension, diabetes, smoking, obesity, high cholesterol). The 2nd approach is the elimination or reduction of carotid stenosis by carotid endarterectomy or angioplasty and stenting. Carotid endarterectomy is the mainstay of therapy for symptomatic, severe carotid stenosis. Although its role for asymptomatic patients appears more limited, it is distinct for severe stenosis. Carotid angioplasty and stenting are techniques in maturation with the attractiveness of being less invasive that face the challenge of at least replicating the results of surgery. In this article, we will discuss the surgical management of symptomatic and asymptomatic carotid stenosis based on the evidence provided by the literature.

Carotid Stenosis↗
PubMed2004

Aneurysms of the ophthalmic (C6) segment of the internal carotid artery: treatment options and strategies based on a clinical series.

AIM: Treatment of ophthalmic segment aneurysms is technically demanding and still associated with a relatively high morbidity and mortality. The refinements of surgical techniques combined with the development of indirect methods of treatment have greatly improved the outcome in treating these lesions. We present our clinical experience and discuss treatment strategies. METHODS: Seventy-eight consecutive patients with 88 ophthalmic segment aneurysms were admitted to our service from January 1997 to June 2003. Forty-three patients presented with unruptured aneurysms and 35 presented with subarachnoid hemorrhage (SAH). Management strategies included surgical clipping alone in 53 patients, clipping and hemicraniectomy in 2, coiling in 17, external carotid artery-middle cerebral artery (ECA/MCA) by-pass in 2, and coil occlusion of the internal carotid artery in 2. Two patients underwent no treatment. RESULTS: In the group of 41 treated patients with unruptured aneurysms, 40 (97.6%) had good outcomes (GOS 1-2) and 1 patient had poor (GOS 3) outcome at discharge. Procedure-related morbidity was 15.7% (8/51 procedures), and permanent morbidity was 9.75% (4/41 patients). In the 35 patients who presented with SAH, mortality was 14.3% (5 patients); at discharge, 21 patients (60%) had good (GOS 1-2) and 9 (25.7%) poor (GOS 3) outcomes. The overall outcome was good (GOS 1-2) in 63 patients (80.8%) and poor (GOS 3-4) in 10 patients (12.8%). Overall mortality was 6.4% (5 patients all with SAH). CONCLUSIONS: Direct obliteration of the aneurysm utilizing advanced surgical techniques is our preferred treatment approach, whenever possible. In case of unclippable large or giant aneurysms, the surgical or endovascular occlusion of the proximal internal carotid artery with or without an extracranial-intracranial by-pass is an option. A highly skilled team including a cerebrovascular and an endovascular surgeon is essential to achieve good outcomes in treating these lesions.

Adult↗
PubMed2003

Visceral leishmaniasis and HIV co-infection: a rare case of pulmonary and oral localization.

Visceral leishmaniasis (VL) has increased as a complicating infection in subjects with human immunodeficiency virus (HIV) in countries bordering the Mediterranean sea. The clinical course as well as organ involvement of VL are often atypical in HIV positive subjects. In this study a case of VL with pulmonary and oral mucose localisation in a patient with acquired immune deficiency syndrome (AIDS), is reported. These findings, together with the presence of the parasite in the peripheral blood smear, confirm that in HIV positive patients the impaired immune system allows the spreading and the atypical localisation of the Leishmania amastigotes more easily than in immuno-competent individuals. In endemic areas and in HIV positive subjects a systemic and careful parasitological follow-up is necessary to ensure that any clinical form of leishmaniasis is not overlooked.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Expanding the boundaries of the transsphenoidal approach: a microanatomic study.

The anatomic features of a transsphenoidal approach are reviewed, focusing on the microsurgical anatomy of parasellar structures. Pertinent microsurgical anatomy is described in sufficient detail for the neurosurgeon to successfully extend a standard transsphenoidal approach for treatment of lesions involving the region of the tuberculum sellae, planum sphenoidale, supradiaphragmatic intradural space, and medial cavernous sinus. The parasellar region of 50 formalin-fixed cadaveric heads was examined by using magnification 3x to 40x. The arterial and venous systems of five cadaveric specimens were injected under pressure with colored silicone rubber. The sellar region of three specimens was examined histologically. Important anatomic landmarks identified in the roof of the sphenoid sinus include a carotid and trigeminal prominence, as well as a tubercular, clival, and opticocarotid recess. The diaphragma sella is actually comprised of two layers of dura, with a venous system (circular sinus) interposed between the layers. The dura mater of the pituitary gland separates the gland from the medial compartment of the cavernous sinus. The microanatomic detail necessary to extend the transsphenoidal approach to the supradiaphragmatic intradural space and medial compartment of the cavernous sinus is described. These data are presented to facilitate the clinical application of these extended approaches.

Cadaver↗
PubMed2001

Intraoperative magnetic resonance imaging to determine the extent of resection of pituitary macroadenomas during transsphenoidal microsurgery.

OBJECTIVE: Well-established surgical goals for pituitary macroadenomas include gross total resection for noninvasive tumors and debulking with optic chiasm decompression for invasive tumors. In this report, we examine the safety, reliability, and outcome of intraoperative magnetic resonance imaging (iMRI) used to assess the extent of resection, and thus the achievement of preoperative surgical goals, during transsphenoidal microneurosurgery. METHODS: Our magnetic resonance operating room contains a Hitachi AIRIS II 0.3-T, vertical-field open magnet (Hitachi Medical Systems America, Inc., Twinsburg, OH). A motorized scanner tabletop moves the patient between the imaging and operative positions. For transsphenoidal surgery, the patient is positioned directly on the scanner tabletop so that the surgical field is located between 1.2 and 1.6 m from the magnet isocenter. At this location, the magnetic field strength is low (<20 G), thus permitting the use of many conventional surgical instruments. Thirty consecutive patients with pituitary macroadenomas underwent tumor resection in our magnetic resonance operating room by use of a standard transsphenoidal approach. After initial resection, the patient was advanced into the scanner for imaging. If residual tumor was demonstrated and deemed surgically accessible, the patient underwent immediate re-exploration. RESULTS: iMRI was performed successfully in all 30 patients. In one patient, iMRI was used to clarify the significance of hemorrhage from the sellar region and resulted in immediate conversion of the procedure to a craniotomy. In the remaining 29 patients, initial iMRI demonstrated that the endpoint for extent of resection had been achieved in only 10 patients (34%) after an initial resection attempt, whereas 19 patients (66%) still had unacceptable residual tumor. All 19 of these latter patients underwent re-exploration. Ultimately, re-exploration resulted in the achievement of the planned endpoint for extent of resection in all of the 29 completed transsphenoidal explorations. Operative time was extended in all cases by at least 20 minutes. CONCLUSION: iMRI can be used to safely, reliably, and objectively assess the extent of resection of pituitary macroadenomas during the transsphenoidal approach. The surgeon is frequently surprised by the extent of residual tumor after an initial resection attempt and finds the intraoperative images useful for guiding further resection.

Adenoma↗
PubMed2001

Early carotid endarterectomy for critical carotid artery stenosis after thrombolysis therapy in acute ischemic stroke in the middle cerebral artery.

BACKGROUND AND PURPOSE: Tissue plasminogen activator (tPA) has been shown to be effective for acute ischemic stroke. However, if a high-grade cervical carotid stenosis remains despite tPA therapy, patients are at risk for recurrent stroke. Carotid endarterectomy (CEA) has been shown to be effective in symptomatic patients with high-grade cervical carotid stenosis in reducing the risk of stroke, but it is unknown whether CEA can be performed safely after tPA thrombolysis. We describe our experience with 5 patients who underwent early (<48 hours) CEA for residual high-grade cervical carotid stenosis after thrombolytic therapy for acute ischemic stroke in the middle cerebral artery territory. METHODS: All patients had a critical (>99%) carotid artery stenosis on the symptomatic side after tPA therapy. All patients received intravenous tPA; 3 patients also received intra-aortic tPA. Three patients received intravenous heparin infusion immediately after administration of tPA. All patients showed marked improvement in their National Institutes for Health Stroke Scale scores after treatment with tPA. CEA was then performed within 45 hours (6 hours in 1 patient, 23 hours in 2, 26 hours in 1, and 45 hours in 1). RESULTS: All 5 patients underwent successful CEA. There were no complications related to surgery. At discharge, 2 patients had a normal examination, and the remaining patients had mild deficits. In a long-term follow-up of 5 to 22 months, no patient had a recurrent cerebrovascular event. CONCLUSIONS: Early CEA can be performed safely and successfully in patients after tPA treatment for acute ischemic stroke in appropriately selected patients.

Acute Disease↗
PubMed2001

Treatment strategy for patients with unruptured intracranial aneurysms.

The increased sensitivity of neuroimaging techniques has enabled the more frequent diagnosis of unruptured aneurysms. Because the most devastating complication of an unruptured aneurysm is subarachnoid hemorrhage, it has been considered desirable to treat these aneurysms before they rupture. However, the optimal treatment strategy for patients with unruptured aneurysms remains controversial. The management decision requires knowledge of the natural history and an accurate assessment of the risks related to various treatment options. On December 10, 1998 the New England Journal of Medicine published an article by the International Study of Unruptured Intracranial Aneurysms Investigators. The study retrospectively assessed the natural history of unruptured aneurysms in 1449 patients; in addition, treatment-related mortality and morbidity were examined in a prospective cohort of 1172 patients. The major finding was that the rate of rupture for aneurysms smaller than 10 mm in diameter in patients with no history of subarachnoid hemorrhage was 0.05% per year, and that the mortality and morbidity associated with surgery greatly exceeded the risk of rupture in such patients. This report has generated tremendous controversy in the treatment of unruptured aneurysms and has influenced our decision making. The results of this study are critically analyzed and potential flaws presented. To develop recommendations for treatment, the literature was reviewed. The conclusion of this search is that there is insufficient evidence to recommend a standard of management. Therapeutic guidelines are provided, particularly for patients with small incidental aneurysms and no history of subarachnoid hemorrhage.

Aneurysm, Ruptured↗
PubMed2000

Hypocapnic constriction in rabbit basilar artery in vitro: triggering by serotonin and dependence on endothelin-1 and alkalosis.

This study tested whether hypocapnic constriction of the rabbit basilar artery in vitro can be triggered by serotonin, and whether the resulting constriction is (1) due to the alkaline pH associated with hypocapnia, and (2) endothelin-1 mediated. Hypocapnic alkaline solution (25 mM NaHCO(3); pH 7.76; pCO(2) 14.2) or isocapnic alkaline solution (50 mM NaHCO(3); pH 7.73; pCO(2) 35.0) rarely altered basal tension. Serotonin (3 microM) challenge in hypocapnic or isocapnic alkaline solution resulted in near maximal tension. Washout of the serotonin did not decrease tension in 54% of the tissues, as plateau tension was maintained for 2-2.5 h. The plateau tension of washed tissues was relaxed by 1-3 microM PD145065 (Ac-D-Bhg-L-Leu-Asp-L-Ile-L-Ile-L-Trp), BQ610 (homopiperidinyl-CO-Leu-D-Trp(CHO)-D-Trp), and BQ788 (N-cis-2, 6-dimethyl-piperidinocarbonyl-L-gamma-MeLeu-D-Trp (COOCH(3))-Nle), endothelin ET(A)/ET(B), endothelin ET(A), and endothelin ET(B) receptor antagonists, respectively. In contrast, serotonin-induced tension in normal solution (25 mM NaHCO(3); pH 7.42; pCO(2) 36.9) was maintained for only 40 min (mean). These results demonstrate that (1) constriction due to hypocapnia in vitro can be triggered by serotonin and is endothelin-1 mediated and (2) alkaline pH in the absence of decreased pCO(2) is sufficient to elicit the constriction triggered by serotonin.

Acetylcholine↗
PubMed2000

Hypocapnic constriction in rabbit basilar artery in vitro: triggering by N(G)-monomethyl-L-arginine monoacetate and dependence on endothelin-1 and alkalosis.

This study tested whether hypocapnic constriction of the rabbit basilar artery in vitro can be triggered by a nitric oxide (NO) synthase inhibitor, and whether the resulting constriction is (1) due to the alkaline pH associated with hypocapnia, and (2) endothelin-1 mediated. Hypocapnic (25 mM NaHCO(3); pH 7.76; pCO(2) 14.2) or isocapnic alkaline solution (50 mM NaHCO(3); pH 7.73; pCO(2) 35.0) rarely altered basal tension. N(G)-monomethyl-L-arginine monoacetate (L-NMMA; 0.1 mM) challenge in hypocapnic or isocapnic alkaline solution resulted in near maximal tension that was maintained for 2-2.5 h even following L-NMMA washout. L-NMMA challenge in normal solution (25 mM NaHCO(3); pH 7. 42; pCO(2) 36.9) also induced near maximal tension, although the tension was maintained for only 25 min (mean). Ac-D-Bhg-L-Leu-Asp-L-Ile-L-Ile-L-Trp (PD145065), homopiperidinyl-CO-Leu-D-Trp(CHO)-D-Trp (BQ610), and N-cis-2, 6-dimethyl-piperidinocarbonyl L-gamma-MeLeu-D-Trp (COOCH(3))-Nle (BQ788; 1-3 microM), endothelin ET(A)/ET(B), endothelin ET(A), and endothelin ET(B) receptor antagonists, respectively, completely relaxed the tension that resulted from L-NMMA challenge in hypocapnic or isocapnic alkaline solution. These results demonstrate that constriction due to hypocapnia in vitro can be triggered by an NO synthase inhibitor and is endothelin-1 mediated. Additionally, alkaline pH in the absence of decreased pCO(2) is sufficient to elicit the constriction.

Acetylcholine↗
PubMed2000

Reduced verapamil inhibition of endothelin-1-constricted rabbit basilar artery due to enhanced non L-type Ca(2+)-channel-dependent constriction.

This study tested whether (1) L-type Ca(2+) channel blockade and extracellular Ca(2+) removal prior to endothelin-1, as compared to during the endothelin-1 constriction, resulted in lesser inhibition, and (2) the reduced inhibition due to prior L-type Ca(2+) channel blockade resulted from enhanced non L-type Ca(2+)-channel-dependent constriction. Pretreatment of rabbit basilar artery in vitro with 1 microM verapamil, an L-type Ca(2+) channel blocker, inhibited 3, 10, 30, and 100 nM endothelin-1 constrictions to a lesser extent than verapamil addition during the plateau endothelin-1 constriction. Ni(2+) (0.03 and 0.1 mM), a nonselective cation channel blocker, relaxed the plateau endothelin-1 constrictions in vessels pretreated with verapamil to greater magnitudes than vessels unexposed to verapamil. Extracellular Ca(2+) removal prior to 10, 30, and 100 nM endothelin-1 also inhibited the endothelin-1 constrictions to smaller magnitudes than Ca(2+) removal during the plateau endothelin-1 constrictions. These results suggest that the reduced inhibition of the endothelin-1 constriction following pretreatment with L-type Ca(2+) channel blocker or Ca(2+)-free solution, as compared to addition of these agents during the endothelin-1 constriction, is the result of non L-type Ca(2+) channel opening and enhanced Ca(2+)-independent constriction, respectively.

Animals↗
PubMed2000

Reversal of hypercapnia induces KATP channel and NO-independent constriction of basilar artery in rabbits with acute metabolic alkalosis.

The mechanism of hypocapnic constriction of the cerebral vasculature under conditions of altered acid-base balance has not been investigated. As K(ATP) channels and NO have been implicated in hypocapnic constriction, this study investigated their roles in the constriction due to lowered pCO(2) in hypercapnic rabbits with acute metabolic alkalosis. Metabolic alkalosis was induced acutely following ketamine/xylazine injection. Lowering blood pCO(2) from initial baseline hypercapnic levels to near normocapnic and hypocapnic levels constricted basilar artery by 10.2+/-0.8% (4) and 16.2+/-0.6% (44), respectively (means+/-S.E., n), as determined in an in situ cranial window preparation. The constrictions were maintained for 4-5 h and return of pCO(2) to hypercapnic levels relaxed the constriction. Changing the suffusate pH to either the pH of the cerebral spinal fluid observed during initial baseline hypercapnia or following lowered pCO(2) did not alter the magnitude of constriction due to lowered pCO(2). Neither 0.3 mM N(G)-monomethyl-L-arginine monoacetate, an NO synthase inhibitor, nor 10 microM glibenclamide, a K(ATP) channel blocker, altered the magnitude of hypocapnic constriction. These results demonstrated that under conditions of acute metabolic alkalosis and accompanying compensatory hypercapnia, subsequent pCO(2) reduction induces prolonged constriction of the basilar artery that is independent of (1) cerebral spinal fluid pH over a physiologic range, and (2) NO and K(ATP) channels.

ATP-Binding Cassette Transporters↗
PubMed2000

Reversal of hypercapnia induces endothelin-dependent constriction of basilar artery in rabbits with acute metabolic alkalosis.

We recently concluded that constriction of basilar artery due to respiration-induced hypocapnia in rabbits with acute metabolic alkalosis and accompanying compensatory hypercapnia was independent of NO and K(ATP) channels. Based on reports that endothelin-1-mediated hypocapnic constriction of the rabbit basilar artery in vitro, we further investigated whether the respiration-induced hypocapnic constriction was endothelin-1 mediated. Metabolic alkalosis was induced acutely following ketamine/xylazine injection. The ET(A) plus ET(B) receptor antagonist, PD145065 (1 microM), and the selective ET(A) receptor antagonist, BQ610 (3 microM), completely relaxed the hypocapnic constriction, as determined in a cranial window. Unexpectedly, the ET(B) receptor antagonists, BQ788 and RES-701-1 (3 microM), relaxed the constriction by 72.1+/-2.8% (4) and 77.2+/-8.7% (5), respectively (means+/-S.E. (n)). To investigate whether the large magnitudes of relaxation to both ET(A) and ET(B) receptor antagonists were due to nonselectivity of the antagonists, the effects of the antagonists on the constriction to exogenous endothelin-1 were evaluated. BQ610, BQ788, and RES-701-1 relaxed the 3-5 nM endothelin-1 constriction by only 64.3+/-7.6% (4), 43.5+/-8.5% (5), and 26.7+/-4.8% (3) (means+/-S.E. (n)), respectively, consistent with the selective blocking action of these antagonists. To investigate whether the greater magnitude of BQ610, BQ788, and RES-701-1 relaxation of hypocapnic constricted versus exogenous endothelin-1-constricted vessels was due to differences between constriction elicited by endogenous versus exogenous endothelin-1, the effects of the endothelin receptor antagonists on constriction to isocapnic alkaline suffusate were evaluated. PD145065 (1 microM) and 0.1 mM phosphoramidon, an endothelin-converting enzyme inhibitor, inhibited the constriction to isocapnic alkaline suffusate by 83.8+/-7.8% (6) and 74.3+/-9.7% (8) (means+/-S.E. (n)), respectively, consistent with the endothelin-1 dependency of the constriction. BQ610, BQ788, and RES-701-1 relaxed the isocapnic alkaline suffusate constriction by 74.9+/-6.7% (5), 65.5+/-6.4% (5), and 78.0+/-6.5% (4) (means+/-S.E. (n)), respectively. Thus, the relaxation profile to the selective endothelin receptor antagonists in isocapnic alkaline constricted vessels more closely approximated the relaxation profile observed in hypocapnic constricted as compared to endothelin-1-constricted vessels. Hypocapnia did not alter the 5 nM endothelin-1 constriction. These results suggest that, under conditions of acute metabolic alkalosis and accompanying compensatory hypercapnia, subsequent hypocapnic constriction is endothelin mediated. Both ET(A) and ET(B) receptor activation may mediate the hypocapnic constriction. The hypocapnic constriction is not due to enhanced endothelin-1 constriction and, thus, is due to the release of endothelin-1 and/or additional endothelins.

Alkalosis↗
PubMed2000

Angiolipomas of the central nervous system.

Angiolipomas are neoplasms composed of mature adipocytes admixed with abnormal vascular elements. They are most commonly found in the subcutaneous tissue of the trunk and extremities, but other sites have been reported. The craniospinal axis is an uncommon but significant site. An extensive review of the literature is conducted. We summarize 94 cases of angiolipomas in the central nervous system (CNS) in 92 patients, including five in our own series, to highlight the most prominent features of these tumors. The increasing number of cases of CNS angiolipoma in the era of magnetic resonance imaging raises the question of the rarity of these lesions.

Adult↗
PubMed2000

Role of NO in endothelium-dependent relaxation of rabbit basilar artery in situ.

The purpose of this study was to investigate the possible involvement of endothelium-derived hyperpolarizing factor in endothelium-dependent relaxation of the cerebral vasculature by testing the effectiveness of NO synthase inhibitors at inhibiting endothelium-dependent relaxation in the rabbit basilar artery. Acetylcholine (1.0 microM) and 0.1/0.2 microM sarafotoxin S6c, an endothelinB receptor agonist, relaxed serotonin constricted basilar artery in situ by 100% and 70%, respectively. NG-monomethyl-L-arginine (L-NMMA; 0.1 mM) and 0.3 mM NG-nitro-L-arginine (L-NNA), NO synthase inhibitors, decreased the 1.0 microM acetylcholine- and 0.1/0.2 microM sarafotoxin S6c-induced relaxations by 75% and 45%, respectively. Unexpectedly, the relaxations were abolished by the combination of L-NMMA plus L-NNA. Furthermore, L-arginine (1.0 mM), but not D-arginine, restored the relaxations. Sodium nitroprusside-induced relaxation was also inhibited by L-NMMA plus L-NNA, and the inhibition was reversed by L-arginine. KCl constricted vessels only minimally relaxed in response to sodium nitroprusside, acetylcholine, and sarafotoxin S6c. These results demonstrate that combined NO synthase inhibitors more effectively inhibit endothelium-dependent relaxation than a single inhibitor. The mechanism underlying the greater inhibition due to the combined NO synthase inhibitors may result from both decreased NO release and secondary effects caused by decreased NO release, such as membrane depolarization. The results further suggest that caution should be used with respect to suggestions of the involvement of endothelium-derived hyperpolarizing factor in endothelium-dependent relaxation based upon the partial inhibitory effects of NO synthase inhibitors.

Animals↗