PubMed Health⌕ Search

Biomedical subjects

M Zuccarello

Publications and source records attributed to M Zuccarello.

At least 19 recordsLinked to original sources
PubMed1996

Relaxation of subarachnoid hemorrhage-induced spasm of rabbit basilar artery by the K+ channel activator cromakalim.

BACKGROUND AND PURPOSE: Cerebral vasospasm resulting from subarachnoid hemorrhage (SAH) is refractory to most vasodilators. However, despite evidence that a mechanism underlying the vasospasm may be smooth muscle cell membrane depolarization resulting from decreased K+ conductance, the ability of K+ channel activators to relax the spasm has not been thoroughly investigated. The purpose of this study, therefore, was to investigate whether K+ channel activation selectively relaxes SAH-induced vasospasm. METHODS: Three days after SAH in the rabbit, relaxation of the basilar artery in response to the K+ channel activator cromakalim as well as to staurosporine (protein kinase C antagonist), forskolin (adenylate cyclase activator), and sodium nitroprusside (guanylate cyclase activator) was measured in situ with the use of a cranial window. Relaxation in response to these agents was also investigated in control vessels contracted with serotonin. Membrane potential of the smooth muscle cells of the basilar artery from SAH and control rabbit was measured in vitro with the use of intracellular microelectrodes. RESULTS: Cromakalim completely relaxed the SAH-induced spastic basilar artery, while staurosporine, forskolin, and sodium nitroprusside were significantly less efficacious. In contrast, sodium nitroprusside and forskolin were more efficacious relaxants in serotonin-contracted control vessels than in SAH vessels. The K+ channel blocker glyburide and high [K+] prevented cromakalim-induced relaxation. Glyburide did not inhibit forskolin-induced relaxation of serotonin-contracted control vessels. Cromakalim concentration-dependently repolarized spastic basilar artery smooth muscle cells, and the repolarization was prevented by glyburide. CONCLUSIONS: These results suggest that K+ channel activation selectively relaxes SAH-induced vasospasm. We speculate that the ability of K+ channel activators to selectively relax the spasm may be due, at least in part, to the underlying inhibition of K+ channels after SAH.

Animals↗
PubMed1996

Prevention of subarachnoid hemorrhage-induced cerebral vasospasm by oral administration of endothelin receptor antagonists.

The purpose of this study was to investigate the effectiveness of oral treatment with the endothelin (ET) A/B receptor antagonist Ro 47-0203, 4-tert-butyl-N-[6-(hydroxy- ethoxy)-5-(2-methoxy-phenoxy)-2'-bipyrimidin-4-yl]-benzenesulfonam ide (bosentan), and the ET A receptor antagonist 2-benzo[1,3]dioxol-5-yl-3-benzyl-4-(4-methoxy- phenyl)-4-oxo-but-2-enoic acid monosodium salt (PD155080), in the prevention of subarachnoid hemorrhage (SAH)-induced delayed cerebral vasospasm. Double hemorrhage in the rabbit constricted the basilar artery to 34% if control as determined by angiography. Oral bosentan and PD155080 administration after the initial SAH decreased the magnitude of constriction to 9% and 16% of control, respectively. Plasma and cerebrospinal fluid bosentan levels and plasma PD155808 levels were consistent with concentrations reported to inhibit ET-1 constriction of blood vessels in vitro. These results support the use of oral administration of ET A/B and ET A receptor antagonists as potential specific treatment for vasospasm resulting from SAH in humans.

Administration, Oral↗
PubMed1995

Immunohistochemical localization of endothelial nitric oxide synthase in vessels of the dura mater of the Sprague-Dawley rat.

Nitric oxide (NO) and the dura mater are implicated in the pathogenesis of vascular headache. Many studies have demonstrated the participation of NO in headache; however, few studies have identified NO in the dura mater. In this study, nine Sprague-Dawley rats were examined with immunohistochemistry using two different endothelial nitric oxide synthase (eNOS) monoclonal antibodies, H32 and ECNOS. eNOS was successfully localized to the endothelium of the middle meningeal artery. To the best of our knowledge, this is the first study to report NOS immunopositive endothelial cells in the blood vessels of the rat dura mater. The authors propose that NO plays an active role in dural vasodilation, contributing to the pathogenesis of vascular headache; in the future, NO inhibitors could serve as pharmacological agents to treat vascular headache.

Animals↗
PubMed1995

Decreased endothelium-dependent relaxation in subarachnoid hemorrhage-induced vasospasm: role of ET-1.

The purpose of this study was to test whether endothelium-dependent relaxation is decreased during acute vasospasm following subarachnoid hemorrhage (SAH) and the mechanism underlying the decrease. Basilar artery in situ was 35% constricted 3 days following injection of autologous arterial blood into the rabbit cisterna magna compared with vessels from control rabbits. In situ suffusion with the endothelium-dependent relaxant, acetylcholine (ACh; 10 microM), relaxed resting and serotonin (5-HT)-contracted control vessels but not vasospastic and 5-HT-contracted vasospastic vessels. In contrast, the relaxant potency and efficacy of ACh was similar in control and vasospastic vessels contracted with 5-HT in vitro. In situ suffusion with the ETA-receptor antagonist, BQ-123 (1 microM), reversed the vasospasm by 51% and restored the magnitude of ACh relaxation of vasospastic and 5-HT-contracted vasospastic vessels to that of controls. ACh in situ and in vitro relaxed endothelin-1 (ET-1)-contracted control vessels to a smaller magnitude than 5-HT-contracted control vessels. These results suggest, in contrast to previous studies, that endothelium-dependent relaxation is decreased during acute vasospasm following SAH. The decreased endothelium-dependent relaxation is secondary to the underlying ET-1-mediated spasm. The inhibition of endothelium-dependent relaxation observed in situ following SAH cannot be demonstrated in vitro, presumably due to loss of the ET-1-mediated vasospasm.

Acetylcholine↗
PubMed1994

Endothelin ETA and ETB receptors in subarachnoid hemorrhage-induced cerebral vasospasm.

The relative roles of endothelin ETA and ETB receptor activation in cerebral vasospasm following subarachnoid hemorrhage were investigated in the rabbit. The endothelin ETA receptor antagonist, BQ610 (1 microM; homopiperidinyl-CO-Leu-D-Trp(CHO)-D-Trp-OH), and the endothelin ETA/ETB receptor antagonist, PD145065 (1 microM; Ac-D-Bhg-L-Leu-L-Asp-L-Ile-L-Ile-L-Trp), relaxed the vasospastic basilar artery in situ by 45% and 87%, respectively. These results suggest that subarachnoid hemorrhage-induced vasospasm of the rabbit basilar artery is due to activation of both endothelin ETA and ETB receptors.

Amino Acid Sequence↗
PubMed1994

Nitric oxide synthase immunoreactivity in the rat dura mater.

The dura mater has been implicated as a tissue where vascular headache develops. Identification of the neural components of this tissue is a prerequisite for understanding the mechanisms of this pathological process. The nitric oxide molecule, a potent vasodilator, may contribute to the vascular headache process by dilating dural vasculature. Our immunohistochemical study using nitric oxide synthase (NOS) antibodies revealed NOS-positive nerve fibers and a prominent mast cell population in the rat dura. A majority of the immunopositive fibers were associated with the anterior meningeal artery and its branches and sparse innervation with the middle meningeal artery, its branches, and superior sagittal sinus. We propose that the NOS-positive nerve fibers and mast cells be considered as possible participants in the pathogenesis of vascular headache.

Amino Acid Oxidoreductases↗
PubMed1994

Brain metastasis from endometrial carcinoma. Report of two cases.

The authors report two cases of surgically treated brain metastases from endometrial cancer which are quite unusual occurrences. In one of them the brain lesion was the presenting symptom of malignancy while in the other the metastasis was discovered after the primary tumor had been treated. Both the brain lesions were scarcely differentiated adenocarcinomas which closely resembled the uterine primaries histologically. The authors review the four cases reported in the literature and discuss the clinical features and the treatment of this disease. The analysis of cases shows that the metastatic potential of endometrial cancer is extremely variable and unpredictable but less severe than that observed in ovarian or cervical tumors. The authors suggest that the erratic behaviour of endometrial cancer may justify an aggressive (though necessarily palliative) approach to brain metastases even in the presence of circumscribed metastatic involvement.

Adenocarcinoma, Papillary↗
PubMed1994

Effect of subarachnoid haemorrhage on trigeminovascular calcitonin-gene-related peptide and substance P of the rat dura mater versus cerebral vasculature.

While the presence of a robust perivascular neural network accompanying cerebral and dural blood vessels that contain various neuropeptides is well documented, the functional significance of this innervation is unclear. Following experimentally induced subarachnoid haemorrhage (SAH) in animal models, immunocytochemical studies have revealed that changes occur in the staining intensity of some of these neuropeptides. This study compared the immunostaining intensity of calcitonin-gene-related peptide (CGRP) and substance P (SP) in cerebral and dural perivascular nerve fibers after SAH in the rat. Subarachnoid haemorrhage was produced by injecting 0.3 ml of autologous blood into the cisterna magna of male Sprague Dawley rats. Sham operated animals received an equal volume of buffered lactated Ringer's solution (pH 7.4). Changes in the immunostaining intensity of cerebral and dural vessels were evaluated by independent observers at 6, 24, and 48 hours after SAH. Immunostaining of CGRP was reduced in cerebral vessels at 6 hours and returned to normal by 48 hours. In contrast, CGRP immunostaining of dural perivascular nerve fibers was unchanged at all time periods examined. A marked decrease in SP immunostaining was documented at 6 hours in both the cerebral and dural vessels in all animals; at 48 hours, the staining intensity had returned to control levels. These results support the idea that several subpopulations of trigeminovascular neurons containing CGRP, SP, or both project to cerebral and dural vessels. Since these subpopulations may be differentially activated in pathologic conditions, such as SAH or vascular headache, the potential exists for pharmacologic intervention of specific neuropeptides with the resultant abatement of a pathologic process.

Animals↗
PubMed1994

Effect of remacemide hydrochloride on subarachnoid hemorrhage-induced vasospasm in rabbits.

The purpose of this study was to assess the role of an excitatory amino acid (EAA) receptor antagonist (remacemide hydrochloride) in a rabbit model of subarachnoid hemorrhage (SAH)-induced cerebral vasospasm. Cerebral angiograms were performed on 22 rabbits pre-SAH and 72 h post-SAH: 6 rabbits received an injection of mock cerebrospinal fluid (1 ml/kg) into the cisterna magna (group I, the control group); 6 rabbits were subjected to SAH but received no treatment (group II); autologous blood (1 ml/kg) from the central ear artery was injected into the cisterna magna of these rabbits; 6 rabbits were subjected to SAH (1 ml/kg) and treated with intraperitoneal (IP) bolus injections of remacemide hydrochloride (15 mg/kg) every 12 h beginning 30 minutes after SAH (group III); and 4 rabbits were not subjected to SAH but received IP bolus injections of remacemide hydrochloride every 12 h (group IV). Digital subtraction angiography was used to measure the diameter of the basilar artery. At 72 h post-SAH, vasospasm was evident in all untreated rabbits. The diameter of the basilar artery was reduced significantly below pre-SAH levels by 35.3 +/- 5.8% (mean +/- standard error of the mean). Treatment with remacemide hydrochloride significantly ameliorated vasospasm (27.3 +/- 5.4%, p < 0.001). These findings suggest that in this model EAAs may cooperate in the genesis of SAH-induced cerebral vasospasm and that NMDA receptor antagonism with remacemide hydrochloride can partially prevent the SAH-induced vasospasm of a large cerebral artery.

Acetamides↗
PubMed1993

Serotonin (5-HT) fibers of the rat dura mater: 5-HT-positive, but not authentic serotoninergic, tryptophan hydroxylase-like fibers.

Serotonin (5-HT)-positive, but not tryptophan-5-hydroxylase (TPOH)-positive, authentic serotoninergic fibers were shown in the rat dura mater. 5-HT immunoreactive fibers in the dura are postulated to result from 5-HT uptake from circulating blood elements (e.g. platelets, mast cells) by perivascular sympathetic nerve fibers. A robust TPOH-immunoreactive mast cell population was identified in the dura; this result confirms the TPOH antibody specificity to cells known to synthesize 5-HT. While these results indicate that there are no authentic serotoninergic fibers in the dura mater, the mast cells, platelets and cerebrospinal fluid can serve as a source of 5-HT activating 5-HT receptors known to be present in this tissue.

Animals↗
PubMed1993

Dural neuropeptide changes after subarachnoid hemorrhage in rats.

The effect of subarachnoid hemorrhage (SAH) on the neuropeptides and mast cells of the rat dura mater has not been reported. We examined the outcome of SAH on the rat supratentorial dura mater to determine whether dural nerves undergo effects similar to those of nerves accompanying cerebral blood vessels after SAH. Following the injection of fresh autologous arterial blood into the cisterna magna, animals were sacrificed at 6, 24, and 48 h, and 6 days post-SAH. Dural whole mounts were immunohistochemically reacted with antibodies to calcitonin gene-related peptide (CGRP), substance P (SP), neuropeptide Y (NPY), and serotonin (5-HT). SP-like immunostaining was substantially reduced after SAH and subsequently returned to control levels at 6 days. NPY-like fiber innervation of the dura was markedly reduced after SAH; although immunostaining intensity increased, it had not returned to control levels at 6 days. The 5-HT content of dural mast cells identified by immunostaining markedly decreased at 6 and 24 h and returned to control levels at 48 h. In contrast, CGRP immunostaining was unchanged in all experimental groups. One possible explanation for this differential response is that subpopulations of trigeminovascular neurons containing SP, CGRP, or CGRP and SP respond differently to various stimuli, including SAH. Another possibility is a differential release of SP or CGRP from the same fiber. To the best of our knowledge this is the first documentation that the dura is also a target for intracranial pathological processes, such as SAH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Interaction between free radicals and excitatory amino acids in the blood-brain barrier disruption after iron injury in the rat.

Excitatory amino acids and oxygen free radicals have been reported to cooperate in the genesis of brain injury in vivo and in vitro. In this study, we tested the capacity of a noncompetitive N-methyl-D-aspartate receptor antagonist, MK-801, and a 21-aminosteroid, U-74006F, tirilazad mesylate, to block the opening of the blood-brain barrier after subarachnoid injection of FeCl2, which is believed to cause a primarily "pure" free radical insult. Subarachnoid injection of FeCl2 resulted in a significant 10-fold increase in Evans blue extravasation while sham injection or NaCl injection had no effect. Pretreatment with either MK-801 or U-74006F significantly reduced the FeCl2-induced increase in capillary permeability by 43 and 63%, respectively (p < 0.05). Combined treatment with MK-801 and U-74006F resulted in a 65% reduction in vascular leakage that was not significantly greater than pretreatment with either drug alone. These results show that both excitatory amino acids and free radicals can damage the cerebral microvasculature and that an excitatory amino acid antagonist can partially protect the blood-brain barrier after free radical-induced injury.

Amino Acids↗
PubMed1993

Recovery of vision after transcranial decompression of pituitary apoplexy characterized by third ventricular hemorrhage.

The authors present a case of pituitary apoplexy characterized by massive third ventricular hemorrhage. This rare complication, which caused total blindness in the patient, a 67-year-old man, was treated with transcranial decompression of the pituitary tumor and removal of a blood clot from the third ventricle. After surgery, the patient totally recovered his vision. To the best of our knowledge, this is the first case of a patient with pituitary apoplexy that ruptured into the third ventricle (diagnosed by imaging studies) who was treated by emergency transcranial decompression.

Adenoma↗
PubMed1992

HCV infection in HBsAg positive chronic liver disease.

The prevalence of anti-HCV antibodies was determined for a group of 68 patients with various forms of chronic liver disease. All patients that were anti-HCV positive but did not show signs of HBV replication had severe liver disease. We therefore suggest that HCV may be responsible for liver damage in HBsAg positive subjects when there are no evident signs of HBV replication.

Chronic Disease↗
PubMed1992

Postoperative venous thromboembolism and brain tumors: Part I. Clinical profile.

Forty-six patients who underwent surgery for brain tumors were studied prospectively with 125I labeled Fibrinogen leg scans to detect postoperative venous thrombosis. The incidence of thrombosis was 72% for meningioma patients, 60% for glioblastoma patients, and 20% for brain metastasis patients. Correlation between the occurrence of venous thrombosis and the various clinical factors thought to be responsible for the high incidence of thrombosis generally failed to show statistical significance. This finding, along with the marked variation in the incidence of venous thrombosis between the different brain tumor groups, strongly suggests that biological factors play a more important role than clinical factors in determining which brain tumor patient will suffer a postoperative thrombotic event.

Brain Neoplasms↗
PubMed1991

Influence of the sympathetic nervous system as well as trigeminal sensory fibres on rat dural mast cells.

The dura mater has attracted considerable attention as an exquisitely sensitive tissue implicated as playing a role in various cephalalgias including vascular headache. Because of the potential clinical impact of the relationship/interaction of neural elements and mast cells the influence of sensory and autonomic nerve fibres on mast cells of the rat dura mater was studied. The trigeminal or superior cervical ganglion was electrically stimulated and the mast cells were examined. Wholemount supratentorial dural preparations were stained using berberine sulphate and the number of mast cells with intact vs dispersed granules counted. Unilateral stimulation of either ganglia resulted in a statistically significant increase in the percentage of mast cells with dispersed granules ipsilateral to the side of stimulation. These results support our idea that in addition to the trigeminal system the sympathetic nervous system must be considered as playing a role in the oedema pathophysiology of vascular headache.

Animals↗
PubMed1991

Brain stem abscess treated successfully by medical therapy.

A case of a solitary brain stem abscess in a 55-year-old man is presented. The computed tomographic scan and clinical picture allowed the presumptive diagnosis to be made. The abscess resolved completely after treatment with chloramphenicol, vancomycin, and ceftazidime administered intravenously. Medical therapy should be considered as an effective treatment of a brain stem abscess, provided the antibiotic therapy is administered under close clinical and computed tomographic monitoring.

Brain Abscess↗