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Biomedical subjects

M Zuccarello

Publications and source records attributed to M Zuccarello.

At least 19 recordsLinked to original sources
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

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

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↗
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↗
PubMed1990

Effect of experimental subarachnoid hemorrhage on CSF eicosanoids in the rat.

A simple and inexpensive experimental model of subarachnoid hemorrhage (SAH) was developed in the rat. Based on accumulating data indicating the important role of arachidonic acid metabolites in the etiology of delayed cerebral vasospasm, we investigated changes induced by SAH on cerebrospinal fluid (CSF) levels of prostaglandin E2 (PGE2), F2 alpha (PGF2 alpha), and thromboxane B2 (TXB2). SAH was produced by the cisternal injection of blood via percutaneous suboccipital puncture. SAH rats (n = 200) were injected with 300 microliters of fresh autologous arterial blood; Control rats (n = 100) received the same volume of mock CSF. In 60 additional animals, no injections were made. To follow the changes induced by SAH on both the spectrum and time course of CSF eicosanoids, cisternal CSF samples were collected under basal conditions, 6, 12, and 36 after cisternal injection. PGE2, PGF2 alpha, and TXB2 were assayed in aliquots of CSF obtained by pooling samples from each experimental group. Eicosanoids were assayed using radioimmunoassay techniques. Arterial spasm was verified in parallel groups of SAH and control rats by comparison of the angiographic diameters of the basilar arteries (BA) and middle cerebral arteries (MCA) to that of the stapedial artery. CSF levels of all three eicosanoids were significantly higher in the SAH groups compared to both noninjected and mock-CSF injected control rats. These increases in concentrations of eicosanoids were accompanied by a decrease in the mean vascular diameter (77.5-82.0% of control) on day 2 following cisternal injection. We conclude that marked elevations of spasmogenic eicosanoids in the CSF are associated with experimental SAH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Protective effect of a 21-aminosteroid on the blood-brain barrier following subarachnoid hemorrhage in rats.

The effects of subarachnoid injection of blood on blood-brain barrier permeability to albumin was assessed in a rat model. Subarachnoid injection of blood caused a significant sixfold increase in Evans blue extravasation, whereas sham operation or NaCl injection had no effect. In addition, subarachnoid injections of arachidonic acid or FeCl2 increased blood-brain barrier permeability to Evans blue 16- and 10-fold, respectively. The capillary permeability after subarachnoid injection of blood was normalized by pretreatment with a novel 21-aminosteroid, U-74006F, that has antioxidant and antilipolytic activity. Pretreatment with U-74006F also reduced the vascular leakage induced by subarachnoid injection of arachidonic acid or FeCl2 by 50% and 45%, respectively. We conclude that damage to membrane lipids by peroxidative and/or lipolytic processes is involved in the subarachnoid hemorrhage-induced blood-brain barrier opening and that U-74006F protects the blood-brain barrier against the effects of subarachnoid hemorrhage by preventing or limiting these pathologic membrane lipid changes.

Animals↗
PubMed1989

Acute effect of the Nd:YAG laser on the cerebral arteriovenous malformation: a histological study.

The acute effect of Nd:YAG laser beam on cerebral arteriovenous malformations (AVMs) was examined. Histological examination of the specimens after treatment with the Nd:YAG laser revealed that the most prominent effect of the laser was shrinkage of the collagen of the vessels of the AVM, which led to laser-induced narrowing of blood vessels. The brain tissue confined to the resected AVM did not contain any histological evidence of acute damage. The resection of 10 cases of AVMs was safely accomplished with no morbidity or increased neurological deficits attributable to the laser technique.

Adolescent↗
PubMed1989

Effect of the 21-aminosteroid U-74006F on cerebral vasospasm following subarachnoid hemorrhage.

The purpose of this study was to use a new 21-aminosteroid (U-74006F) with in vitro antioxidant and antilipolytic properties as a pharmacological probe to assess the role of lipid hydrolysis and peroxidation in a rabbit model of subarachnoid hemorrhage (SAH)-induced vasospasm. Cerebral angiograms were performed on 15 rabbits. Eighteen hours later, 1 cc/kg of autologous blood was infused into the cisterna magna of all 15 animals. Six rabbits received no treatment, six received U-74006F starting 30 minutes after SAH, and three rabbits received the vehicle for U-74006F starting 30 minutes after SAH. At 72 hours post-SAH, a second angiogram was obtained. Digital subtraction angiographic techniques were used to measure the diameter of and contrast material flow through the basilar artery. At 72 hours post-SAH, vasospasm was evident in all untreated and vehicle-treated rabbits. The diameter of and the flow through the basilar artery were significantly reduced 42.3% +/- 6.6% and 46.8% +/- 5.8%, respectively, below pre-SAH levels (means +/- standard error of the means). Treatment with U-74006F eliminated the SAH-induced vasospasm; in treated animals, both the flow through and the diameter of the basilar arteries were at pre-SAH levels. These findings indicate that: 1) membrane lipid changes (that is, hydrolysis with eicosanoid production and/or peroxidation) contribute to the chronic vasospasm resulting from SAH, and 2) U-74006F prevents the SAH-induced chronic vasospasm in this model by limiting these pathological membrane events.

Animals↗
PubMed1988

Effect of intracisternal thromboxane A2 analogue on cerebral artery permeability.

Thromboxane, a highly vasoactive substance, is found in the cerebrospinal fluid of patients and experimental animals following subarachnoid haemorrhage. A stable synthetic analogue of thromboxane A2 was administered intracisternally in rabbits. This resulted in an increase in endothelial permeability of the major cerebral arteries to Evans Blue dye and horseradish peroxidase. Thromboxane may be involved in the pathogenesis of cerebral vasospasm and may be related to the contrast enhancement of the arteries in the basal cisterns on CT scans of patients who are prone to develop arterial narrowing.

Animals↗
PubMed1988

Morbidity and mortality of carotid endarterectomy under local anesthesia: a retrospective study.

It has been shown that carotid endarterectomy reduces the incidence of stroke in patients with symptomatic extracranial occlusive vascular disease in the absence of major perioperative complications such as stroke or death. We present a retrospective study of 106 carotid endarterectomies performed under local anesthesia in 100 patients in whom transient ischemic attack (TIA) or minor stroke had occurred. Nonfatal stroke occurred in 2%, and TIA occurred in 1%. There was no perioperative mortality. Our study suggests that, under local anesthesia, even high risk patients can be operated safely and the majority of carotid endarterectomies can be performed without the use of an indwelling shunt. Meticulous surgical technique is of great importance for achieving low perioperative complications.

Adult↗
PubMed1987

Immunohistochemical demonstration of alpha-1-proteinase inhibitor in brain tumors.

Using light microscopy and immunoperoxidase methods (PAP), the presence of alpha-1-proteinase inhibitor (API) was studied in seventeen brain tumors and four normal brain samples. The brain tumors included four glioblastomas, five low-grade gliomas, two metastatic lung carcinomas, two acoustic schwannomas, and four meningiomas. Normal brain displayed a finely granular intracytoplasmic staining confined to neuronal cells. Glial cells were negative for API. Fifteen of the 17 brain tumors were positive for API. Only two of five low-grade gliomas were negative for API. Glioblastoma and metastatic tumors exhibited the strongest positivity followed by acoustic neuroma, meningioma, and low-grade glioma. All positive samples exhibited finely granular intracytoplasmic API, and 50% exhibited extracellular API positivity. Metastatic and glioblastoma tumors demonstrated prominent extracellular API staining. Our results support the concept of a local production of API by brain tumors.

Blood Proteins↗
PubMed1987

Barrier disruption in the major cerebral arteries after experimental subarachnoid hemorrhage in spontaneously hypertensive and normotensive rats.

The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the major cerebral arteries were studied in 24 spontaneously hypertensive rats (SHR) and 13 Sprague-Dawley rats (SDR). Horseradish peroxidase (HRP) was given intravenously before killing the animals to assess the integrity of the barrier. In the acute experimental group, transient elevation of intracranial pressure (ICP) and systemic arterial pressure produced by cisternal injection of whole blood, saline solution, or Elliott's B solution resulted in extensive disturbance of the blood-arterial wall barrier. In the chronic group, only the cisternal injection of whole blood in SHR brought about an extensive and marked disturbance of the arterial permeability. These results suggest that: (a) early breakdown of the blood-arterial wall barrier seems to be due to a sudden rise in the ICP or arterial pressure; (b) in the chronic experiments, the subarachnoid clot is the most important factor responsible for the permeability changes; and (c) in the chronic SAH experiments, the blood-arterial wall barrier seems to be more vulnerable in SHR than in Sprague-Dawley rats. Due to the well-known similarities between SHRs and hypertensive human beings, patients with chronic hypertension should be considered at high risk after SAH for extensive blood-arterial wall barrier disturbances.

Animals↗
PubMed1987

Alpha-1-antitrypsin in human brain tumors.

This study was undertaken to confirm the presence of alpha-1-antitrypsin (alpha 1-AT) in human brain tumors and to attempt to elucidate its significance. Seventy-seven consecutive unselected patients with various brain tumors were entered in this study. The alpha 1-AT and alpha 2-macroglobulin contents of the tumor extracts were qualitatively assessed by Ouchterlony immunodiffusion techniques. Plasminogen activator (PA) activity was assayed electrophoretically on sodium dodecyl sulfate gels. The patients were were divided into two groups according to the positivity of their tumors to alpha 1-AT. Sixty-eight percent of the tumors were positive for alpha 1-AT, and all specimens were negative for alpha 2-macroglobulin. Clinical and biological parameters obtained in all study patients failed to show statistically significant differences between the two groups with the exception of PA activity (p = 0.001), the peritumoral edema as seen on computerized tomography, and the preoperative serum fibrinogen level. These three parameters were higher in the group with specimens positive to alpha 1-AT. This study supports the hypothesis that alpha 1-AT is produced primarily by tumor cells in proportion to the regional proteolytic and inflammatory activity, and may protect the tumor cells.

Brain Neoplasms↗