Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates.

The authors sought to develop a model for assessing in vivo regulation of cerebral vasoregulation by nitric oxide (NO), originally described as endothelial-derived relaxing factor, and to use this model to establish the role of NO in the regulation of cerebral blood flow (CBF) in primates. By using regional intraarterial perfusion, the function of NO in cerebral vasoregulation was examined without producing confounding systemic physiological effects. Issues examined were: whether resting vasomotor tone requires NO; whether NO mediates vasodilation during chemoregulation and autoregulation of CBF; and whether there is a relationship between the degree of hypercapnia and hypotension and NO production.

Transcranial Doppler ultrasound assessment of intracranial hemodynamics in children with diabetic ketoacidosis.

The pathophysiology of acute neurological complications of diabetic ketoacidosis (DKA) in children and adolescents is not completely understood. We sought to establish whether transcranial Doppler (TCD) was able to monitor the changes of cerebral blood flow regulatory mechanisms, as measured by cerebral blood velocities (CBF-V), Gosling's pulsatility index (PI), and cerebral vascular reactivity (VR), prior to and during treatment of DKA. The increased values of PI suggested an increase of intracranial pressure (ICP) due to the existence of cerebral vasoparalysis, based on the low values of VR prior to treatment and 6 hours after initiation of treatment.

Intercellular adhesion molecule-1 (ICAM-1) upregulation in human brain tumors as an expression of increased blood-brain barrier permeability.

The distribution of intercellular adhesion molecule (ICAM-1) binding sites was studied in the microvasculature of several types of human brain tumor biopsies (angioma, glioblastoma multiforme and meningioma). Immunoelectron microscopy was performed with the application of immuno-HRP or -gold probes using a pre-embedding technique. Ultrastructural analysis demonstrated a pronounced ICAM-1 upregulation on the luminal EC and/or perivascular surfaces.

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage.

The continuous release of nitric oxide (NO) is required to maintain basal cerebrovascular tone. Oxyhemoglobin, a putative spasmogen, rapidly binds NO, implicating loss of NO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). If vasospasm is mediated by depletion of NO in the vessel wall, it should be reversible by replacement with NO.

Complete cerebral ischemia with short-term survival in rat induced by cardiac arrest. II. Extracellular and intracellular accumulation of apolipoproteins E and J in the brain.

The distribution of apolipoprotein E (apo E) and apolipoprotein J (apo J) was investigated immunocytochemically in rats at various time intervals after 10 min global cerebral ischemia (GCI) induced by cardiac arrest. Strong apo E and weaker apo J immunoreactivity was found extracellularly in multiple deposits located close to the microvessels. These deposits appeared 3 h after GCI and were present, but not in all the animals, at all time intervals studied post-GCL.

Ultrastructural studies of cerebral vascular spasm after cardiac arrest-related global cerebral ischemia in rats.

The present investigation was undertaken to study the ultrastructural morphology of brain blood vessels during vasospasm following total cerebral ischemia. Global cerebral ischemia was produced in rats by compression of the cardiac vessel bundle (i.e.

Complete cerebral ischemia with short-term survival in rats induced by cardiac arrest. I. Extracellular accumulation of Alzheimer's beta-amyloid protein precursor in the brain.

The distribution of beta-amyloid protein precursor (APP) was investigated immunocytochemically in rats subjected to global cerebral ischemia (GCI) induced by cardiac arrest. Rats underwent 10 min of GCI with 3, 6, and 12 h and 2 and 7 days of survival. APP immunostaining was found extracellular and intracellularly.

Long-term effects of radiation therapy for a catecholamine-producing glomus jugulare tumor. Case report.

A 42-year-old woman presented with otorrhea 22 years after extracranial resection of a norepinephrine-secreting glomus jugulare tumor with intravascular embolization and radiation therapy to the intracranial portion of the tumor. Tumor growth was arrested and was associated with a decrease in blood and urine norepinephrine levels. Extensive evaluation of the otorrhea, including computerized tomography-cisternography, gadolinium-enhanced magnetic resonance imaging, and arteriography showed marked diffuse necrosis of the temporal bone and skull base with limited tumor vascularity.

Early blood-brain barrier changes in the rat following transient complete cerebral ischemia induced by cardiac arrest.

This study examined regional patterns of increased vascular permeability following transient global cerebral ischemia. Rats underwent 3.5, 5 or 10 min of cardiac vessel bundle occlusion, i.

Complete cerebral ischemia, prostacyclin deficiency, and therapeutic possibilities.

This report summarizes the results of our studies on the effects of prostacyclin (PGI2) on the outcome of global cerebral ischemia (GCI). GCI was produced for 15 and 20 min. In vivo dialysis of the hippocampus was used to determine the changes in extracellular concentrations of calcium (Ca/2e) and blood-brain barrier (BBB) permeability.

Abnormalities of the blood-brain barrier in global cerebral ischemia in rats due to experimental cardiac arrest.

The aim of the study was to characterize the impact of global cerebral ischemia resulting from cardiac arrest on the BBB permeability. Survival time of experimental animals after 3.5, 5 or 10 min ischemia range from 3.

Platelet occlusion phenomenon after short- and long-term survival following complete cerebral ischemia in rats produced by cardiac arrest.

Platelet interaction with cerebral microvessels was studied in rats after global brain ischemia. Studies were performed with a model of global central nervous system ischemia produced by cardiocirculatory arrest in normothermic rats. The ischemic period of 5-min was followed by times of recirculation lasting 5 and 15 mins, 1, 3, 6, 24, and 48 hrs, and 6, 10, and 12 months.

Thrombin is a regulator of astrocytic endothelin-1.

Endothelin-1, a potent vasoconstrictor of cerebral vessels, is produced by rat primary astrocytes and is subject to autostimulatory regulation in these cells. In this study we examined the effect of thrombin on astrocytic endothelins and report that endothelin-1 is released into the culture fluid in response to thrombin treatment. However, increased production of endothelin-1 is not accompanied by a concomitant increase in steady-state levels of endothelin-1 mRNA as assessed by reverse transcriptase-polymerase chain reaction, even though thrombin stimulation leads to increased inositolphospholipid turnover and activation of the nuclear factor AP1.

Local nimodipine application improves early functional recovery in the rabbit hippocampus after 15-min global cerebral ischemia.

Microdialysis was used to apply 10 microM nimodipine to the hippocampus of rabbits submitted to 15-min global cerebral ischemia. Analysis of dialysate allowed determination of changes in extracellular fluid concentrations of calcium (Ca2+e) and amino acids and in blood-brain barrier (BBB) permeability to fluorescein. General physiological parameters and EEG were recorded throughout the experiments, and morphological changes in the hippocampus 3 h following ischemia were evaluated.

Is vasospasm related to proliferative arteriopathy?

Although proliferative arteriopathy has been postulated to play a role in the etiology of vasospasm after subarachnoid hemorrhage (SAH), histological and morphological studies examining cerebral vasospasm have produced conflicting results. To help settle this controversy, the authors used an in vivo label of cell division, bromodeoxycytidine, to assess cell proliferation in a primate model of SAH. Fifteen cynomolgus monkeys received a clot of either whole blood (11 animals) or red blood cells (four animals) placed around the right middle cerebral artery (MCA).

Neuropeptide Y in the primate model of subarachnoid hemorrhage.

The cause of cerebral vasospasm after subarachnoid hemorrhage (SAH) remains unknown. Recently, an association between the potent vasoconstricting peptide, neuropeptide Y, and delayed cerebral vasospasm after SAH has been postulated. This was based on the findings of increased neuropeptide Y levels in the cerebrospinal fluid (CSF) and plasma after SAH in animals and humans.

The effect of some exogenous factors on the formation of intranuclear membranaceus inclusions in the nerve cells.

The intranuclear membranaceus inclusions (IMI) appear as encapsulated irregular vacuoles surrounded by a single, rarely double, membrane. The vacuoles include floccular, fine granular content or they are translucent. They were found in neurones of particularly old or very young laboratory animals.

Prostacyclin attenuates in the rabbit hippocampus early consequences of transient complete cerebral ischemia.

The effects of prostacyclin (PGI2) on ischemic changes of extracellular calcium concentration (CaE+2) and the blood-brain barrier (BBB) permeability were studied by microdialysis of the rabbit hippocampus. This was combined with morphological and neurophysiological observations. Complete cerebral ischemia lasting 15 min was produced by ligation of the brachiocephalic trunk, the left subclavian and both internal thoracic arteries.

Mechanisms of inflammatory cell attachment in chronic relapsing experimental allergic encephalomyelitis: a scanning and high-voltage electron microscopic study of the injured mouse blood-brain barrier.

Brain and spinal cord blood vessels from mice subjected to chronic relapsing experimental allergic encephalomyelitis were examined by scanning (SEM) and high-voltage electron microscopy (HVEM). SEM analysis of veins and venules from affected tissue regions demonstrated inflammatory cells (ICs), primarily lymphocytes or monocytes, attached to the luminal endothelial cell (EC) surface adjacent to the junctional complexes. In transverse section these cells were shown by HVEM to extend and to insert filopodia (lymphocytes) or flap-like lamellapodia (monocytes) into the luminal EC surfaces.

Blockade of N-methyl-D-aspartate-sensitive excitatory amino acid receptors with 2-amino-5-phosphonovalerate reduces ischemia-evoked calcium redistribution in rabbit hippocampus.

To evaluate the participation of excitatory amino acid receptors sensitive to N-methyl-D-aspartate (NMDA) in ischemia-evoked redistribution of Ca2+ ions from the extra- to the intracellular compartment of the hippocampus, 2-amino-5-phosphonovalerate (APV), a specific antagonist of NMDA receptors, was administered to the rabbit hippocampus through a dialysis probe before, during, and after complete reversible 15-min cerebral ischemia. Microdialysis of the hippocampus allowed us to determine the changes in extracellular calcium and amino acid concentrations and to monitor the permeability of the blood-brain barrier (BBB) to fluorescein. Moreover, EEG and general physiological parameters were registered.

Reassessment of a new model of complete cerebral ischemia in rats. Method of induction of clinical death, pathophysiology and cerebrovascular pathology.

The present study was undertaken to ascertain the role of the microcirculation in the phenomenon of hypoperfusion following complete cerebral ischemia. The experiments were performed on rats under superficial ether anesthesia. Cerebral ischemia was induced by cardiac arrest for 3.

The effects of prostacyclin on early ultrastructural changes in the cytoplasm and nuclei of neuroglial cells following complete cerebral ischemia.

Twelve rabbits were submitted to 20-min global cerebral ischemia. Half of them were treated continuously with prostacyclin (PGI2) for 3 min before and during ischemia, and for 15 min after it. Untreated animals were not given PGI2 medication.

Diverse mechanisms of neuronal protection by nimodipine in experimental rabbit brain ischemia.

The purpose of this study was to verify the possible involvement of nimodipine-sensitive calcium channels in ischemic Ca2+ influx to hippocampal neurons to assess their role in nimodipine neuroprotection. We induced 15-minute global cerebral ischemia in pentobarbital-anesthetized and relaxed rabbits, which had been implanted with a transhippocampal dialysis probe, by intrathoracic artery occlusion combined with hypotension. A part from electroencephalographic and morphologic observations, changes in the extracellular concentrations of calcium, amino acids, and blood-brain barrier permeability to fluorescein were detected by microdialysis of the hippocampus.

Recovery of breathing pattern after 15 min of cerebral ischemia in rabbits.

The study was undertaken to ascertain the neural control of breathing and vagal reflexes during and after cerebral ischemia. The experiments were performed on anesthetized, paralyzed, and artificially ventilated rabbits. Cerebral ischemia was induced by reversible intrathoracic occlusion of the brachiocephalic trunk and the left subclavian and both internal thoracic arteries for 15 min.

Combined conventional transmission, scanning, and high-voltage electron microscopy of the same blood vessel for the study of targeted inflammatory cells in blood-brain barrier inflammation.

The microvasculature of brains and spinal cords from mice subjected to chronic relapsing experimental autoimmune encephalomyelitis (CREAE) was studied using three different electron microscopic techniques. Blood vessels were initially examined by scanning electron microscopy. This allowed for the investigation of topographical changes of the luminal aspects of endothelial cells (ECs) and identification of targeted inflammatory cells (ICs) attached to the ECs.