Studies on stimulation and properties of antiglobulin antibodies. II. Antiglobulin antibodies against homologous globulins and antigens of thermally denatured autologous sera in the sera of rabbits immunized with various antigens.

Sera of 48 rabbits after long-term immunization with suspensions of Diplococcus pneumoniae, Klebsiella friedländeri, Proteus OX19 and solution of bovine albumin were examined for antibodies reacting with homologous gamma-globulins and antigens of thermally denatured autologous sera. Appearance of antibodies of this type was related to duration of immunization, but not related to the type of antigen used. The experimental results were explained as a result of altered antigenic properties of antibodies following reaction with homologous antigen.

Studies on stimulation and properties of antiglobulin antibodies. I. Influence of heatig at 56 degrees C and 60 degrees C on antigenicity.

The autoimmunogenic properties of whole rabbit serum heated at 56 degrees C and 60 degrees C were studied in rabbits. Autologous rabbit serum heated 20 min at 60 degrees C was immunogenic. The state of induced immunity manifested itself by the appearance of antibodies to antigens of heterologous sera: human, goat and guinea pig. No antibodies for autologous sera were found, including autologous sera heated 20 min at 60 degrees C. The antibodies for heterologous sera directed against gamma-globulins were detected by the passive hemagglutination test and by precipitation in agar gel.

Studies on stimulation and properties of antiglobulin antibodies. III. Antiglobulin antibodies with different specificity in patients with bronchial asthma complicated by suppurative catarrh of the respiratory tract.

Sera from 14 of 50 patients suffering from bronchial asthma complicated by suppurative catarrh of the respiratory tract contained antibodies to homologous and heterologous gamma-globulins. The findings were attributed to hyperimmunization causing changed in antigenic properties of antibodies. Antigenically altered antibodies can act as autoimmunogenic stimuli inducing an immune response manifested by the appearance of antibodies to autologous gamma-globulins and cross reacting with homologous and heterologous gamma-globulins.

Atrial natriuretic peptide secretion following subarachnoid hemorrhage in spontaneously hypertensive rats.

Atrial natriuretic peptide (ANP) is released excessively in spontaneously hypertensive rats (SHR), and vasodepression is its main effect on the blood vessels. The aim of the study was to investigate the changes in ANP secretion in the cerebral vasospasm following subarachnoid hemorrhage (SAH) in SHRs. The SAH was induced by the injection of 100 microliters of unheparinized, autologous blood into the cerebrospinal fluid (CSF), via a canule formerly inserted into the cisterna magna (CM). In the sham SAH group the SAH was imitated with 0.9% saline injection. The concentrations of ANP in the blood samples obtained in the acute and chronic stages of vasospasm were radioimmunoassayed with commercial RIA kits (Peninsula RIK 9103). It was found that both SAH and sham SAH induced a significant increase in plasma ANP in the chronic phase of vasospasm. No such changes were observed in the acute phase. This shows that the chronic cerebral vasospasm following SAH considerably enhances the ANP secretion in SHRs, probably through the increased endothelin release. These compensatory and regulatory mechanisms help prevent the development of brain oedema and the progression of vasopasm through secondary vasodilation.

Influence endothelin ETA receptor antagonist--BQ-123--on changes of endothelin-1 level in plasma of rats with acute vasospasm following subarachnoid hemorrhage.

Endothelin participates in regulating the vascular tone, and it is also involved in the pathogenesis of vasospasm following subarachnoid hemorrhage (SAH). Endothelin-1 (ET-1) induced cerebral vasospasm is inhibited by ETA receptors specific antagonist-BQ-123; this protects the neurons from ischemic damage. The present study evaluates the dynamics of ET-1 concentration changes in the plasma of rats in the acute phase of vasospasm after SAH, which was induced by administering 100 microliters non-heparinized fresh autologous arterial blood into the brain cisterna magna (CM). The study also assesses the effect of blocking ETA receptors on the changes in ET-1 level. BQ-123, the specific ETA receptors antagonist, was administered to cerebrospinal fluid (CSF) through a cannula inserted into CM; the antagonist--40 nmol in 50 microliters CSF--was given 20 minutes prior to SAH. In the control group, sham SAH was induced by administering 100 microliters artificial CSF (aCSF) to CM. ET-1 concentration in the plasma of rats in the acute phase of vasospasm was assessed by radioimmunoassay 30 and 60 minutes after SAH or sham SAH. It has been showed that both SAH and sham SAH cause significant increase in the ET-1 concentration (p < 0.05) in the rat plasma after 30 minutes; the concentration returns to an initial value after following 30 minutes, which may suggest that ET-1 released binds to its receptors in the acute phase of the vasospasm. On the other hand, in the two groups of rats with blocked ETA receptors there was a significant rise in ET-1 concentration 30 minutes after SAH or sham SAH, and a still further rise was observed 60 minutes after the procedure. The rise was significantly higher in animals with SAH (p < 0.05). The dynamics of the ET-1 concentration changes observed in rats with blocked ETA receptor suggests that SAH is an ET-1 production stimulator significantly more potent than other factors assessed in the study, such as a rise in the intracranial pressure resulting from administering aCSF to CM. Blocking ETA receptors makes it impossible for the ET-1 released to bind to the receptors, which may be a factor preventing the occurrence of cerebral vasospasm following SAH.

Effect of endothelin-1 receptor antagonist BQ-123 on basilar artery diameter after subarachnoid hemorrhage (SAH) in rats.

Aim of the study was to quantify cerebral vasospasm in rats after subarachnoid hemorrhage (SAH) by morphometric examination of basilar artery and to evaluate the influence of endothelin receptor blocker BQ-123 on basilar artery constriction. The rat cisterna magna (CM) was cannulated and after 7 days SAH was developed by administration of 100 microl autologic, non-heparinized blood to the CM. The sham subarachnoid hemorrhage was developed by intracisternal administration of 100 microl of artificial cerebrospinal fluid. Endothelin receptor blocker BQ-123 was injected into the CM in a dose of 40 nmol diluted in 50 microl of cerebrospinal fluid 20 min. before SAH, and 24h and 48 h after SAH. After perfusion fixation the brains were removed from the skull and histological preparations of basilar artery were done. The internal diameter and wall thickness of basilar arteries was measured by interactive morphometric method. The most severe vasospasm was found in rats after SAH. The presence of numerous infiltrations composed of neutrophils and macrophages correlated with advanced vasospasm (index of constriction 5 times lower than in normal), suggesting the role of other factors participating in the late phase of vasospasms after SAH. Administration of BQ-123 in the late phase after SAH caused the dilatation of basilar artery. Following the administration of BQ-123 in the late phase (48 h after SAH) the basilar artery dilated, its wall became thinner, and the number of leukocyte infiltrations in the subarachnoid space decreased compared to the values after SAH alone.

Influence of the corticotropin releasing hormone (CRH) on the brain-blood barrier permeability in cerebral ischemia in rats.

The increase in the blood-brain barrier (BBB) permeability and a developing cerebral oedema due to the ischemic infarction appear a few hours, and intensify during a few days, after closing the carotid arteries. It fails to be clear, however, what causes the increase in the microvessels damage, and whether the damage is a secondary result of the vasoactive substances released by the neurones and glia cells damaged by the ischemia. CRH, which plays an essential role in integrative the nervous, endocrine, and immunological systems, has a positive effect on the decrease in the permeability of the BBB damaged by various physical and chemical factors. Therefore, the examination of the CRH role in the cerebral ischemia may prove useful for explaining the processes taking place in the foci of the cerebral infarction and their environment. The experiment was carried out on rats which, 20 minutes before closing of both internal carotid arteries, was administered 10 microg CRH to cerebrospinal fluid via cisterna magna of the brain. The BBB permeability was measured 30 minutes, 3 hours, 3 days, and 7 days after closing the arteries. The experiment has shown the CRH protective effect on the BBB and its consequent effect on the decrease in the BBB permeability which appears in the 3 hours after closing the arteries (p<0.05), and is high significant during the chronic phase of the cerebral ischemia (p<0.03). It can be thus concluded that CRH, by affecting directly the endothelium of the cerebral vessels, decreases the endothelial damage in the acute phase of the ischemia. The decrease is noted to be more significant in the chronic phase of the ischemia; such an effect can be attributed to CRH stimulating the hypothalamic-adrenal axis, and to the secondary activation of the mechanisms decreasing the BBB permeability.

Cerebral angiogenesis after subarachnoid hemorrhage (SAH) and endothelin receptor blockage with BQ-123 antagonist in rats.

The aim of the study was to determine the effect of chronic vasospasm after SAH on angiogenesis and the effect of endothelin-1, the main causative factor in vasospasm, on this process. Male Wistar rats, 220-250 g, were examined. Seven days after cannulation of the cisterna magna (CM), a 100 microl dose of non-heparinized blood was administered to induce SAH. Sham SAH (aSAH) was induced by intracisternal injection of 100 microl of artificial cerebrospinal fluid. Endothelin receptor antagonist BQ-123 in a dose of 40 nmol in 50 microl of cerebrospinal fluid was given three times: 20 min. before SAH and aSAH, 60 min and 24 hours after SAH and aSAH. The same pattern of BQ-123 administration was used in the nonSAH group. The brains were removed 48 hours later for histological evaluation. Vascular surface density was measured in cerebral hemisphere sections (at the level of the dorsal part of the hippocampus) and brain stem sections (1/2 of the pons). An increase in angiogenesis was observed after SAH, compared to control values. The administration of BQ-123, a specific endothelin receptor blocker inhibits angiogenesis in cerebral hemispheres after SAH.

Expression of vascular endothelial growth factor (VEGF) in rat brain after subarachnoid haemorrhage and endothelin receptor blockage with BQ-123.

Cerebral vasospasm is one of the most severe complications of subarachnoid haemorrhage (SAH), leading to pathological changes in the vessel wall itself and in the nervous tissue, due to ischaemia of endothelial cells and neurones. Amongst the known substances inducing vasospasm, the most potent spasmogenic effect is exerted by endothelin-1 (ET1). The constriction of cerebral arteries and obliteration of capillaries highly stimulates the secretion of growth factors by endothelial cells and induces compensatory formation of collateral circulation in response to brain ischaemia. Expression of vascular endothelial growth factor (VEGF), the main factor responsible for angiogenesis and vascular permeability, was found to be increased in hypoxic cells (irrespective of the cause of hypoxia) as well as in neoplastic cells in the brain. The aim of the study was to determine whether chronic vasospasm and hypoxia of endothelial cells stimulate expression of VEGF, and whether blockage of the endothelin receptor ET(A) reduces this expression. The SAH was induced experimentally in male Wistar rats and the ET(A) receptor antagonist--BQ-123 was administered into the cisterna magna. After 48 hours the brain was removed and expression of VEGF studied immunohistochemically on paraffin sections. We found that hypoxia of endothelial cells, induced by chronic vasospasm after SAH, caused increased expression of VEGF in brain vessels and neurones of the cerebral hemispheres, brain stem and cerebellum. After administration of the endothelin receptor antagonist BQ-123, no changes in VEGF expression in the brain were found.

[Multiple spinal meningeal cysts in the thoracic region associated with lymphedema of the legs (Milroy's disease)]. / Mnogie torbiele nadoponowe w odcinku piersiowym kregoslupa wspólistniejace z zespolem obrzeku limfatycznego konczyn dolnych (choroba Milroya).

Intraspinal extradural meningeal cysts are uncommon cause of spinal compression. Either the classification or the etiopathology of these changes are indistinct in the literature. A rare case of multiple extradural meningeal cysts associated with lymphedema of the legs is presented. The total surgical removal was followed by the quick neurological improvement. Some etiological, diagnostic and therapeutic aspects of these pathologies have been discussed.

[Cerebral ischemia in young patients]. / Zespól niedokrwienny mózgu u ludzi mlodych.

The clinical, angiographic and computed tomography (CT) examinations of 19 patients aged from 12 to 30 years with signs of ischaemic brain syndrome are presented. On the basis of these examinations and data obtained from literature it is supposed that in a majority of patients the disease is caused by basal arteriopathies + i.e. pathological changes in the wall of cerebral arteries, mainly of the circulus Willis. The features distinguishing this syndrome from ischaemic disease in adults are presented and discussed. These are first of all: sudden onset connected with physical effort, deep neurological deficit, narrowing or occlusion of basal cerebral arteries seen in angiography and signs of ischaemia within deep cerebral structures visible in CT. The methods of treatment are discussed, mainly STA-MCA anastomosis used in most cases. The results of treatment are discussed. Finally the problem of the cerebral ischaemic syndrome in young people is presented from the point of view of haemodynamics, principally in the aspect of haemodynamic reserve of cerebral blood flow.

[Visual system function in patients after surgery for intracranial tumors]. / Ocena stanu funkcjonalnego narzadu wzroku u pacjentów po przebytych operacjach guzów wewnatrzczaszkowych.

UNLABELLED: Visual function was studied in patients after operations for brain tumours. The study group comprised 7 cases. Visual acuity, field of vision by kinetic and static methods and visual evoked potentials were studied before and after operations. The follow up time was from 1 to 51 months, mean 20 months. In all patients decreased visual acuity, visual field defects and VEP abnormalities were found, before operation. The first control examination after operation showed improvement of visual acuity in 2 cases after removal of pituitary tumours, and worsening of vision in all the remaining ones. In two cases of tumours spreading to the basis of the frontal lobe blindness of one eye developed. Static and kinetic perimetry showed in all cases enlarged visual field defects. VEP confirmed that removal of pituitary tumours compressing visual tract can improve vision: P100 amplitudes increased and latencies become shorter. Further VEP improvement occurred even 6-20 months after achieving of good visual acuity. No improvement of vision developed if the visual pathway had been damaged during the operation. CONCLUSIONS: Pituitary tumours can be removed without damage to the surrounding structures and vision can improve after that. Meningiomas and gliomas lying in immediate vicinity of optic nerves and their chiasma or growing out from them are usually large and often their removal is associated with damage to the visual pathway leading to visual field defects to blindness. The assessment of vision should be based on static and kinetic perimetry and visual evoked potentials (VEP) since these methods are mutually complementary and only their comparison provides a full result.

[Giant osteoma of the paranasal sinuses passing into the anterior cranial fossa]. / Olbrzymi kostniak zatok przynosowych penetrujacy do przedniego dolu czaszkowego.

A case of giant osteoma of paranasal sinus passing into anterior cranial fossa was presented. The frontal craniotomy in order to removing this tumor was applied. In any case of such tumor the CT seems to be a necessary examination.

[The orbito-zygomatic craniotomy in the treatment of giant tumor penetrating from maxillary-ethmoidal region to the anterior cranial fossa]. / Kraniotomia oczodolowo-jarzmowa w leczeniu olbrzymiego guza penetrujacego z masywu szczekowo-sitowego do przedniego dolu czaszki.

The orbitozygomatic craniotomy was presented in resection of giant tumour of maxillary-ethmoidal region, orbital cavity and anterior cranial fossa. As a result of this approach the possibility of whole tumour resection was obtained. Also, easy closure of anterior fossa and avoidance of the facial deformation was achieved.

Influence of 5-aminoisoquinolin-1-one (5-AIQ) on neutrophil chemiluminescence in rats with transient and prolonged focal cerebral ischemia and after reperfusion.

Stimulation of neutrophils by different factors increases their oxidative activity and the free radicals produced can report on the degree of activation. Poly(adenosine 5'-diphosphate ribose)polymerase-1 (PARP-1), a nuclear enzyme activated by strand breaks in DNA, plays an important role in the tissue injury associated with ischaemia-reperfusion injury and inflammation. 5-aminoisoquinolin-1-one (5-AIQ) is a potent inhibitor of PARP-1 activity in vitro and in vivo in rats. Acute (80 min) and prolonged (24h) focal cerebral ischaemia was induced in rats by obstruction of the median cerebral artery, with or without reperfusion, with or without administration of 5-AIQ. The oxidative activity of neutrophils was measured by chemiluminescence. Administration of 5-AIQ.HCl (3.0 mg kg(-1) b.w. - i.v.) caused a significant decrease in the oxidative activity of neutrophils in the group which had experienced chronic ischaemia for 24h but had no significant effect in the group which had received 80 min ischaemia, when compared to the control group. Increase of the oxidative activity of neutrophils was confirmed in rats with prolonged cerebral ischaemia, followed by reperfusion. 5-AIQ probably may decrease this activity through inhibition of PARP-1 in focus of local ischaemia as well as hence lowering the expression of inflammatory mediators by activated neutrophils.

[The role of endothelin in regulation of vascular tone in physiology and pathology]. / Rola endoteliny w regulacji napiecia scian naczyn w fizjologii i patologii.

This paper discuss importance of the endothelin, present in the plasma and other fluids, on the vascular smooth muscles in physiology and pathology. Endothelin-1 as one of the very strong vasoconstructive peptides influences the vascular tone. We discuss the competitive action of vasoconstrictors and vasodilators in promoting of vasospasm, especially in the states, where endothelial cells are injured.

Vascular endothelial growth factor (VEGF) and its effect on angiogenesis.

The article discusses the role of vascular endothelial growth factor(VEGF) in angiogenesis in embryonic development, particularly the effect of VEGF on capillary formation in response to chronic tissue ischemia and hypoxia. The sources and action of numerous angiogenic and angiostatic factors responsible for morphologic development of endothelial cells and disturbances in VEGF and FGF secretion are also presented. Increased VEGF and VEGF receptor expression enhances vascular permeability and angiogenesis, and is the cause of tissue edema as well as tumor and metastasis formation. VEGF appears to have a beneficial effect only in ischemic diseases of the heart and peripheral vessels. The article highlights the therapeutic implication of VEGF suppression in other areas of ischemia.

Reactivity of cerebral arteries after subarachnoid hemorrhage in rats after phosphoramidon administered.

The aim of the study was to quantify cerebral vasospasm in rats after subarachnoid hemorrhage (SAH) by morphometric examination of basilar artery and to evaluate the influence of Phosphoramidon on basilar artery constriction. The rat cisterna magna (CM) was cannulated and after 7 days SAH was developed by administration of 100 microliters autologic, non-heparinized blood to the CM. The sham subarachnoid hemorrhage was developed by intracisternal administration of 100 microliters of artificial cerebrospinal fluid. After 60 min and after 24 h Phosphoramidon was injected into the CM in a dose of 40 nmol diluted in 50 microliters of cerebrospinal fluid. After perfusion, the brain was removed from the skull and histological preparations of the basilar artery were made. The internal diameter and wall thickness of basilar arteries were measured by interactive morphometric method. The most severe vasospasm was found in rats after SAH and the administration of Phosphoramidon in the late phase after SAH caused the dilatation of the basilar artery. The presence of numerous infiltrations composed of neutrophils and macrophages correlated with advanced vasospasm (index of constriction 5 times lower than normal), suggesting the role of other factors participating in the late phase of vasospasms after SAH.

Effect of phosphoramidon on brain tissue angiogenesis in the chronic phase of vasospasm after subarachnoid hemorrhage in the rat.

BACKGROUND: Subarachnoid hemorrhage (SAH) frequently leads to prolonged cerebral vasospasm resulting in vascular pathology due to endothelial cell ischemia and neuronal hypoxia. Posthemorrhagic vasospasm can be counteracted by the administration of phosphoramidon, which blocks the endothelin converting enzyme (ECE) responsible for the conversion of big endothelin into a fully active ET1 peptide. The aim of the study was to determine the effect of chronic vasospasm after SAH on angiogenesis and the effect on this process of endothelin-1, the main causative factor in vasospasm. MATERIAL AND METHODS: Male Wistar rats were examined. Seven days after cannulation of the cisterna magna, blood was administered to induce SAH. The ECE inhibitor phosphoramidon was administered in a dose of 40 nmol in 50 microl of cerebrospinal fluid three times: 20 min before SAH, 60 min after SAH, and 24 hours after SAH. The brains were removed 48 hours later for histological evaluation. The vascular surface density was measured in cerebral hemisphere sections (at the level of the dorsal part of the hippocampus) and brainstem sections (1/2 of the pons). CONCLUSION: Increased angiogenesis was observed in the cerebral hemispheres after SAH. The administration of phosphoramidon inhibits angiogenesis in cerebral hemispheres after SAH.