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Biomedical subjects

B B Johansson

Publications and source records attributed to B B Johansson.

At least 19 recordsLinked to original sources
PubMed1992

NBQX, an AMPA antagonist, reduces glutamate-mediated brain edema.

Glutamate (2.5 mg) was administered after the blood-brain barrier had been opened by a unilateral intracarotid infusion of 5 mg protamine sulfate in rats. Whereas the brain specific gravity, measured 24 h later, did not differ between the injected and non-injected side after protamine alone, glutamate significantly reduced the specific gravity in the right hemisphere indicating brain edema (P less than 0.01). NBQX, a potent AMPA receptor antagonist, significantly reduced the edema (P less than 0.01) and completely inhibited the glutamate mediated increase in albumin content in cerebrospinal fluid (P less than 0.01).

Animals↗
PubMed1992

Fetal neocortical grafts implanted in adult hypertensive rats with cortical infarcts following a middle cerebral artery occlusion: ingrowth of afferent fibers from the host brain.

This study is focused on the survival of fetal neocortical grafts placed in the infarcted adult host cortex of the spontaneously hypertensive rat and describes the ability of host axonal regeneration into the graft after a focal ischaemic lesion. Five to seven days following ligation of the right middle cerebral artery, dissociated neocortical primordium from fetuses of gestational age 12-18 days was implanted into the infarcted cortical area. Surviving transplants were seen in all rats, although grafts derived from gestational age 12-14 days displayed an irregular morphology rich in sinusoid-like cavities and containing fewer cells of apparently mature neuronal morphology. Grafts from older donors contained perikarya of neuronal appearance; however, they lacked normal cortical lamination. Ten days postgrafting, fibers stained by acetylcholinesterase histochemistry, dopamine-beta-hydroxylase, and 5-hydroxytryptamine immunohistochemistry were found in the grafts, and by 10-23 weeks after transplantation the fiber density had increased substantially. When the retrograde tracer Fluoro-Gold was injected into the grafted tissue, labeled cells were found in several subcortical nuclei of the host, including the nucleus basalis of Meynert, ventral pallidum, thalamus, dorsal raphe, locus coeruleus, as well as the ipsilateral and contralateral neocortex. This study shows that grafts of dissociated neocortical tissue exhibit good survival and growth potential when implanted into infarcted neocortex and that several nerve fiber systems of the adult host have a regenerative capacity sufficient to innervate the grafted tissue.

Acetylcholinesterase↗
PubMed1992

Vascularization of fetal neocortical grafts implanted in brain infarcts in spontaneously hypertensive rats.

The vascularization of neural grafts in ischemic brain was studied in spontaneously hypertensive rats grafted with a suspension of fetal neocortical tissue into the infarcted area five to six days after ligation of the middle cerebral artery. The brain vasculature was examined by scanning electron microscopy of corrosion vascular casts and the cortical microvasculature was stereologically quantified in light microscopy three months after the occlusion. Patent anastomoses were present between the middle cerebral artery distal to occlusion and the proximal part, as well as to the anterior and posterior cerebral arteries, in both grafted and non-grafted rats. A vascular plexus covering the infarct cavities and the grafts contained leptomeningeal vessels intermingled with a thin capillary network which is not normally found on the brain surface. The graft vessels were derived from this vascular plexus. The regular pattern of arterioles and venules penetrating from the cortical surface in normal neocortex was absent in the grafts but the capillary morphology was similar in both types of tissue. The grafts had a lower capillary density than normal tissue and lacked the laminar distribution of capillaries characteristic of normal neocortex. The results demonstrate the plasticity of the vascular system where remodeling of the vascular tree after an ischemic insult provides suitable conditions for the vascularization of neocortical grafts.

Animals↗
PubMed1992

Experimental models of altering the blood-brain barrier.

The passage of a substance from blood to brain can be enhanced by altering the permeability of the substance itself or by altering the BBB characteristics. Example of the former is to increase lipid solubility, glycosylation and cationization, liposome entrapment and coupling to carriers. Unselective opening of the BBB can be obtained by a local or systemic increase of the intravascular pressure, by intracarotid injection of hyperosmolar solutions or by substances that alter the endothelial surface charge such as protamine sulphate. Substances that alter the fluidity of membranes can reduce or enhance the permeability of the BBB. In experimental models involving temporary opening of the BBB possible long-term hazardous effects must be considered.

Animals↗
PubMed1992

Plasma lipids and lipoproteins in subtypes of stroke.

We determined plasma lipid and lipoprotein concentrations in 131 patients (95 males, 36 females, mean age 71 years) 6 months after acute stroke onset. Compared to a reference population, the alterations of plasma lipid concentrations in stroke patients were moderate. However, the stroke patients had higher levels of triglyceride and lipoprotein (a) and lower concentrations of cholesterol, high density lipoprotein cholesterol and low density lipoprotein cholesterol. Patients with different subtypes of stroke showed significant differences when compared with each other by analysis of covariance (with adjustment for age, sex, smoking, hypertension and diabetes). Patients with carotid or vertebral artery disease had the higher levels of cholesterol, triglyceride and apolipoprotein B, whereas high density lipoprotein triglyceride concentrations were higher in patients with cardioembolic infarcts.

Adult↗
PubMed1992

Rat melanin-concentrating hormone stimulates adrenocorticotropin secretion: evidence for a site of action in brain regions protected by the blood-brain barrier.

Melanin-concentrating hormone (MCH) is a peptide reported to inhibit ACTH and cortisol secretion in teleost fish. Its ability to modify the activity of rat corticotrophs, however, remains controversial. We report here that while the peripheral injection of rat (r) MCH failed to alter plasma ACTH levels of conscious rats with an intact blood-brain barrier (BBB), it significantly activated the hypothalamic-pituitary-adrenocortical axis of rats with increased BBB permeability induced by protamine sulfate administration into the internal carotid artery. Similarly, the intracerebroventricular injection of this peptide into rats with intact BBB measurably released ACTH. The ACTH response to rMCH was markedly, but not totally, inhibited by passive immunoneutralization of CRF. These results indicate that rMCH acts within the central nervous system to stimulate the hypothalamic-pituitary-adrenocortical axis of rats, and that the site of action of the peptide is located in brain structures protected by the BBB. Activation of CRF-secreting neurons represents an important final pathway, although other regulatory factors also seem to be involved.

Adrenocorticotropic Hormone↗
PubMed1992

Vascular mechanisms in hypertensive cerebrovascular disease.

Hypertension causes vascular changes of essentially three types: structurally adaptative changes, degenerative alterations unrelated to atherosclerosis, and atherosclerosis. Structural changes result in an increased peripheral resistance, even in the relaxed vascular bed, and a reduced collateral capacity, thus predisposing to ischemia distal to an arterial stenosis/occlusion and to "watershed" infarcts in connection with a drop in blood pressure. Degenerative changes in the small intracerebral arteries can lead to plasma extravasation and focal brain edema, lacunar infarcts, and intracerebral hemorrhages. Hypertension also predisposes to saccular aneurysms and subarachnoid hemorrhages. Finally, atherosclerotic changes including stenoses or occlusions of predominantly extracranial and pial arteries give rise to transitory ischemic attacks and brain infarcts by artery-to-artery embolism or distal hemodynamic perfusion insufficiency.

Cerebrovascular Disorders↗
PubMed1992

Evaluation of long-term functional status in first-ever stroke patients in a defined population.

Medical, social and ADL variables were registered within 48 hours of stroke onset and 6 and 12 months later in 346 first-ever stroke patients. One year after stroke onset 27% of the patients were dead. 78% of the surviving patients were living in their own homes, 10.6% in old people's homes with no medical facilities and 9.5% in nursing homes. A health index was used for ADL evaluation and the quality of life was estimated according to Nottingham Health Profile (NHP). 16% of the patients had domestic social service assistance before stroke onset. The help given by relatives and friends far exceeded that given by the society before as well as after stroke onset. Right hemispheric stroke patients had a worse outcome than left-sided with respect to ADL and life satisfaction.

Activities of Daily Living↗
PubMed1991

Sensorimotor performance and rotation correlate to lesion size in right but not left hemisphere brain infarcts in the spontaneously hypertensive rat.

In order to correlate behavioural deficits to lesion size and to reveal possible functional asymmetries in the rat brain, locomotor activity, rotation and sensorimotor integration to touch were studied in spontaneously hypertensive rats (SHR) subjected to right or left middle cerebral artery occlusion. Control and infarcted rats showed no difference in locomotor activity. Infarcted rats tended to rotate towards the side of the lesion. A large sensorimotor deficit was found contralateral to the infarcted hemisphere. The absolute values of the side-biases for the rotation and sensorimotor tests were of the same degree irrespective of lesion side. Whereas the left hemisphere lesion size did not correlate to the behavioural outcome, the size of the right hemisphere lesion was highly correlated to the total sensorimotor deficit. Furthermore, the sensorimotor deficit of specific body parts was found to correlate to the damage of certain brain regions in a rostrocaudal fashion, reminiscent of a somatotopical organization. The extent of ipsilateral rotation correlated to brain tissue loss at the level of the posterior caudate-putamen. The present results indicate an asymmetrical organization for brain functions involved in the performance of the rotation and sensorimotor tests.

Animals↗
PubMed1991

The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction.

Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.

Animals↗
PubMed1991

Dixyrazine, a phenothiazine derivative, can prevent brain oedema induced by intracarotid injection of protamine sulphate.

The present study was performed to determine whether an opening of the blood-brain barrier (BBB) induced by intracarotid infusion of protamine sulphate necessarily leads to brain oedema and, if so, whether dixyrazine, a phenothiazine, can prevent the oedema. Evans blue albumin was used to detect BBB opening. Endogenous serum albumin was determined in CSF sampled before and after protamine infusion. The brain specific gravity, a sensitive indicator of brain oedema, was determined one hour after intracarotid infusion of 5 or 10 mg protamine sulphate in 100 or 200 microliters solvent in rats. Both doses opened the BBB and the CSF albumin was significantly increased (p less than 0.05 for 5 mg and p less than 0.01 for 10 mg protamine sulphate). However, only 10 mg protamine significantly reduced the specific gravity in the cerebral cortex and basal ganglia in the right (injected) hemisphere. Pretreatment with dixyrazine 10 mg/kg completely prevented the brain oedema and significantly reduced the albumin increase in CSF. We conclude that a) a moderate opening of BBB induced by 5 mg protamine sulphate does not lead to brain oedema and b) dixyrazine can prevent the brain oedema induced by 10 mg protamine sulphate.

Animals↗
PubMed1991

Changes in physiological parameters of rat cerebrospinal fluid during chronic sampling: evaluation of two sampling methods.

Although rat cerebrospinal fluid (CSF) is increasingly being used in pharmacological and biochemical research, methodological studies on basic physiological data are lacking. We have determined the albumin content and number of erythrocytes and leukocytes in CSF obtained by two different methods of sampling from cisterna magna-repeated sampling from an implanted cannula and by repeated punctures. In the initial samples the albumin content was 0.08 +/- 0.03 micrograms/microliters. Chronic cannulation of the cisterna magna resulted in a meningeal reaction with increased cell and albumin content: a reaction that could be reduced but not prevented by using a sterile cannula. The number of leukocytes but not erythrocytes was highly correlated to the albumin content. Repeated sampling in the absence of a permanent cannula did not significantly increase albumin content but carried a higher risk for erythrocyte contamination.

Animals↗
PubMed1991

Bilirubin-induced changes in brain energy metabolism after osmotic opening of the blood-brain barrier.

Acute and residual effects of blood-brain barrier disruption and bilirubin on brain metabolism were studied in a rat model after osmotic opening of the blood-brain barrier under pentobarbital anesthesia. Arabinose (1.5 M) was infused via the right external carotid artery over 30 s, resulting in opening of the barrier within the right hemisphere. Two min later, bilirubin was infused i.v. over 3 min, raising the serum bilirubin concentration to 37-44 mg/dL (633-752 mumol/L). The animals were euthanized at 15 min or 4 h by freezing the brain in situ. Opening the blood-brain barrier produced small changes in cerebral energy metabolism in some animals at 15 min. Compared with saline-infused control animals, two out of nine rats had decreased brain phosphocreatine and three out of nine developed increased brain lactate levels. Infusion of bilirubin in rats with a disrupted blood-brain barrier produced profound decreases in brain energy metabolites, glucose, and glycogen and a markedly increased lactate/pyruvate ratio at 15 min. The markedly increased lactate in the presence of normal or low pyruvate in bilirubin-treated animals indicates accumulation of NADH and probably reflects severe mitochondrial dysfunction. Four h after the arabinose/bilirubin infusions, the barrier would be expected to be repaired and bilirubin levels were negligible, but two out of five arabinose and three out of six bilirubin rats continued to have severely altered brain metabolism indicating residual brain injury in some animals.

Animals↗
PubMed1990

The physiology of the blood-brain barrier.

The BBB is a dynamic interface between blood and the central nervous system enabling the brain to keep an optimal internal environment. The endothelial cells of the brain capillaries are unique epithelial-like cells that are fused together by tight junctions and have a low pinocytotic activity. The entry of a specific substance will, therefore, mainly depend on its lipid solubility, and whether or not it has access to any of the carriers in the endothelial cells. Enzymatic degradation in the endothelium can prevent entry into the brain of substances that do enter the endothelial cells. Astrocytes may have an important role by inducing and upholding some barrier functions. An intact BBB is evidently important for optimal brain function. Manipulation of the BBB to allow entry of therapeutic agents may be justified under certain circumstances but should be done with caution until we know more about the long-term consequences of such manipulation.

Animals↗
PubMed1990

Albumin content in brain and CSF after intracarotid infusion of protamine sulfate: a longitudinal study.

The endogenous serum albumin content was determined by immunoelectrophoresis in brain and cisternal CSF 1, 24, and 72 h after a transient opening of the blood-brain barrier. Protamine sulfate, 5 mg in 100 microliters 0.9% NaCl, was infused during 30 s into the internal carotid artery via a catheter in the external carotid artery in conscious rats. The albumin content in CSF was 0.08 +/- 0.03 g/liter before protamine infusion and 0.09 +/- 0.02 g/liter in rats infused with saline only. The levels were significantly increased one and 24 h after protamine infusion (0.37 +/- 0.19 and 0.23 +/- 0.09 g/liter, P less than 0.001) but not at 72 h (0.14 +/- 0.05 g/liter). The albumin content in the right (injected) hemisphere decreased with time but was significantly higher than that in the left hemisphere at all times (P less than 0.001 1 and 24 h after protamine; P less than 0.01 at 72 h). There was no correlation between the albumin contents in brain and CSF. Pretreatment with dixyrazine, a phenothiazine derivate, significantly reduced the protamine-induced leakage of endogenous serum albumin into brain and CSF.

Animals↗
PubMed1989

Endogenous serum albumin content in brain after short-lasting epileptic seizures.

Epileptic seizures can transiently alter the blood-brain barrier. We have determined the content of extravasated endogenous serum albumin in the brain and its change with time after bicuculline (0.3 mg/kg) induced epileptic seizures of a few minutes' duration in conscious rats. The brains were perfused with saline in situ 5 min, 2 h, 24 h, 3 or 7 days after the injection of bicuculline. The content of endogenous serum albumin in the cerebral cortex, diencephalon, mesencephalon, pons and cerebellum was determined by rocket immunoelectrophoresis. At 5 min the extravasation was most marked in the diencephalon with levels above 99% of the confidence limit of control brains in 8 out of 9 brains. Higher levels were seen at 2 h than at 5 min in the cerebral cortex and the cerebellum. Since it is known that the barrier rapidly normalizes after seizures, these findings suggest redistribution probably along clearance pathways into the cerebrospinal fluid (CSF) and possibly re-entry of albumin into the parenchyma from the CSF. Four out of 6 rats still had increased albumin levels in the cerebral cortex at 24 h. At 72 h and 7 days no values differed from controls.

Animals↗