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Biomedical subjects

J Van Reempts

Publications and source records attributed to J Van Reempts.

At least 37 records · Page 2Linked to original sources
PubMed1991

Singlet oxygen induced cerebral vasospasm: an experimental study in rats.

A new experimental model is described which can be used as an alternative to study the effects of subarachnoid hemorrhage (SAH) in rats. Vasospasm of the basilar artery is induced photochemically after transpalatal illumination of intracisternally injected rose bengal in two different rat strains. Singlet oxygen, generated in the subarachnoid space, elicits vasospasm which has been demonstrated angiographically at 90 min and 24 h after photosensitisation. Sprague Dawley rats responded better than Wistar rats. Dilution of rose bengal in water was more vasospastic than dilution of rose bengal in artificial CSF. Since the action of singlet oxygen is similar to that of free radicals, this experiment gives an argument for the hypothesis that free radicals play a leading role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage.

Animals↗
PubMed1990

Fiberoptic intracranial pressure monitoring in rats.

An adaptation of a fiberoptic intracranial pressure monitoring system for clinical use is described. The method allows easy and reliable acute and chronic intracranial pressure registration in anesthetized as well as conscious rats. The disposable fiberoptic probes, originally designed for human use, can be re-used limitlessly. The fiberoptic method is compared with conventional monitoring procedures under different experimental conditions. The validity of intraparenchymal and epidural measurements is discussed. The importance of chronic intracranial pressure registration in conscious laboratory animals is stressed.

Animals↗
PubMed1990

Cerebroprotective effects of flunarizine in an experimental rat model of cardiac arrest.

A rat cardiopulmonary arrest model was used to study the effects of flunarizine on survival and on the development of postischemic brain damage. Ischemia was induced by a combination of hypovolemia and intracardiac injection of a cold potassiumchloride solution. To validate the model; survival rate and histological damage were assessed after ischemic periods ranging from 5 to 20 minutes. A 6-minute cardiac arrest period was withheld for further therapeutic investigations. In one group (n = 12), flunarizine was administered successively in doses of 0.5 mg/kg intravenous at 5 minutes, 10 mg/kg intraperitoneal at 1 hour, and 20 mg/kg orally at 16 and 24 hours after recirculation. The second group (n = 13) received only the vehicle. Flunarizine, although not affecting mortality; significantly reduced the mean number of ischemic neurons in CA1 hippocampus from 83% in the control to 44% in the drug-treated series (P = 0.014). The results are indicative of the usefulness of this cardiac arrest model to study morphologic aspects of cerebral injury. The results obtained with flunarizine show the effectiveness of this drug even when it is administered after a severe ischemic insult such as global complete ischemia.

Animals↗
PubMed1989

Favourable effect of flunarizine on the recovery from hemiparesis in rats with intracerebral hematomas.

In 25 rats, an intracerebral hematoma was created in the foreleg area of the motor cortex by injection of 50 microliters blood. After the lesion, 13 were treated with flunarizine and 12 with the solvent. Neurological testing was performed by measuring the running time on a rotating platform. In animals with hemiparesis, the flunarizine group (n = 7) showed a significantly (P less than 0.05) better recovery than the control group (n = 8). No significant differences occurred in animals without neurological deficits (flunarizine: n = 6, control: n = 4). So the effect of the drug is not due to a non-specific activation; it may partially cure neurological deficits caused by intracerebral hematoma.

Animals↗
PubMed1989

Dorsal-ventral gradient in vulnerability of CA1 hippocampus to ischemia: a combined histological and electrophysiological study.

Transverse hippocampal slices were prepared after 7 days survival from rats subjected to 8 min of global incomplete ischemia by temporary occlusion of both carotid arteries and hypotension. The slices demonstrated a dorsal-ventral gradient in the amount of ischemic neuronal necrosis in the CA1 region. Histologically ischemic cell change decreased from 90% dorsoseptally to 10% ventrotemporally. Electrophysiological analysis of the number of slices with viable synaptic transmission in CA1 also revealed a septotemporal gradient in susceptibility to ischemia.

Action Potentials↗
PubMed1989

Photochemical stroke model: flunarizine prevents sensorimotor deficits after neocortical infarcts in rats.

We produced unilateral photochemical infarcts in the hindlimb sensorimotor neocortex of 186 rats by intravenous injection of the fluorescein derivative rose bengal and focal illumination of the intact skull surface. Infarcted rats showed specific, long-lasting deficits in tactile and proprioceptive placing reactions of the contralateral limbs, mostly the hindlimb. Placing deficits were most prominent during transition to immobility and/or when independent limb movements were required. Administration of flunarizine, a Class IV calcium antagonist, 30 minutes after infarction resulted in marked sparing of sensorimotor function in 30 rats. In contrast to 20 vehicle-treated rats, which remained deficient for at least 21 days, 15 (75%) of the rats treated with 1.25 mg/kg i.v. flunarizine showed normal placing on Day 1 after infarction, whereas the remaining five (25%) recovered within 5 days. Oral treatment of 10 rats with 40 mg/kg flunarizine was also effective. Neocortical infarct volume and thalamic gliosis, assessed 21 days after infarction, did not differ between 30 flunarizine- and 30 vehicle-treated rats. However, when 4-hour-old infarcts were measured in 16 rats, posttreatment with intravenous flunarizine reduced infarct size by 31%. In combination with appropriate behavioral analyses, photochemical thrombosis may constitute a relevant stroke model, in which flunarizine preserved behavioral function during a critical period, corresponding to the spread of ischemic damage.

Animals↗
PubMed1988

Purine nucleoside phosphorylase: a histochemical marker for glial cells.

The distribution of purine nucleoside phosphorylase activity has been investigated histochemically in rat and guinea-pig brain. At the light microscopical level, enzyme activity was most pronounced in glial cells in various anatomical regions of the rat brain. In contrast, the guinea-pig brain presented only a weak activity. Endothelial cells of both species were also reactive. These findings were confirmed by electron microscopy. Based upon anatomical position and morphologic characteristics, positive glial cells were identified as astrocytes. Precipitate-rich astrocytic processes could be easily demonstrated in between barely reactive neuronal fibers and around microvessels. A minority of astrocytes was devoid of reaction product. The present method may offer a valuable tool for the histopathological study of several types of disorders in which glial cells play a functional role.

Animals↗
PubMed1988

A new method to study activated oxygen species induced damage in cardiomyocytes and protection by Ca2+-antagonists.

It has been proposed that oxygen derived free radicals contribute to reperfusion injury in ischemic tissue: radical induced lipid peroxidation is believed to cause membrane destruction, eventually evolving to cell death. A method is introduced which investigates the effect of exogenously generated reactive O2 species on isolated Ca2+-tolerant rat cardiomyocytes. Singlet oxygen (O2(1)), generated by photo-excitation of the photosensitive dye rose bengal, induced the transformation of elongated rod-shaped cells into hypercontracted rounded cardiomyocytes. These shape changes were prevented by removal of extracellular Ca2+ or by addition of radical scavengers. Pre-treatment with various classes of Ca2+-antagonists dose-dependently reduced the number of hypercontracted cardiomyocytes after exposure to O2(1). Compounds not active on the slow Ca2+-channel (e.g. flunarizine-like) provided a better degree of protection than the genuine slow Ca2+-channel blockers (e.g. dihydropyridines). Ultrastructurally, cardiomyocytes exposed to O2(1) showed a loss of cytochemically demonstrable sarcolemma-associated Ca2+ and the presence of clustered Ca2+-deposits in the mitochondria. Drug pre-treated cells displayed a Ca2+-distribution pattern comparable to unchallenged control cells.

Animals↗
PubMed1987

Cytoprotective effects of disodium cromoglycate on rat stomach mucosa.

The cytoprotective effects of the anti-asthmatic drug, disodium cromoglycate (DSCG), on gastric mucosal necrosis induced by ethanol in rats were studied. Subcutaneous, but not oral, DSCG prevented the formation of gastric lesions and this effect was dose-dependent between 1.25 and 40 mg kg-1, with an ED50 value of 6.8 mg kg-1. Maximal cytoprotection occurred 15-30 min after DSCG treatment. Histological examination revealed that DSCG effectively protected the gastric mucosa against ethanol-induced vascular congestion, haemorrhage, epithelial desquamation and mucosal oedema. Enhanced production of endogenous prostaglandins, which are known cytoprotective compounds, could not explain the mucosal protection. At a dose of 40 mg kg-1, DSCG did not change prostaglandin E2 or 6-keto-prostaglandin F1 alpha concentrations in gastric mucosal tissue, although its cytoprotective activity was partially inhibited by prior treatment of the animals with indomethacin.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Ischemic brain injury and cell calcium: morphologic and therapeutic aspects.

Histopathological data obtained from different experimental models of hypoxia and ischemia were evaluated in order to extend current knowledge of mechanisms responsible for delayed neuronal cell death. Special attention is given to the distribution of calcium (Ca2+) in vulnerable areas during the postischemic period. Between an initial defensive Ca2+ sequestration, which is completely reversible, and final toxic Ca2+ overload, which is associated with irreversible neuronal necrosis, important Ca2+ shifts could be demonstrated cytochemically. Such shifts occur mainly at excitatory presynaptic sites and seem to precede structural ischemic cell change in postsynaptic areas. Recent results obtained with some Ca2+ entry blockers indicate that prophylactic treatment and postischemic intervention prevent cytosolic Ca2+ overload and reduce delayed brain injury.

Animals↗
PubMed1984

The hypoxic brain: histological and ultrastructural aspects.

A brief review of structural damage to cerebral cells resulting from experimentally induced hypoxia or ischemia is presented. The histological aspect of the brain is compared in different animal models with respect to the onset and progression of damage. Cell changes detected in the early post-hypoxic period consist of microvacuolation and seem to be fully reversible. Coagulative cell change and edematous cell change which may be considered as the morphologic equivalent of irreversible cell death, develop in a later phase, often as a result of secondary events such as microcirculatory impairment or tissue lactic acidosis. A striking difference in vulnerability exists between cerebral cell types or anatomic brain regions. Possible determinant factors for this phenomenon are discussed. Finally, the special contribution of calcium in cell destructive processes is demonstrated with the aid of ultrastructural calcium distribution studies.

Acid-Base Equilibrium↗
PubMed1984

Histologic changes in the hypoxic brain.

Two animal models were used for the morphologic study of hypoxic or ischemic cerebral injury. In the first model ("Levine preparation") rats were subjected to a unilateral carotid artery ligation, followed by intermittent exposure to pure nitrogen. Damage, which was examined 24 h after this bypoxic insult, was largely restricted to the ipsilateral cerebral cortex. In the second model ("Pulsinelli preparation") severe bilateral transient ischemia was induced by permanent occlusion of both vertebral arteries, followed by temporary ligation of both carotid arteries. Damage was examined after short recirculation times and after a 3-day survival period. Injury was largely confined to the CA1 layer of the hippocampus. In both experimental models two types of cell change were prominent: coagulative cell change which was restricted to neurons, and edematous cell change which was largely confined to astrocytes. Studies on cerebral microcirculation revealed a close relationship between areas of reduced flow and areas with structural damage. Cytochemical demonstration of subcellular calcium indicated an early and important redistribution of this cation, indicative for toxic calcium overload in the cytosol. Data on therapeutic intervention with Ca2+-overload blocker flunarizine are included.

Animals↗
PubMed1983

The role of calcium in cellular dysfunction.

In order to study the effects of substances with selective Ca2+ entry blocking properties which enhance the tolerance to ischemia by preventing a toxic calcium overload, attempts are made to localize calcium ultrastructurally. Under normoxic conditions, a mobile pool of Ca2+ is localized in synaptic vesicles and in mitochondria of brain cells; in mitochondria of cardiac, skeletal and vascular smooth muscle; and in the junctional SR of fast skeletal muscle. A plasmalemmabound pool of Ca2+ is present in cardiac and slow skeletal muscle. Ischemia or hypoxia induce marked shifts in calcium of both the mobile and the plasmalemma-bound pools. Cardiac and skeletal muscle mitochondria scavenge huge amounts of calcium, especially during the reperfusion period following prolonged circulatory arrest. The membrane-bound Ca2+ is lost under these conditions. In the hypoxic brain, the amount of intracellular calcium clearly parallels the degree of damage. Observations made on peripheral and brain blood vessels show that high amounts of precipitated Ca2+ cover the myofilaments upon induction of spasm. The antispasmodic effect of the selective Ca2+-entry blockers flunarizine and lidoflazine is morphologically characterized by the absence of Ca2+ over the myofilaments in muscle treated as such whereas the extracellular Ca2+ remained the same. This observation indicates that the entry of Ca2+ is blocked at the level of the plasma membrane. In the heart and brain these drugs preserve the structural integrity of the plasmalemma-surface coat complex and thereby protect the cells against the devastating consequences of cellular calcium overload.

Animals↗
PubMed1983

Protection with flunarizine against hypoxic-ischaemic damage of the rat cerebral cortex. A quantitative morphologic assessment.

The protective effect of flunarizine against cerebral cortical damage was evaluated in the "Levine preparation" after 24 hr of a combined hypoxic-ischaemic insult. Ligation of the right carotid artery, followed by intermittent exposure of the rats to pure nitrogen resulted in two major types of cellular damage in the ipsilateral hemisphere: coagulative necrosis of neurones (ischaemic cell change) and extreme cellular swelling (severe cell change). Quantification of the degree of damage was obtained by calculating the number of both types of cell change per mm3 of cortex. Flunarizine given orally at doses of 20 mg/kg and 10 mg/kg 5 hr before mild hypoxia and at doses of 40 mg/kg and 10 mg/kg 5 hr before severe hypoxia, led to a significant reduction of ischaemic and severe cell change. The calcium entry blocking properties of flunarizine are held responsible for these beneficial effects.

Animals↗