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E Koźniewska

Publications and source records attributed to E Koźniewska.

13 recordsLinked to original sources
PubMed2003

Acute decrease of cerebrocortical microflow and lack of carbon dioxide reactivity following subarachnoid haemorrhage in the rat.

Experiments were designed to study the extent, duration and severity of the impairment of cerebrocortical microciroflow during acute ischemia following experimental SAH in the rat. Twenty five male, adult anesthetized and mechanically ventilated Wistar rats were used. SAH was induced by perforation of the middle cerebral artery (MCA) using intravascular filament. Cerebrocortical microflow (LDF) was recorded bilaterally in the territory supplied by the MCA at normocapnia before SAH and up to 180 min thereafter. Reactivity of microcirculation to CO2 was also studied. In order to further explain mechanisms of post-SAH microcirculatory changes, L-arginine--a precursor of NO and 17-octadecynoic acid (17-ODYA)--an inhibitor of the enzymes of cytochrome P-450 family were administered. SAH resulted in acute decrease of microflow on both sides although during the first 20 min this effect was much better pronounced on the side ipsilateral to ruptured MCA (p < 0.05). Pretreatment with L-arginine or 17-ODYA didn't improve microflow after SAH. On the contrary, in rats pretreated with 17-ODYA LDF on the side ipsilateral to bleeding significantly deteriorated (p < 0.05 vs. control group at all times beginning 10 min after SAH). Following SAH the impairment of CO2 reactivity was also observed.

Animals↗
PubMed2003

Early neutrophilic expression of vascular endothelial growth factor after traumatic brain injury.

The formation of edema after traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. However, the molecular and cellular mechanisms underlying these phenomena have not been fully understood. One possible factor involved in edema formation is vascular endothelial growth factor (VEGF). This growth factor has previously been demonstrated to increase the blood-brain barrier permeability to the low molecular weight markers and macromolecules. In this study, we analyzed the temporal changes in VEGF expression after TBI in rats. In the intact brain, VEGF was expressed at relatively low levels and was found in the cells located close to the cerebrospinal fluid space. These were the astrocytes located under the ependyma and the pia-glial lining, as well as the epithelial cells of the choroid plexus. In addition, several groups of neurons, including those located in the frontoparietal cortex and in all hippocampal regions, were VEGF-positive. The pattern of VEGF-immunopositive staining of neurons and choroidal epithelium suggested that in these cells, VEGF binds to the cell membrane-associated heparan sulfate proteoglycans. Following TBI, there was an early (within 4 h post-injury) increase in VEGF expression in the traumatized parenchyma associated with neutrophilic invasion. The ipsilateral choroid plexus appeared to play a role in facilitating the migration of neutrophils from blood into the cerebrospinal fluid space, from where many of these cells infiltrated the brain parenchyma. VEGF-immunopositive staining of neutrophils resembled haloes and was found ipsilaterally within the frontoparietal cortex and around the velum interpositum, a part of the subarachnoid space. These haloes likely represent the deposition of neutrophil-derived VEGF within the extracellular matrix, from where this growth factor may be gradually released during an early post-traumatic period. The maximum number of VEGF-secreting neutrophils was observed between 8 h and 1 day after TBI. In addition, from 4 h post-TBI, there was a progressive increase in the number of VEGF-immunoreactive astrocytes in the ipsilateral frontoparietal cortex. The maximum number of astrocytes expressing VEGF was observed 4 days after TBI, and then the levels of astroglial VEGF expression declined gradually. Early invasion of brain parenchyma by VEGF-secreting neutrophils together with a delayed increase in astrocytic synthesis of this growth factor correlate with the biphasic opening of the blood-brain barrier and formation of edema previously observed after TBI. Therefore, these findings suggest that VEGF plays an important role in promoting the formation of post-traumatic brain edema.

Animals↗
PubMed1997

Dependence of basal cerebral blood flow and cerebral vascular resistance in spontaneously hypertensive rats upon vasoconstrictor prostanoids.

The effects of indomethacin (inhibitor of cyclooxygenase), imidazole (inhibitor of thromboxane A2 synthase) and SQ 29548 (antagonist of TxA2/PGH2 receptors) on basal CBF and CVR were studied in normocapnic and normoxic SHR and WKY rats. CBF was measured by the intracarotid 133Xe technique. CVR was calculated as ratio of mean arterial blood pressure and CBF. Resting CBF did not differ between SHR and WKY. MABP and CVR were significantly higher (p < 0.01) in SHR than in WKY. Indomethacin (6 mg/kg, i.v.) produced a significant long-lasting decrease of CBF and increase of CVR in both strains, although these effects were more pronounced (p < 0.01) in WKY. Imidazole (20 mg/kg, i.v.) had no effect on measured variables in either strain. SQ 29548 (1 mg/kg, i.v.) produced a significant increase of CBF in SHR (p < 0.001) but not in WKY. CVR decreased in SHR parallel to the increase of CBF but remained unchanged in WKY. Our results demonstrate that, in contrast to WKY, basal CBF and CVR in SHR depend upon vasoconstricting prostanoids which act on TxA2/PGH2 receptors but are distinct from thromboxane A2.

Animals↗
PubMed1992

Evidence against participation of V2 receptors in the increase of cerebral blood flow during hypoxemia in the rat.

Cerebral blood flow (CBF) and cerebral utilization of oxygen (CMRO2) were studied in anesthetized and artificially ventilated rats during normoxemia and hypoxemia before and during intravenous infusion of a selective blocker of V2 vasopressinergic receptors (d(CH2)5 [D-Ile2,Abu4] AVP, 15 micrograms/kg per hour i.v.). CBF was measured by means of the intracarotid 133-Xe injection method. CMRO2 was calculated from the oxygen arteriovenous difference using the Fick principle. Infusion of V2 antagonist did not influence CBF, CMRO2 or blood pressure (BP) during normoxia. It also did not change the response of cerebral circulation to hypoxemia. Increase in CBF and decrease in cerebrovascular resistance (CVR) during hypoxemia were similar during the infusion of V2 blocker or without it. However, the decrease in BP observed during hypoxemia in the control group of rats was prevented in the group of animals which were infused with V2 blocker.

Angiotensin Receptor Antagonists↗
PubMed1992

Effects of endothelium-derived nitric oxide on cerebral circulation during normoxia and hypoxia in the rat.

The aim of this study was to determine the effects of endogenous nitric oxide (NO) on cerebral blood flow (CBF) and cerebrovascular resistance (CVR) under conditions of normoxia and hypoxia. Experiments were performed on anesthetized, mechanically ventilated Wistar rats. CBF was measured using the intracarotid 133Xe injection technique. NO formation was inhibited by NG-monomethyl-L-arginine (L-NMMA). Administration of L-NMMA (100 mg kg-1 i.v.) during normoxia resulted in an increase in mean arterial blood pressure from 113 +/- 4 to 145 +/- 4 mm Hg (p less than 0.001), a decrease in CBF of 21% (from 91 +/- 4 to 75 +/- 5 ml 100 g-1 min-1, p less than 0.001), and an increase in CVR of 53% (from 1.3 +/- 0.1 to 2.0 +/- 0.2 mm Hg ml-1 100 g min, p less than 0.001). These effects were reversed by i.v. administration of 300 mg kg-1 of L-arginine but not D-arginine. Moreover, the administration of L-NMMA abolished the enhancement of CBF and the diminution in CVR observed during intracarotid infusion of acetylcholine (ACh). The increase in CBF and decrease in CVR during hypoxia in the group of rats that received L-NMMA were similar to that in the control group, although CBF and CVR levels attained during hypoxia in both groups were different. The results show that NO is involved in the maintenance of basal CBF and CVR, and is responsible for the ACh-elicited increase in CBF and the decrease in CVR in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

V2-like receptors mediate cerebral blood flow increase following vasopressin administration in rats.

Experiments were performed on anesthetized (chloral hydrate) Wistar rats to determine the effect of vasopressin (VP) on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebrovascular resistance (CVR), and mean arterial blood pressure (MAP) before and after V1 or V2 VP receptor blockade. Influence of synthetic V2 receptor agonist (dVDAVP) on these variables was also tested. Intracarotid administration of 5 mU VP (Pitressin, n = 15) significantly increased CBF by 28% and CMRO2 by 27% and reduced CVR by 20% of control value. Intravenous (i.v.) infusion of dEt2AVP (V1 antagonist, 15 micrograms kg-1 h-1, n = 7) did not influence the effect of VP on CBF, CMRO2, and CVR but abolished MAP increase after VP. Intravenous (i.v.) infusion of d(CH2)5[D-Ile2,Abu4] AVP (V2 antagonist, 15 micrograms kg-1 h-1, n = 8) abolished the effect of VP on CBF, CMRO2, and CVR without changing its influence on MAP. Intracarotid administration of 12.5 ng dVDAVP (n = 7) increased CBF by 43% and CMRO2 by 29% and decreased CVR by 29% of control value. MAP was not affected. The results suggest that VP-induced CBF increase is, at least partly, caused by the rise of CMRO2 and mediated by V2-like receptors.

Animals↗
PubMed1988

Enhanced reactivity towards flunarizine in cerebrovascular bed of spontaneously hypertensive rats.

Cerebral blood flow (CBF) was measured and cerebrovascular resistance (CVR) was calculated in anesthetized spontaneously hypertensive rats (SHR) and normotensive rats (NR) following the administration of incremental dosages of i.v. flunarizine or papaverine. CBF and CVR changes following papaverine were the same in both groups of rats irrespective of the dose of the drug. The effect of flunarizine was much more pronounced in SHR than in NR. The results point out the greater dependency of basal cerebrovascular tone in SHR upon Ca2+ influx into vascular smooth muscle cells.

Animals↗
PubMed1979

Impairment of cerebral blood flow autoregulation after hypertonic urea administration.

The effect of unilateral intracarotid administration of 3 M urea on resting cerebral blood flow, arterial blood pressure, perfusion pressure-cerebral blood flow relation, ECoG and Evans blue permeability was tested in dogs. The injection of urea was without effect on ECoG and enhanced the arterial blood pressure temporarily. Cerebral blood flow measured 10 min after the urea injection was not affected. Extravasation of Evans blue was observed in the urea-perfused hemisphere for about 40 min following the urea administration. Cerebral perfusion pressure-blood flow relation for the urea affected hemisphere studied at the time when blood-brain barrier to protein was restored revealed loss of the normal autoregulatory response, despite that it was preserved in the control hemisphere.

Animals↗
PubMed1978

Cerebrovascular response to intracarotid infusion of 5-hydroxytryptophan and L-DOPA in cats.

Intracarotid administration of 5-hydroxytryptophan (10 mg/kg) results in a slight vasoconstriction of cerebral vessels. L-DOPA (20 mg/kg) administered by the same route enhances cerebral blood flow. The effect on cerebral blood flow of L-DOPA (20 mg/kg) following intracarotid 5-hydroxytryptophan (10 mg/kg) administration shows a potentiation of cerebral blood flow response in non-pretreated as well as in nialamide- and reserpine-pretreated cats.

5-Hydroxytryptophan↗
PubMed1977

Disturbances in the blood-brain barrier and cerebral blood flow after rapid brain decompression in the cat.

The effect of sudden decompression of the brain on the blood-brain barrier and cerebral blood flow was studied in cats. The decompression experiments were performed on 9 cats which had been subjected to two hours of compression with an epidural balloon and on 10 cats subjected to four hours of balloon compression. In both experimental groups one could observe haemorrhages and disturbances in the blood-brain barrier in the cortex of the previously compressed hemisphere and in the basal nuclei. The extent of these changes depended on the duration of the epidural compression. At the same time, a decrease in cerebral blood flow, mainly in the brain cortex, was observed in both experimental groups.

Animals↗
PubMedDate not supplied

Lack of autoregulatory response of the cerebral circulation after osmotic opening of the blood-brain barrier in dogs.

The reversibility of osmotic opening of the blood-brain barrier was studied in dogs one hour after intracarotid 3 M urea injection. At that time the permeability of cerebral blood vessels to albumin is restored as evidenced by lack of Evans blue extravasation. Despite that, the response of the urea-perfused hemisphere to changes of perfusion pressure was abnormal. Blood flow in that hemisphere followed passively blood pressure changes in contrast to the contralateral hemisphere in which the blood flow remained independent of the perfusion pressure.

Animals↗