Wyniki wyszukiwania

1

Vasopressin in vascular regulation and water homeostasis in the brain

100%

Kozniewska E., Romaniuk K.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 8

2

Blood-brain barrier and cerebral blood flow disturbances after intracarotid administration of hypertonic urea

100%

Kozniewska E., Skolasinska K.

Acta Physiologica Polonica

|

1979

|

tom 30

|

nr 1

3

Dilation of the middle cerebral artery exposed to low extracellular sodium depends on the integrity of the endothelium

100%

Romaniuk K., Kozniewska E.

Acta Neurobiologiae Experimentalis

|

2006

|

tom 66

|

nr 4

4

Disturbed regulation of the rat middle cerebral artery during hypo-osmotic hyponatremia

100%

Aleksandrowicz, Kozniewska E.

Acta Neurobiologiae Experimentalis

|

2011

|

tom 71

|

nr 1

Objectives: Hyponatremia is diagnosed in approximately 30% of neurosurgical patients after head trauma, subarachnoid or intracerebral haemorrhage. It is well documented that hyponatremia deteriorates the general state of the patients, aggravates brain damage and increases mortality. Its influence on the regulatory mechanisms of cerebral blood vessels is unknown. The aim of our experiments was to study the impact of acute and chronic hyponatremia on the regulation of the isolated middle cerebral artery (MCA) of the rat. Material and Methods: Seventy five vessels were studied in the organ chamber. Acute hyponatremia (AH, 120mM Na+) was induced in vitro 1 hour prior to the study of MCA reactivity. Chronic hyponatremia (CH) was induced in vivo with a help of vasopressin and liquid diet (AIN-76). Vasopressin was delivered continuously from subcutaneously implanted ALZET osmotic minipumps. After 3.5 days, plasma Na+ concentration ranged from 114 to 122 mM in these rats. MCAs were isolated and studied in the organ chamber containing 120 mM Na+ buffer. MCAs placed in normonatremic bath (Na+=144 mM) served as a reference group. The reactivity tests comprised responses to acidosis (pH=7.0), to hyperkalemia (20 mM K+) and to changes in perfusion pressure. Results: In normonatremia MCA dilated on average by 19±2% (p<0.05) during decrease of pH from 7.4 to 7.0 and by 30±3% (p<0.05) during increase of K+ concentration in the bath from 3.5 to 20 mM. Hyponatremia impaired reactivity of the MCA to both acidosis and hyperkalcemia. There were differences in the severity of this impairment depending on the duration of hyponatremia. During AH decrease of pH induced constriction of the MCA by 13±3% (p<0.05) whereas during CH constriction was only 4±1% (p<0.05 vs. AC and normonatremia). The impairment of the response to 20 mM K+ (constriction by 18±2%, p<0.05 vs. normonatremia) was observed only during AH. The response to changes in perfusion pressure was well preserved both during AH and CH. Conclusion: Our results demonstrate for the first time that hyponatremia selectively disturbs the regulatory mechanisms of cerebral blood vessels. They also show that acute hyponatremia impairs regulation of the MCA more than chronic hyponatremia. In conclusion, vascular impairment may be an important component of intracranial pathology during hyponatremia. Acknowledgements: This study was financially supported by the grant N401 19032/3924 from the Ministry of Science and Higher Education.

5

The role of reverse mode of Naplus/Ca2plus exchanger in vascular response to acute hyponatremia

100%

Klapczynska K., Kozniewska E.

Acta Neurobiologiae Experimentalis

|

2009

|

tom 69

|

nr 1

In a previous study we have found that dilation of the middle cerebral artery (MCA) of the rat during acute hyponatremia depends on endothelium and NO/cGMP signalling. The production of NO in the endothelium is stimulated by the increase of intracellular concentration of Ca2+ which can occur either as a result of the release of calcium ions from intracellular stores or their infl ux from the extracellular space. The latter requires opening of specifi c Ca2+ channels of the cell membrane and/or operation of Na+ /Ca2+ exchanger (NCX) in the reverse mode. In the present study we sought the participation of the reverse mode of NCX in the response of MCA to acute hyponatremia. Experiments were performed on MCAs harvested from the brains of male Wistar rats and mounted in the organ chamber under the inverted microscope equipped with video camera and monitor. The diameter of the vessel was measured directly from the screen and recorded. The vessel was perfused at a transmural pressure of 80 mm Hg, temperature of 37°C and pH 7.4. Hyponatremia was induced by decreasing the intra- and extraluminal concentration of Na+ from 144 to 120 mM. In some experiments hyponatremia was preceded by the administration to the chamber of the inhibitor of the reverse mode of NCX (KB-R7943, 10 microM) or the inhibitor of L-type Ca2+ channel (Nimodipine, 0.1 microM). In the last experiment endothelium was removed before administration of KB-R7943 (10 microM) and lowering of Na+ . Hyponatremia resulted in the dilation of the MCA by 17% (P<0.05). This response was abolished by the pretreatment with KB-R7943 but not with Nimodipine. The results show that small decrease in the concentration of extracellular Na+ may stimulate reverse mode of NCX in the endothelium but not in the smooth muscle cells.

6

Modulation of the rat middle cerebral artery response to acidosis in hyponatremia by the opener of large-conductance calcium-dependent potassium channels (BKCa)

100%

Aleksandrowicz M., Kozniewska E.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Objectives: It is well known, that acidosis-induced dilation of the middle cerebral artery (MCA) in normonatremia depends on BKCa channel activation in smooth muscle cells of the arterial wall. Our studies on the effect of hyponatremia on the regulation of the rat MCA have demonstrated, that acute hyponatremia causes BKCa channel dysfunction manifested by its reduced sensitivity to agonists. The aim of our present experiments was, therefore, to study whether the response of MCA to acidosis is decreased during hyponatremia and if so, whether BKCa channel activator applied in subthreshold dose restores the response of MCA to lowering of extravascular pH. Method: MCAs were isolated from male Wistar rats brains and placed in the arteriograph chamber filled 3-(N-morpholino) propanesulfonic acid (MOPS) buffered saline solution containing 1% BSA. The vessels were perfused (100 µl/ min) and set at a hydrostatic pressure of 80 mmHg. The MCA images were recorded using a microscope equipped with a camera coupled to a monitor. The measured parameter was the internal diameter of the vessel. Acute hyponatremia was induced in the chamber by decreasing Na+ concentration in the extra- and intravascular fluid from 144 mM to 120 mM. After equilibration of the MCA for 1 hour in normonatremic buffer, responses of this artery to BKCa channel activator (NS1619, 10- 5M) in normo- and hyponatremia, to lowering of extravascular pH from 7.4 to 7.0 in normonatremia, in hyponatremia and in hyponatremia in the presence of NS1619 (10-5M) were studied. Results: NS1619 administration led to MCA dilation by 16 ± 1% (P<0.001) in normonatremia but had no effect on the vessel diameter in hyponatremia. Reducing pH from 7.4 to 7.0 resulted in the dilation of MCA by 18 ± 2% (P<0.001) in normonatremia whereas in hyponatremia constriction of the MCA by 4 ± 2% (P<0.01) in response to reduced pH was observed. The presence of BKCa channel activator restored the response of the MCA to acidosis during hyponatremia. Conclusion: These results confirm our previous findings that during acute hyponatremia, BKCa channels sensitivity in the wall of MCA is reduced. This explains lack of the dilation of this artery to extracellular acidosis in hyponatremia. This study was financially supported by statutory activities of the Mossakowski MRC PAS

7

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

100%

Kozniewska E., Skolasinska K.

Acta Physiologica Polonica

|

1980

|

tom 31

|

nr 4

8

Impact of focal cerebral ischemia/reperfusion on the microcirculation in the cerebral cortex, selective vascular protection with free radical scavengers

81%

Kozniewska E., Reszka R., Lisdat F., Radomska L.

Acta Neurobiologiae Experimentalis

|

1999

|

tom 59

|

nr 3

9

Neuroprotective effects of Y2 and Y5 neuropeptide Y receptor agonists

61%

Smialowska M., Domin H., Zieba B., Michalik R., Piotrowski P., Kozniewska E.

Acta Neurobiologiae Experimentalis

|

2009

|

tom 69

|

nr 1

Neuropeptide Y (NPY), a 36 amino acid peptide widely distributed in the nervous system, inhibits glutamatergic transmission and decreases hippocampal epileptiform activity which may lead to neuroprotection. Such effects were observed in some earlier studies, but results are divergent and the role of particular Y receptors remains unclear. In the present study we investigated a possibility of neuroprotective action of neuropeptide Y1, Y2 and Y5 receptor specifi c ligands in rats in two in vivo models of brain damage. In the fi rst model, kainic acid (KA)(2.5 nmol/1 μl) was microinjected into the CA1 region of the rat dorsal hippocampus and the peptide compounds (470 pmol/1 μl) were injected in the same region 30 min, 1 h or 3 h after the kainate. Seven days later the brains were taken for histology and number of neurons in CA pyramidal layer was evaluated by stereological counting. It was found that, Y2 agonist (NPY13- 36) and Y5R agonist ([CPP1-17,NPY19-23,Ala31,Aib32Gln34] hPP), injected 30 min or 1 h but not 3 h after the KA, signifi cantly diminished KA-induced hippocampal lesion. Contrary Y1 agonist ([Leu31,Pro34]-NPY) did not induced any protection but had a tendency towards an increase of the degeneration. The most promising Y2 agonist was tested also in the second model, focal cerebral ischemia after transient middle cerebral artery occlusion (MCAO). The peptide was injected icv (10 μg/6 μl,), 30 min after MCA occlusion. It signifi cantly diminished MCAO-induced brain damage evaluated by TTC staining. Our results indicated neuroprotective effects of Y2 and Y5 activation. Moreover we found that the peptides may be effective after delayed (30ñ60 min) application.

10

Increase of cerebral blood flow in rats after human beta-amyloid peptide infusion

61%

Pluta R., Oseka M., Januszewski S., Misicka A., Lipkowski A. W., Barcikowska M., Kozniewska E.

Folia Morphologica

|

1996

|

tom 55

|

nr 4

11

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

51%

Kozniewska E., Michalik R., Rafalowska J., Gadamski R., Walski M., Frontczak-Baniewicz M., Piotrowski P., Czernicki Z.

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 11

145-160

The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.

Ograniczanie wyników

Vasopressin in vascular regulation and water homeostasis in the brain

Blood-brain barrier and cerebral blood flow disturbances after intracarotid administration of hypertonic urea

Dilation of the middle cerebral artery exposed to low extracellular sodium depends on the integrity of the endothelium

Disturbed regulation of the rat middle cerebral artery during hypo-osmotic hyponatremia

The role of reverse mode of Naplus/Ca2plus exchanger in vascular response to acute hyponatremia

Modulation of the rat middle cerebral artery response to acidosis in hyponatremia by the opener of large-conductance calcium-dependent potassium channels (BKCa)

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

Impact of focal cerebral ischemia/reperfusion on the microcirculation in the cerebral cortex, selective vascular protection with free radical scavengers

Neuroprotective effects of Y2 and Y5 neuropeptide Y receptor agonists

Increase of cerebral blood flow in rats after human beta-amyloid peptide infusion

Mechanisms of vascular dysfunction after subarachnoid hemorrhage