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R M Pluta

Publications and source records attributed to R M Pluta.

26 records · Page 2Linked to original sources
PubMed1992

Neuropeptide Y in the primate model of subarachnoid hemorrhage.

The cause of cerebral vasospasm after subarachnoid hemorrhage (SAH) remains unknown. Recently, an association between the potent vasoconstricting peptide, neuropeptide Y, and delayed cerebral vasospasm after SAH has been postulated. This was based on the findings of increased neuropeptide Y levels in the cerebrospinal fluid (CSF) and plasma after SAH in animals and humans. For this study, the primate model of SAH was used to assess the possible role of neuropeptide Y in delayed vasospasm after SAH. Fifteen cynomolgus monkeys underwent placement of a clot of either whole blood or red blood cells in the subarachnoid space around the middle cerebral artery (MCA). Sequential arteriography for assessment of MCA diameter and sampling of blood and CSF for neuropeptide Y were performed: before SAH (Day 0); 7 days after SAH, when signs of delayed cerebral vasospasm peak in this model and in humans; 12 days after SAH; and 28 days after SAH. Subarachnoid hemorrhage did not evoke changes in CSF or plasma levels of neuropeptide Y. Nine monkeys had arteriographic evidence of vasospasm on Day 7, but no change in neuropeptide Y levels occurred in plasma or CSF. In addition, neuropeptide Y levels did not change, even after resolution of vasospasm on Day 12 or Day 28. Neuropeptide Y levels were substantially higher in CSF than in arterial plasma (p less than 0.003 at each interval). No correlation was found between neuropeptide Y levels in CSF and in plasma. These results do not confirm a relationship between neuropeptide Y levels in the CSF or peripheral plasma and delayed cerebral vasospasm in SAH.

Analysis of Variance↗
PubMed1992

Is vasospasm related to proliferative arteriopathy?

Although proliferative arteriopathy has been postulated to play a role in the etiology of vasospasm after subarachnoid hemorrhage (SAH), histological and morphological studies examining cerebral vasospasm have produced conflicting results. To help settle this controversy, the authors used an in vivo label of cell division, bromodeoxycytidine, to assess cell proliferation in a primate model of SAH. Fifteen cynomolgus monkeys received a clot of either whole blood (11 animals) or red blood cells (four animals) placed around the right middle cerebral artery (MCA). On the day of surgery continuous intravenous infusion of bromodeoxycytidine was begun and continued until the animal was sacrificed immediately after arteriography on Day 7, 12, or 27 following surgery. Sections from the right and left MCA's were stained with a monoclonal antibody against bromodeoxcytidine, and labeled cells were counted. Arteriographic evidence of vasospasm occurred in nine monkeys on Day 7. On Day 12 and Day 27 no monkeys had persistent vasospasm. Placement of subarachnoid clot around the right MCA increased proliferative activity across all layers of the arterial wall. Most of the labeled cells were in the adventitia and the endothelium. Although there were more dividing cells in all layers of the right MCA than the left MCA (p < 0.01), the number of stained cells per section was limited (range 0.1 to 21.2, mean 8) and the occurrence of vasospasm was not associated with the number of dividing cells in the right MCA on Day 7, 12, 27, or for all days combined (p > 0.6). Cerebral vasospasm after SAH was not associated with the extent of proliferation of cells in the vessel wall, nor could the intensity of the limited proliferative changes have been responsible for narrowing of the vessel diameter.

Animals↗
PubMedDate not supplied

Transcranial Doppler ultrasound assessment of intracranial hemodynamics in children with diabetic ketoacidosis.

The pathophysiology of acute neurological complications of diabetic ketoacidosis (DKA) in children and adolescents is not completely understood. We sought to establish whether transcranial Doppler (TCD) was able to monitor the changes of cerebral blood flow regulatory mechanisms, as measured by cerebral blood velocities (CBF-V), Gosling's pulsatility index (PI), and cerebral vascular reactivity (VR), prior to and during treatment of DKA. The increased values of PI suggested an increase of intracranial pressure (ICP) due to the existence of cerebral vasoparalysis, based on the low values of VR prior to treatment and 6 hours after initiation of treatment. At 24 hours, the correction of hematocrit and pH was associated with a significant decrease of PI, suggesting a decrease of ICP, likely due to a return of vascular tone in response to the low PaCO2. This was further supported by an increase of VR in all patients. At 48 hours, when PaCO2 returned to normal, the PI remained low and the VR increased further, suggesting a complete reversal of vasoparalysis and a return of cerebral blood flow regulatory mechanisms.

Adolescent↗
PubMedDate not supplied

[Results of early surgical treatment of intracranial aneurysm. Preliminary report].

The authors report their preliminary experiences with early (within 72 hours after haemorrhage) operations in cases of intracranial aneurysms. Out of 131 patients operated on from April 1985 to March 1986 in the Department of Neurosurgery, Medical Academy in Warsaw 20 were qualified for surgical intervention immediately after haemorrhage. In 13 cases Nimodipine (Nimotop) was given locally during the operation and in the postoperative period. The schedule of drug administration is shown. In 15 cases (75%) a very good result was noted, in 3 (15%) major signs of focal brain damage were observed within 6 months after the operation. Two patients (20%) died. In 4 cases neurological focal signs developed 4-5 days after subarachnoid haemorrhage due to ischaemia confirmed with CT. The operative conditions during early operations, and the approach to the vessels at the base of the brain were as good as during delayed operations.

Adult↗
PubMedDate not supplied

[A case of angioma of the spinal cord].

A case of angioma situated in the lumbosacral spinal cord is described in a man aged 35 years. During 10 months of conservative treatment and rehabilitation therapy the condition of the patient deteriorated, paralysis of lower extremities developed. The angioma was diagnosed during myelography. The patient was treated surgically, the angioma was removed, and after the operation and rehabilitation therapy an improvement of the neurological state was obtained.

Adult↗