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Biomedical subjects

O R Blaumanis

Publications and source records attributed to O R Blaumanis.

7 recordsLinked to original sources
PubMed1992

Noninvasive fetal ECG mode fetal heart rate monitoring by adaptive digital filtering.

Beat-to-beat variability (BTBV) of the fetal heart rate (FHR) is considered an indication of the neural integrity and is an important prognostic indicator of fetal well-being. We report the initial evaluation of a recently developed abdominal fetal ECG (AFECG) mode of FHR monitoring using Adaptive Digital Filtering (ADF) to accurately obtain BTBV noninvasively. Five women in labor at term were monitored with the direct fetal scalp electrode (FSE) and simultaneously with the AFECG using ADF. A computer analysis of 3298 seconds (55 minutes) of data provided a one-to-one comparison of the R-R intervals. One analysis of the direct FSE data with a second simultaneous analysis from the same electrode, to serve as control, was compared with the noninvasive AFECG data. The study group has a standard deviation of only 1.50 bpm compared to 0.79 bpm for the control group. The AFECG method agrees with the direct FSE method within 1 bpm for 92.6% of the reported R-R intervals and within 2 bpm for 98.9% of the reported intervals. This new noninvasive AFECG technique with ADF provides a continuous record of instantaneous FHR and BTBV that may be relied upon to provide an accurate continuous clinical record. The reliability of the technique has yet to be determined over a wide range of subjects.

Computers↗
PubMed1990

Focal cerebral edema impedes convective fluid/tracer movement through paravascular pathways in cat brain.

Cerebral blood vessels are accompanied by longitudinal paravascular fluid pathways that communicate with the subarachnoid space. After infusion into the subarachnoid space, the tracer protein, HRP, distributes throughout the brain with such rapidity as to suggest that the paravascular fluid transport system serves to flush the entire brain parenchyma. However, it was found that the tracer is largely excluded from regions of experimental vasogenic brain edema as well as from remotely situated white matter in the cold-lesioned hemisphere. The results suggest that the persistence and spread of vasogenic edema may be related to an impairment or disruption of the normal paravascular fluid transport system of the brain.

Animals↗
PubMed1990

Rapid solute transport throughout the brain via paravascular fluid pathways.

Solutes in CSF have rapid access to ECS throughout the CNS (within 5-10 min). This occurs by solute/fluid influx through PVS around penetrating arteries, followed by longitudinal spread along the BL of capillaries to reach venules and veins. These paravascular pathways can be demonstrated light-microscopically by infusion of the tracer protein, HRP, into SAS and the subsequent localization of this probe molecule in brain sections using the sensitive histochemical method based on TMB. This unidirectional tracer/fluid movement along the intraparenchymal vascular network, with accompanying spread into the cerebral interstitium, appears to be facilitated by the pulsation of penetrating arterioles within their PVS with each cardiac contraction.

Animals↗
PubMed1977

Spinal cord injury. The role of vascular damage in the pathogenesis of central hemorrhagic necrosis.

We postulated that damage to the endothelial lining of the spinal cord vasculature is a major factor in the pathogenesis of the characteristic lesion of the spinal cord (progressive, central, hemorrhage necrosis) that occurs after acute trauma. Endothelial damage may occur as a result of primary injury to the vessels or after arterial spasm. This damageresults in deposition of platelets and formation of thrombi on the exposed subendothelial tissues and embolization of such thrombi to smaller vessels of the spinal cord parenchyma.

Animals↗