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Biomedical subjects

O R Blaumanis

Publications and source records attributed to O R Blaumanis.

15 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↗
PubMed1988

Physiologic parameters of the Cushing reflex.

The effects of increased intracranial pressure and blood gas tensions on systemic blood pressure were examined in this study. Intracranial pressure was raised hydrostatically and blood gas tensions, blood pressure, and respiration were monitored in anesthetized dogs. Small gradual increments in intracranial pressure resulted in increased cerebral venous carbon dioxide tension, followed by increased respiration, a gradual rise in blood pressure, and finally an increase in heart rate. The results of this study indicate that blood pressure changes appear to be determined by alterations in carbon dioxide tension following increases in intracranial pressure; small increases in intracranial pressure elicit a cluster of physiologic responses, all directed toward stabilization of local cerebral carbon dioxide tension.

Animals↗
PubMed1987

Adaptive filtering in ECG monitoring of the fetal heart rate.

There has long been an interest in noninvasively monitoring the fetal electrocardiogram (ECG). In the past twenty years a clinical need has developed to monitor the instantaneous fetal heart rate (FHR) and changes in the heart rate from one beat to the next, i.e., beat-to-beat FHR variability as well as an interest in understanding the development of cardiac arrhythmias. The purpose of this paper is to present initial results obtained from an Electrocardiographic Adaptive Processor (EAP) to noninvasively monitor in real-time continuous tracings of the fetal ECG, FHR, and FHR variability. Twenty-five sets of noninvasive fetal ECG data were collected from pregnant subjects during the third trimester of pregnancy using maternal abdominal paste-on electrodes. The fetal QRS amplitude and shape varied from 5 to 30 microvolts with fetal position, gestational age, and relative electrode configuration. Results have been obtained in three specific areas: 1) The development and initial testing of a microprocessor based Electrocardiographic Adaptive Processor (EAP) implemented as an FHR monitor has been completed. The EAP has been implemented to adaptively cancel, in real-time, the maternal ECG component from maternal abdominal ECG leads to provide a continuous tracing of the fetal ECG complex, or FHR and FHR variability. 2) Maternal and thoracic ECG data stored on computer disk were used to test the adaptive techniques to cancel the strong interfering maternal ECG. Studies continue to effectively reduce background electromyographic (EMG) noise. 3) Tracings of the fetal QRS complex, instantaneous FHR, and short term FHR variability have been obtained in real-time.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1985

Evidence for a 'paravascular' fluid circulation in the mammalian central nervous system, provided by the rapid distribution of tracer protein throughout the brain from the subarachnoid space.

The protein tracer, horseradish peroxidase (HRP), was infused into the lateral cerebral ventricles or subarachnoid space of anesthetized cats and dogs after insertion of a cisternal cannula to permit drainage of cerebrospinal fluid (CSF) and tracer solution. The intracerebral distribution of the tracer was then determined by light microscopy of serial brain sections after postinfusion intervals of 4 min-2 h. For the localization of HRP, sections were incubated with diaminobenzidine (DAB) or the much more sensitive chromogen, tetramethylbenzidine (TMB). The TMB reaction showed a consistent 'paravascular' distribution of tracer reaction product, within the perivascular spaces (PVS) around large penetrating vessels and in the basal laminae around capillaries, far beyond the termination of the PVS. After infusion of HRP over 4 min, arterioles were surrounded by the tracer, but capillaries and venules were usually less densely demarcated; by 6 min, however, the intraparenchymal microvasculature was outlined in toto throughout the forebrain and brainstem. Electron microscopy of sections incubated in DAB after 10 or 20 min HRP circulation confirmed the paravascular location of the reaction product, which was also dispersed throughout the extracellular spaces (ECS) of the adjacent parenchyma. Our results demonstrate that solutes in the CSF have access to the ECS throughout the neuraxis within minutes via fluid pathways paralleling the intraparenchymal vasculature. The rapid paravascular influx of HRP could be prevented by stopping or diminishing the pulsations of the cerebral arteries by aortic occlusion or by partial ligation of the brachiocephalic artery. The exchange of solutes between the CSF and the cerebral ECS has generally been attributed to diffusion, however, HRP enters the neuraxis along the intraparenchymal microvasculature far more rapidly than can be explained on this basis. This apparent convective tracer influx may be facilitated by transmission of the pulsations of the cerebral arteries to the microvasculature. We postulate that a fluid circulation through the CNS occurs via paravascular pathways.

Anesthesia, General↗
PubMed1985

A method for microscopic studies of cerebral angioarchitecture and vascular-parenchymal relationships, based on the demonstration of 'paravascular' fluid pathways in the mammalian central nervous system.

A new method is described for morphological studies of blood vessels and related cellular elements in the mammalian central nervous system (CNS). The tracer protein, horseradish peroxidase (HRP), in solution, is infused intraventricularly or intracisternally in anesthetized animals over 5-10 min. During this period, HRP in the subarachnoid space enters the perivascular spaces around penetrating arterioles and rapidly permeates the gliovascular basal laminae surrounding capillaries. After fixation by intravascular perfusion of aldehydes, brain sections are incubated with the highly sensitive chromogen, tetramethylbenzidine. Intraparenchymal blood vessels throughout the CNS are vividly demonstrated for light microscopy by HRP reaction product in their perivascular spaces or basal laminae. Correlative ultrastructural investigations of specific blood vessels and related parenchymal elements can be conducted using adjacent sections.

Animals↗
PubMed1982

Experimental cerebral vasospasm: resolution by chlorpromazine.

Vasospasm of the cat basilar artery was produced by electrical, mechanical, or chemical stimuli or by subarachnoid hemorrhage. The vasospasm induced by these stimuli was relieved by the topical application of chlorpromazine to the vascular wall. Chlorpromazine appears to be a nonspecific vasoparalytic agent. Unlike previously used substances, it is effective in resolving vasospasm caused by mechanical as well as chemical irritation.

Angiotensin II↗
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↗
PubMedDate not supplied

Cerebral venous blood gas tensions in elevated intracranial pressure.

Cerebral venous blood gas tensions were correlated with elevated intracranial pressure in spontaneously breathing dogs lightly anesthetized with nitrous oxide/halothane. Intracranial pressure was elevated by infusion of artificial cerebrospinal fluid into a lateral ventricle. Respiration and blood pressure were monitored. The results of these experiments indicate that cerebral venous carbon dioxide tension is increased in association with elevation in intracranial pressure. Moreover, it appears that cerebral venous pCO2 is effectively regulated at a mean of about 52 mm Hg over a wide range of intracranial pressure.

Animals↗
PubMedDate not supplied

CT characteristics of a transplantable canine glioma model: preliminary kinetic analysis.

Experimental brain tumors can be produced in dogs through the intracerebral injection of 3 X 10(6) live tumor cells in either neonates or adult animals. Tumors are visible by computed tomography on day 8 postinjection. Most tumors appear as ring lesions with central lucencies and shaggy borders. By postinjection day 12, tumor volumes increase more than 10 times; the cell cycling time is about 1-3 days. The initial doubling time is about 1-2 days and corresponds to the in vitro doubling time of about 24 hr. The use of computed tomography to perform noninvasive kinetic analysis deserves further study. The transplantable canine glioma model would appear to be ideal for this purpose.

Animals↗