PubMed Health⌕ Search

Biomedical subjects

M Rau

Publications and source records attributed to M Rau.

53 records · Page 3Linked to original sources
PubMed1990

Dose-dependent blood flow velocity changes in the Basal cerebral arteries following low-dose ketamine.

The effects of low-dose ketamine on blood flow velocity and pulsatility index (PI) in the basal cerebral arteries were studied in two groups of healthy volunteers (group A: 0.25 mg/kg, n = 10; group B: 0.5 mg/kg, n = 10) by means of a 2 MHz pulsed transcranial Doppler ultrasonic system (TCD) for an observation period of 70 min. In addition, mean arterial pressure (MAP), heart rate (HR), end-tidal CO2 (petCO2), and oxygen saturation (saO2) were recorded. The mean blood flow velocity (Vmean) increased significantly by 28% in group A and by 68% in group B within 2-9 min. In group B, the PI was reduced by 32% for a period of 2-7 min (p < 0.05). MAP (group A: -20%; group B: -26%) and HR (group A: -39%; group B: -54%) increased significantly (p < 0.05). Vmean and PI were significantly different between groups A and B, suggesting a dose-dependent stimulation of cerebral hemodynamics. The flow velocity increases cannot be entirely explained by systemic hemodynamic changes since there was no intergroup difference with respect to MAP and HR. No significant differences were observed with regard to petCO2 and saO2. With the assumption that the diameter of the insonated vessel is not changed by ketamine, the dose-dependent increase in Vmean with a concomitant decrease in PI may be interpreted as indicating an increase in cerebral blood flow.

Journal Article↗
PubMed1990

Transcranial Doppler sonography as a supplement in the detection of cerebral circulatory arrest.

The effects of compromised cerebral hemodynamics on intracranial blood flow velocity patterns (BFV) were studied by noninvasive transcranial Doppler sonography (TCD). Pulsatility index (PI) as an estimation of peripheral cerebral vascular resistance was additionally analyzed. TCD patterns were determined in 19 mechanically ventilated brain dead patients (group A) and 8 resuscitated or severely head injured patients (group B) with intermittent elevated intracranial pressure (ICP). Group A and B TCD data were compared to control measurements obtained in 20 healthy volunteers (group C). Normal TCD recordings (group C) were characterized by anterograde Doppler wave-forms with a predominantly high diastolic flow pattern and PI values of <1. In brain dead patients (group A), flow velocity profiles were significantly decreased. The flow curve consisted of low systolic anterograde spikes, while early diastolic flow components of low amplitudes revealed retrograde phases with a late diastolic zero flow. In some cases, total diastolic circulatory arrest was obtained. PI in brain dead patients was increased by a factor of 10 and was infinite in situations of zero net flow. The low systolic spikes and retrograde diastolic flow may be explained by the effects of reduced intracranial compliance due to increased intracranial pressure (ICP). The detection of bidirectional signals, indicating anterograde and retrograde movements of the blood column or low systolic spikes without diastolic signals, seems to be specific for the condition of brain death. Insonation of the basilar artery should be performed in order to exclude preserved perfusion of infratentorial brain regions during supratentorial circulatory arrest and vice versa. In group B patients, episodes of increased ICP predominantly affected the diastolic flow velocity component. In these patients, resistive Doppler signals with normal or reduced systolic peaks and decreased diastolic flow velocities were expressed as increases in PI. Noninvasive transcranial Doppler sonography appears to confirm cerebral circulatory arrest. Additionally, TCD may be of value for the early detection of impaired cerebral hemodynamics due to changes in intracranial compliance.

Journal Article↗
PubMed1990

[The effect of postural changes on cerebral hemodynamics during general anesthesia].

Anesthesia may compromise the regulation of systemic and cerebral hemodynamics following changes in body position. Sudden decreases in cerebral perfusion pressure due to changes from a horizontal to a head-elevated position may cause decreases in cerebral blood flow (CBF), particularly in patients with preexisting cerebrovascular disease. Transcranial Doppler sonography (TCD) permits on-line measurement of blood flow velocity (BFV) in human basal cerebral arteries, and there is evidence that monitoring of BFV may indicate relative changes in CBF. The present study compares the effects of changes from a horizontal to a head-elevated position on blood flow velocity in the middle cerebral artery (MCA) in 30 patients (ASA I) with different levels of steady state anesthesia (group A: n = 20, isoflurane = 1.0 vol% end-tidal; group B: n = 10, isoflurane = 0.4 vol% end-tidal; O2/N2O; FiO2: 0.3; 6 1/min). The MCA was insonated by transtemporal approach using a 2 MHz Doppler ultrasound system (TC2-64 B, EME) with a range-gating mechanism, adjustable sample volume depth, and flow direction discrimination. Systolic (Vsyst, cm/s) and mean flow velocity (Vmean, cm/s), pulsatility index (PI), mean arterial blood pressure (MAP, mmHg), heart rate (HR, b/min) and end-tidal CO2 (pet-CO2, mmHg) were recorded with the subjects lying flat (baseline values) and for 5 min following adjustment to a 35-40 degrees head-elevated position. There was a significant reduction of 25% for Vsyst from 79 +/- 17 cm/s (baseline) to 59 +/- 13 cm/s and a 33% decrease for Vmean from 52 +/- 9 cm/s (baseline) to 35 +/- 9 cm/s in group A immediately after repositioning.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Increase in blood flow velocity in the middle cerebral artery following low-dose ketamine].

Low-dose ketamine is recommended in patients requiring sufficient analgetic support in emergency situations. There is still controversy in the discussion on ketamine-induced effects on cerebral blood flow and intracranial pressure. We investigated the effect of 0.25 mg x kg-1 ketamine i.v. on the blood flow velocity in the basal cerebral arteries in 10 healthy volunteers by transcranial Doppler sonography (TCD). Peak and mean blood flow velocities, pulsatility index, arterial blood pressure, heart rate, oxygen saturation and end tidal carbon dioxide tension were measured during the study. There was a significant increase in the hemodynamic parameters and in blood flow velocities, paralleled by a decrease in pulsatility index and constant values for oxygen saturation and CO2-tensions following injection of ketamine. The results indicate a transient stimulation of the cardiocirculatory system with a concomitant reduction of the cerebral vascular resistance. The question of informative detection of intracranial hemodynamics following application of intravenous anesthetics will be discussed.

Adult↗
PubMed1987

Vanadate-stimulated NADH oxidation in microsomes.

Addition of vanadate, stimulated oxidation of NADH by rat liver microsomes. The products were NAD+ and H2O2. High rates of this reaction were obtained in the presence of phosphate buffer and at low pH values. The yellow-orange colored polymeric form of vanadate appears to be the active species and both ortho- and meta-vanadate gave poor activities even at mM concentrations. The activity as measured by oxygen uptake was inhibited by cyanide, EDTA, mannitol, histidine, ascorbate, noradrenaline, adriamycin, cytochrome c, Mn2+, superoxide dismutase, horseradish peroxidase and catalase. Mitochondrial outer membranes possess a similar activity of vanadate-stimulated NADH oxidation. But addition of mitochondria and some of its derivative particles abolished the microsomal activity. In the absence of oxygen, disappearance of NADH measured by decrease in absorbance at 340 nm continued at nearly the same rate since vanadate served as an electron acceptor in the microsomal system. Addition of excess catalase or SOD abolished the oxygen uptake while retaining significant rates of NADH disappearance indicating that the two activities are delinked. A mechanism is proposed wherein oxygen receives the first electron from NAD radical generated by oxidation of NADH by phosphovanadate and the consequent reduced species of vanadate (Viv) gives the second electron to superoxide to reduce it H2O2. This is applicable to all membranes whereas microsomes have the additional capability of reducing vanadate.

Animals↗
PubMedDate not supplied

Effects of succinylcholine and related substances administered into the medial preoptic area on the local EEG, body temperature, heart rate, galvanic skin resistance and biogenic amines.

Succinylcholine (Sch) which is a cholinergic neuromuscular blocker has been known to occasionally lead to episodes of malignant hyperthermia in swine and humans. In order to find whether it produces any hyperthermic effects through action on medial preoptic area, experiments were carried on by administering intracerebrally the chemical into the medial preoptic area through an in-dwelling cannula-cum-electrode in the free moving rat. The changes in body temperature and the local EEG were studied. For comparison purpose, the effects of carbachol, atropine and phenylephrine were also studied. Further, in the curarized state of no muscular activity, the effect of SCh on the preoptic area was again tested and also the changes in the other autonomic parameters of heart rate and galvanic skin resistance (GSR) were studied. It was observed that SCh given into preoptic area caused a clear hyperthermic effect. The effect was countered by prior administration of atropine into the site. After SCh the local EEG changed into a high amplitude slow wave format. The heart rate was not altered but the GSR increased by two-fold. Carbachol caused a rise in body temperature, heart rate and also GSR. SCh also caused a reduction in noradrenaline content of the hypothalamus by 23% while no change in dopamine and serotonin occurred. Serotonin increased by 28% in the brainstem with no change in the other amines. Septum showed an increase of noradrenaline and dopamine contents by 40% and 25% respectively. Keeping in view the monoaminergic connections and thermoregulatory role of the preoptic area, one may postulate that SCh could inhibit the warm sensors and the controls of the dual sympathetic mechanism which normally leads to an increase of sudomotor activity and a decrease of vasomotor activity, the inhibition resulting in rise of body temperature.

Animals↗