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Biomedical subjects

S Hoyer

Publications and source records attributed to S Hoyer.

At least 127 records · Page 7Linked to original sources
PubMed1977

Influence of systemic and cerebral vascular factors on the cerebrospinal fluid pulse waves.

In anesthetized, artificially ventilated dogs, the intracranial cerebrospinal fluid (CSF) pulse waves were studied simultaneously with the central aortic pressure, central venous pressure (CVP), and the sagital sinus pressure under physiological conditions and in normovolemic arterial hypotension and hypertension, in acute cardiac insufficiency of the right atrium, in raised intracranial pressure (ICP), and in arterial hypoxemia. The physiological CSF pulsations are shown to be mainly arterial in origin. In the diastolic phase, the descending part of the pulse curve can be modified by venous superpositions coinciding with the right atrial "A" wave. With increase of ICP the configuration of the CSF pulsations changes: the venous superpositions disappear and the waves become more and more arterial in shape. Furthermore, the pulse amplitude increases considerably. The same change can be observed when cerebral vessels are dilated by arterial hypoxemia. During cardiac insufficiency and consecutive increase of CVP, the CSF pulse curve is venous in shape and the right atrial "A" wabe predominates. In arterial hypotension, CSF pressure decreased. Conversely, in angiotensin-induced systemic arterial hypertension, CSF pressure and its pulse amplitude increased. It is concluded that both systemic arterial blood pressure and cerebrovascular reactivity are major determinants for the shape and the pressure amplitude of the intracranial CSF pulse waves. In the presence of cerebral vasodilatation, systemic arterial blood pressure may be an important factor in raising ICP and altering the brain tissue compliance, because cerebral vascular damping of the arterial pulse is diminished and the arterial pressure head may be directly transmitted to the cerebral capillary bed.

Animals↗
PubMed1977

Effect of pyritinol-GCl on blood flow and oxidative metabolism of the brain in patients with dementia.

In order to test whether and in what way pyritinon-HCl affects cerebral blood flow and oxidative metabolism in patients with organic brain disorders, the following parameters were measured in a group of 87 patients: cerebral blood flow using the Kety and Schmidt method, cerebral consumption of oxygen and glucose, and also CO2 and lactate ouptut. 45 out of the 87 patients were given pyritinol in a dose of 900 or 1000 mg/day, 42 out of 87 patients formed a control group and were given 500 mgof 5% laevulose i.v. daily for the average duration of the study of approximately 3 weeks. The results can be summarised as follows: 1. Cerebral blood flow and oxidative metabolism are changed in patients with organic brain disorders in different ways voth as regards quality and quanitity. Findings from earlier investigations could thus be confirmed. 2. When laevulose only was used, the parameters measured did not alter on average. In addition to deteriorations in the findings, spontaneous improvements or normalisationof previously disturbed cerebral blood flow and cerebral metabolism values were also abserved. 3. Pyritinol-HCl usually improved previously disturbed cerebral glucose metabolism significantly. An effect on disturbed cerebral blood flow or pathologically changed cerebral oxygen consumption was not found.

Adult↗
PubMed1976

Disturbed oxidative metabolism in organic brain syndrome caused by bismuth in skin creams.

Two patients are described with an organic brain syndrome thought to be due to bismuth (Bi) absorbed from a skin cream. Both patients had intellectual impairment and memory loss punctuated by periods of confusion, tremulousness, clumsiness, difficulty in walking, and myoclonic jerks. A similar clinical picture has been reported from Australia and France in patients taking insoluble bismuth salts by mouth. Bi was found in cerebral venous blood in both patients and in the cerebrospinal fluid in one. It is suggested that bismuth can cross the blood/brain barrier and disturb oxidative cerebral metabolism, because increased lactate production was found with decreased consumption of oxygen and glucose and lowered cerebral blood-flow.

Adult↗
PubMed1976

Cerebral blood flow and oxidative brain metabolism during and after moderate and profound arterial hypoxaemia.

In anaesthetized artificially ventilated dogs, the effect of graded arterial hypoxaemia on cerebral blood flow (CBF) and on the oxidative carbohydrate metabolism of the brain was tested. It is shown that the hypoxic vasodilatory influence on cerebral vessels is present even at moderate systemic hypoxaemia, provide that PaCO2 is kept within normal limits. At PaO2 of about 50 Torr, CBF increased from 56.6 to 89.7 ml/100g/min. With increasing cerebral hyperamia (CBF increased to 110.9 ml/100g/min, at PaO2 of 30 Torr), CMRO2 (4.2 ml/100g/min) was not significantly raised above its normal level (4.7 ml/100g/min) even with profound arterial hypoxaemia. This shows that CMRO2 levels are poor indices of hypoxic hypoxia. A disproportionately high increase in cerebral glucose uptake (CMR glucose levels rose from 4.4 to 10.4 mg/100g/min) and enhanced cerebral glycolysis (CMR lactate changed from 0.2 to 1.6 mg/100g/min) at moderately reduced PaO2 (50 Torr) indicated early metabolic changes which became more marked with further falls in arterial oxygen tension. However, 60 minutes after restoration of a normal PaO2 level, CBF and brain metabolism were found to have completely recovered. It is concluded that a short period of profound systemic hypoxaemia does not produce long lasting metabolic and circulatory disorders of the brain provided the cerebral perfusion pressure does not vary, and is kept at normal levels.

Animals↗
PubMed1975

Comparative studies of the electroencephalogram and the cerebral oxidative metabolism in patients with liver cirrhosis.

In two groups of patients with liver cirrhosis and normal EEG (Group A) and with pathological EEG (Group B) it was possible to demonstrate a correlation between the severity grade of the EEG changes, the livertypical deviations of serum chemistry and alterations in cerebral oxidative metabolism. The metabolism of the brain showed a reduced oxygen consumption and carbon dioxide output in the patients with pathological EEG changes. All patients showed a raised glucose uptake, an increased lactate release, a raised ammonia uptake and glutamine output. These findings in patients with liver cirrhosis indicate a disturbance of the oxidative energy metabolism of the brain with secondary intensification of glycolysis. Pathological changes in the EEG only appear if the oxygen consumption of the brain is limited (as in the patients of Group B). These EEG changes have a poor prognosis in respect to life expectancy. With consideration of the data from animal experiments and the reported results of cerebral blood flow and oxydative metabolism in patients with liver cirrhosis it might be assumed that liver insufficiency with elevated serum ammonia results in a deranged oxydative cerebral metabolism which might explain hepatic encephalopathy.

Ammonia↗
PubMed1975

[Blood flow and oxidative metabolism of the brain in patients with dementia (author's transl)].

The purpose of this retrospective study was to investigate how the blood flow and oxidative metabolism of the brain was changed in dementia and the influence of the age factor. Cerebral blood flow (CBF) was measured in 115 patients aged from 40 to 83 years by means of the Kety-Schmidt technique with the modification of Bernsmeier and Siemons. The cerebral metabolic rates of oxygen and CO2 were determined by the van Slyke method and by gaschromatography respectively and of glucose and lactate by standard enzymatic methods. All cases of dementia due to head injuries, cerebral infections, cerebral infarctions, exogenous or endogenous intoxications or circulatory diseases were excluded from this study, but no classification of the dementias was made. Statistical calculations were carried out by means of the analysis of variance for a two-way design. Cerebral blood flow did not show a normal distribution curve but was at least triphasic; CBF in demented patients was either lower than normal, normal or higher than normal. The distribution curves showed further that a low cerebral blood flow of mean 32.5 ml/100 g min coincided with a low CMR oxygen of 2.50 ml/100 g min; however, CMR glucose was either low (2.50 mg/100 g min), or nearly normal (4.50 mg/100 g min) or elevated (7.50 mg/100 g min). A normal (45.0 ml/100 g min) or enhanced (62.5 ml/100 g min) CBF correlated with a CMR oxygen which was either decreased to 2.75 ml/100 g min or increased to 4.75 ml/100 g min; CMR glucose was either decreased to 1.50 mg/100 g min, or nearly normal (4.50 mg/100 g min), or was elevated to 6.50 and 10.50 mg/100 g min with respect to the peaks of the distribution curves. It is assumed that the variability of the findings with respect to the blood flow and oxidative metabolism of the brain in dementia is due to different pathophysiological and pathobiochemical disturbances in the brain. A significant influence of age on CBF and metabolism in patients with dementia was not found.

Adult↗
PubMed1975

[Changes in cerebral blood flow and oxidative cerebral metabolism after extensive acute head trauma (author's transl)].

Total cerebral blood flow and oxidative cerebral metabolism were measured at normal pCO2, hypocapnia and hypercapnia in 15 unconscious patients in the acute phase after head trauma. In the basal position (normal CO2) measurements were within normal limits and did not correspond to the severity of the clinical picture. But on altering arterial pCO2 there were market changes in oxidative cerebral metabolism, which suggests an abnormal cerebral regulatory mechanism. Measurement of the same functions 14 days later indicated, on the one hand, persistence of changes, but, on the other, a return to normal of previously markedly elevated cerebral glucose uptake. Comparing cerebral blood flow and metabolism between patients who survived and those who died in the acute phase after brain damage, there were no significant differences.

Adult↗
PubMed1975

The effect of carbon dioxide on cerebral blood flow and cerebral metabolism in dogs.

In 11 normally oxygenated, normotensive mongrel dogs, blood flow and oxidative metabolism of the brain was studied during normocapnia and during respiratory alkalosis and respiratory acidosis. During respiratory alkalosis (mean PaCO2 17.8 mm Hg) CBF decreased significantly from 61.0 to 33.9 ml/100 g/min (44%) while arteriovenous-substrate differences increased and the rates of oxygen and glucose metabolism remained constant. Cerebral venous-arterial difference of lactate was increased significantly as compared with the resting state. During hypercapnia CBF increased significantly from 61.0 (resting state) to 115.7 ml/100 g/min (89%) (mean PaCO2 64.7 mm Hg). The arteriovenous-substrate differences decreased while the cerebral metabolic rates remained constant. The data show that the relationship between PaCO2 and CBF in the range 20-65 mm Hg PaCO2 is expressed by a linear relationship: y = 2.88 + 1.69x; in this range, the oxidative metabolism of the brain is unchanged and the increased cerebral lactate production in respiratory alkalosis is not necessarily linked to tissue hypoxia.

Acidosis, Respiratory↗
PubMed1975

Blood flow and oxidative metabolism of the brain in patients with schizophrenia.

55 patients with schizophrenia were divided into three groups according to the clinical symptoms: (1) productive schizophrenias, i.e. patients with hallucinations, catatonic excitation and stupor; (2) paranoia and schizophrenia simplex, and (3) non-productive schizophrenias, i.e. patients with schizophrenic defects and hebephrenia. Total cerebral blood flow (CBF) and the rates of cerebral oxygen, carbon dioxide, glucose and lactate metabolism were investigated. Patients with productive schizophrenias displayed a significant increase in CBF (to an average of 101.4 ml/100 g min), CMR oxygen (to an average of 6.26 ml/100 g min) and CMR glucose (to an average of 12.11 mg/100 g min), i.e. CBF and CMR oxygen nearly doubled and CMR glucose more than doubled in comparison with normal findings. In patients with paranoia and schizophrenia simplex CBF and oxidative metabolism did not vary much and were within the normal range. Non-productive schizophrenias showed a significant decrease in CBF (to an average of 36.7 ml/100 g min), CMR oxygen (to an average of 2.20 ml/100 g min) and CMR glucose (to an average of 3.86 mg/100 g min) in comparison with both other groups of schizophrenias and the group of healthy young men. The results demonstrated variations in CBF and oxidative metabolism of the brain in patients with distinct types of schizophrenia. It was possible to find a correlation between the mental state of the psychosis on the one hand and CBF and metabolism on the other. The high CBF and metabolic rates of the brain in productive schizophrenias might be due to disturbances in the cerebral metabolism of biogenic amines.

Adolescent↗