Biomedical subjects
Publications and source records attributed to E Alberti.
Using a computerized gamma camera regional cerebral blood flow and regional cerebral blood transit time are measured after injection of Xenon 133 and Technetium 99m respectively into the internal carotid artery. Equipment, technical procedures and methodology are described. Typical cases are presented to describe the usefullness of this procedure.
Continuous monitoring of the cerebrospinal fluid pressure and observation of the pressure during intrathecal infusion of normal saline at two rates were performed in patients with communicating hydrocephalus and cerebral atrophy of other causes. Constant or temporarily increased cerebrospinal fluid pressure was observed only in communicating hydrocephalus. Reduction of intracranial pressure by a ventriculoatrial shunt was associated with clinical improvement. The intrathecal infusion test was capable of detecting reduced absorption of cerebrospinal fluid if more than one infusion rate was employed. Using both tests it is easier to determine which patients with communicating hydrocephalus should be treated with a shunt operation.
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.
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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.
The combination of Klippel-Trénaunay-Weber syndrome (KTWS) with intracranial vascular malformations is documented by angiography in a 25 year old man with the classical features of KTWS: systematized naevi, hypertrophy of the right side, and varicosis. In addition, the syndrome was associated with "cuts laxa", a coincidence of somar rarity. The patient suffered from an ischaemic infarct of the brain stem with several neurological deficits.
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Using a gamma camera and the stochastic method, regional cerebral blood flow was measured in a patient with the diagnosis of idiopathic orthostatic hypotension. Blood pressure was altered by tilting the patient in supine position head-up and head-down. A partial defect in the autoregulation and CO2 sensitivity was found. Sensitivity to Norepinephrine was checked by intravenous infusion of 0.02 mug/min/kg body weight. An immediate marked rise in blood pressure was observed. Clinical symptoms, therapeutic guidelines, and histopathological findings are discussed.
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.
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Toxoplasmic encephalitis (TE) is a mayor cause of central nervous system infection in patients with acquired immunodeficiency syndrome (AIDS). Toxoplasma antibodies were detected in 56 of 79 patients with AIDS (71%), in the present study. Fourteen out of 57 seropositive patients developed TF (25%) and had Toxoplasma gondii antigen detected in their urine. For this, most of them received an effective therapy, with the subsequent disappearance of the symptoms and discontinuity of excretion of the T. gondii antigens. Our results suggest that the monitoring of T. gondii antigen in the urine of AIDS patients may be useful to decide on the proper time for therapy, as well as to avoid the beginning of neurologic signs in these patients.
A simple and rapid staphylococcal coagglutination test for the detection of Toxoplasma gondii antigens in mice urine is described. A suspension of protein-A containing Staphylococcus aureus coated with rabbit hyperimmune serum was used as reagent. The sensitivity of the antigen assay was found to be at least 118 ng of the antigen protein per ml. No coagglutination was observed when the reagent was challenged against antigenic solutions of other parasites. The suitability of the method for detecting antigens of T. gondii in urine samples was studied by experimental toxoplasma infection in mice. Before the staphylococcal test, the urine samples were double serially diluted in 0.1 M PBS. From the second day on all samples from infected mice were positive at 1/16 dilution. At this dilution, all samples from non infected mice were negative or did not produce coagglutination. This method might be used in the rapid etiological diagnosis also in human cases of acute toxoplasmosis.