[Severe deglutition disorders in a patient with a mediastinal space-occupying lesion].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Hartmann.
Explore the source record for details and available documents.
Vascular relaxation in rabbit aortic preparations by acetylcholine is endothelium-dependent. Because of the short half-life of the endothelium-derived relaxing factor(s) (EDRF), a constant source of this material is necessary to study its effect in perfused hearts or hearts in situ (reported half-life 6-50 sec). To investigate the effect of EDRF(s) on the large coronary arteries and the resistance vessels of the isolated working rabbit heart, freshly harvested porcine endothelial cells were used. The cells were stimulated with acetylcholine to produce EDRF(s). To extend the half-life of EDRF, superoxide dismutase was added to the cell suspension. Left atrial infusion of these cells increased coronary flow and reduced total coronary resistance. No significant effect on the diameter of the endothelium-deprived obtuse marginal coronary artery was noted. The vasoconstrictor effect on resistance vessels of topically applied histamine was significantly reduced during the infusion of activated endothelial cells. It can be concluded that EDRF(s) released from freshly harvested endothelial cells increases coronary flow and diminishes total coronary vascular resistance in the working heart. In this preparation coronary arterioles are more sensitive to EDRF(s) than large coronary arteries. EDRF may contribute to the regulation of regional myocardial flow.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
After supratentorial infarction crossed cerebellar diaschisis has been described. This report concerns the rare phenomenon of crossed cerebral diaschisis in cerebellar infarction. Relative distribution of cerebral and cerebellar blood flow was measured using three-dimensional, qualitative single-photon-emission-computed-tomography (SPECT) with a rotating gamma camera and 123I-IMP. Regional cerebral blood flow was calculated with the two-dimensional, quantitative 133Xe-inhalation-technique. Reduced uptake was observed in the left cerebral hemisphere (-13.9%) contralateral to the cerebellar infarction with the most marked reduction in the left premotor region (-21%). This might be explained by the functional depression of cerebello-ponto-thalamo-cerebral pathways.
Perfluorochemicals are widely used in clinical and experimental studies as volume expanders with high oxygen carrying capacity. We noticed that contractions of rabbit aortic strips, induced by norepinephrine, were inhibited in FC-43 emulsion as compared to Krebs-Henseleit solution (KH). To study this inhibition, a comparative evaluation was made of the contractile responses of norepinephrine, serotonin and histamine in FC-43 emulsion and KH. The effect of these agents was significantly diminished in FC-43 emulsion; concentration-response curves were shifted to the right and the maximum response was diminished. A search was made for the individual constituents of FC-43 responsible for diminution of contraction of vascular smooth muscle. After centrifugation of FC-43 emulsion, the supernatant caused a reduction of contractility and reduced EC50-values of norepinephrine to the same degree as the fully constituted emulsion. This excluded perfluorotributylamine, the oxygen carrying particles, as being responsible for this inhibition. When the detergent Pluronic F-68 was added to KH in concentrations equal to that in FC-43 emulsion, inhibition of contraction occurred and EC50-values increased. Contractions induced by norepinephrine were equally inhibited by the addition to KH of a volume expander, hydroxyethylstarch, in a concentration equal to that in FC-43 emulsion. It is concluded that FC-43 emulsion inhibits vasoactive agents and attenuates its pharmacologic effects on vascular smooth muscle. The fractions of FC-43 emulsion responsible for inhibiting the effect of vasoactive agents are Pluronic F-68 and hydroxyethylstarch.
A controlled study of the effect of hypervolaemic haemodilution on cerebral blood flow (CBF) was performed using 10% hydroxyethylstarch (HES) in 27 patients with acute cerebral ischaemia. Of the patients, 12 were randomly allocated as controls without HES infusion and 15 received 500 ml HES daily, infused over a period of 5-7 h, for 7 days. CBF was measured on days 1, 2 and 7 by the xenon 133 inhalation method and calculated as initial slope index. In the HES-treated group, CBF increased in both hemispheres (P less than 0.001) from day 1 to day 2 and, in addition, in the infarcted hemispheres from day 2 to day 7 (P less than 0.01). In the control group, the hemispheric flow of the involved side had decreased (P less than 0.001) by day 2 and had not significantly changed by day 7; however, in the contralateral hemisphere flow did not change. In hypaemic regions the increase in flow was larger than in other regions in both groups. Regional flow had increased more in the HES-treated group than in controls at both day 2 (P less than 0.01) and day 7 (P less than 0.002). Hypervolaemic haemodilution with HES was able to improve hemispheric and regional flow significantly, particularly in infarcted hemispheres and hypaemic regions with acute cerebral ischaemia.
Regional cerebral blood flow (rCBF) was measured using the inhalation xenon 133 technique in 25 patients undergoing superficial temporal artery-middle cerebral artery anastomotic surgery. rCBF was measured once before and 3 times after operation, up to one year. Data were compared to rCBF-measurement in 16 patients with similar diagnosis, age distribution and medical treatment except that they were not operated on. Mean rCBF increased in some patients 4-8 weeks after surgery on the ipsilateral side. Compared to the non-surgical patients mean rCBF at this time was higher over both hemipheres. However, taking a flow increase of at least 15% as being significant only one third of all patients presented with a significant flow increase. Regional flow data indicated that the amount of hypoaemic areas in the operated side decreased significantly. Areas with normal flow increased in number from CBF 1 to the 4-8th week. There were no significant changes in flow distribution over the contralateral side. It was concluded that extracranial-intracranial bypass improves flow in patients with TIA or PRIND respectively only in some cases. Also a return to normal flow distribution can be achieved in only a few cases.
From the relationship between the degree of air pollution due to tobacco and its acute effects on healthy persons it is possible to estimate the still tolerable level of air pollution for healthy adults. The results and conclusions of the studies published by now on acute effects of passive smoking on patients with bronchial asthma are partially contradictory and do not allow a reliable estimation of the upper limit of tobacco smoke exposure for this particularly sensitive group. Because of methodological problems in studies with symptomatic asthmatics, further studies should be conducted which investigate patients with hayfever and asthma out of the pollen season, clinically healthy subjects with nonspecific bronchial hyperreactivity upon pharmacological challenge, and subjects who claim sensitivity to tobacco smoke.
Cerebral blood flow (CBF) and hemorheological parameters, such as hematocrit, plasma viscosity, and erythrocyte aggregation, were measured before and up to 7 h after 60-min infusions with 10% hydroxyethyl starch (HES), or 0.9% NaCl solution and 10% low molecular weight dextran (LMWD) in a total of 12 normal baboons. Infusion of HES increased CBF up to 48% from the resting level, and decreased hematocrit without an increase in plasma viscosity. Infusion of LMWD decreased hematocrit with an increase in CBF of up to 9.6%, but increased plasma viscosity at the same time. The disaggregating effect for erythrocytes was rather more obvious with LMWD than with HES but without significant difference between them. These data show different rheological effects with infusions of HES and LMWD on the physiological conditions of normal baboons.
Studies were carried out to demonstrate the presence of the endothelium derived relaxing factor (EDRF) in coronary arteries in situ and the effect of hydroquinone on this factor. The studies revealed the presence of EDRF in coronary arteries of rabbit hearts remaining in situ. EDRF was inactivated by left atrial injection of hydroquinone. In situ constriction of coronary arteries by vasopressin was markedly increased following exposure to hydroquinone, and the dilatory response to acetylcholine was absent. The experiments confirm the presence of the endothelium derived relaxing factor in coronary arteries in situ and its inactivation by hydroquinone.
Isolated rabbit coronary arteries, aortic strips, and a working rabbit heart preparation were used to assess the positive inotropic and vasodilator effects of a newly developed positive inotropic compound, CI 914. The substance had a relaxing effect on histamine preconstricted coronary arteries and aortic strips. At concentrations of 10(-4) mol.litre-1 the relaxing effect on the coronary arteries was significant only at a histamine concentration of 3 x 10(-4) mol.litre-1 (p less than 0.01) whereas at a concentration of 10(-3) mol.litre-1 the relaxing effect was significant at histamine concentrations of from 3 x 10(-5) mol.litre-1 to 3 x 10(-4) mol.litre-1. Aortic strips were more sensitive to the relaxing effect of CI 914, which was significant with 10(-4) mol.litre-1 at histamine concentrations of 3 x 10(-6) to 3 x 10(-4) (p less than 0.05 to p less than 0.01). In the isolated working heart preparation topically sprayed histamine significantly increased total and large coronary artery resistances (p less than 0.001 and p less than .01). This effect was significantly reduced (p less than 0.01 and p less than 0.02) when CI 914 10(-4) mol.litre-1 was present in the perfusion fluid. These findings show that the phosphodiesterase inhibitor CI 914, a positive inotropic agent, induces vasodilation in isolated coronary arteries and aortic strips of the rabbit and reduces the constriction of coronary arteries induced by histamine in the isolated working rabbit heart preparation.
The nitrogenase activity of the microaerophilic bacteria Azospirillum brasilense and A. lipoferum was completely inhibited by 2.0 kPa of oxygen (approximately 0.02 atm of O2) in equilibrium with the solution. The activity could be partially recovered at optimal oxygen concentrations of 0.2 kPa. In contrast to the NH4+ switch off, no covalent modification of the nitrogenase reductase (Fe protein) was involved, as demonstrated by Western-blotting and 32P-labeling experiments. However, the inhibition of the nitrogenase activity under anaerobic conditions was correlated with covalent modification of the Fe protein. In contrast to the NH4+ switch off, no increase in the cellular glutamine pool and no modification of the glutamine synthetase occurred under anaerobic switch-off conditions. Therefore, a redox signal, independent of the nitrogen control of the cell, may trigger the covalent modification of the nitrogenase reductase of A. brasilense and A. lipoferum.
Effects of hypocapnia on cerebral oxygen consumption (CMRO2) and blood flow (CBF) in cerebral ischemia were studied in 19 patients. The CMRO2 did not change significantly during hypocapnia within the whole group of patients, because 10 out of 19 cases showed a decrease (p less than 0.001) and other 9 showed an increase (p less than 0.01) of CMRO2 during hypocapnia. The first 10 showed higher resting CMRO2 (p less than 0.001) and arteriovenous differences of oxygen content (AVDO2; p less than 0.02) than the other 9. However, the resting CBF and CO2 reactivity to hypocapnia were not different between them, and clinical situations were also similar. A dissociation between flow and metabolism was suggested in the first 10 with rather preserved CMRO2, while reduced metabolic demands were suggested in the other 9. Different responses of CMRO2 to hypocapnia are expected in cerebral ischemia, i.e. in cases with rather preserved CMRO2 it decreases despite an AVDO2 increase, suggesting a capability of CMRO2 to respond to CBF reduction, while it increases in cases with more decreased CMRO2, as the AVDO2 increase exceeds the CBF reduction to maintain the decreased CMRO2 for a further CBF reduction. The vascular CO2 reactivity, therefore, might be maintained to be constant between these patients.
Isolated supraclinoid occlusive disease of the internal carotid artery is a rare cause of cerebral ischemia. The authors of the only review of this subject concluded that it is caused predominantly by factors other than atherosclerosis. We examined 6 patients with isolated supraclinoid occlusive lesions. Five of them had one or more risk factors for atherosclerosis. Thus, the isolated stenosis of that part of the internal carotid artery does not seem to represent a particular pathologic entity.
The effect of nisoldipine on coronary vascular resistances, cardiac performance and myocardial oxygen consumption was determined. Rabbit hearts were perfused with a perfluorochemical (FC-43) emulsion. Endothelium was removed from the obtuse marginal and the upper portion of the anterior descending coronary artery. Changes in the internal diameter of these arteries were visualized using injection of Patent Blue Dye (color arteriography). Mean internal diameter of coronary arteries and surface area/unit length were computer calculated. Nisoldipine reduced the constriction of coronary arteries and the decrease on coronary flow induced by histamine. Nisoldipine abolished or reduced the decrease in cardiac output, LVESP, dP/dt and myocardial oxygen consumption. The results demonstrate that in the supported rabbit heart preparation, nisoldipine is an effective dilator of large subepicardial coronary arteries, deprived of endothelial lining, and counteracts constriction of coronary resistance vessels. As a consequence nisoldipine improves performance of the ischemic myocardium.
Vascular relaxation in rabbit aortic preparations induced by acetylcholine is endothelium-dependent. The nature of the endothelium-derived relaxing factor (EDRF) has not been ascertained because it is very labile (reported half-life 6-50 seconds). To obtain a stable source of EDRF, a system was developed in which the relaxing factor was continuously produced by freshly harvested porcine endothelial cells. Endothelial cells were collected from aortas by exposing the endothelial lining to collagenase 0.1%. Cells were washed and concentrated by repeated centrifugation to obtain a high cell count (7.2 X 10(6) cells/ml). Endothelium-deprived aortic strips from rabbits were incubated in these cells suspended in tissue culture medium and fetal calf serum. The strips were precontracted with histamine. Acetylcholine was added to induce EDRF release. Significant relaxation of endothelium-deprived aortic strips was observed. Superoxide dismutase, an enzyme known to protect EDRF against inactivation, caused further relaxation, which was inhibited by the addition of hemoglobin, an agent known to inhibit the relaxing action of EDRF. Even without the addition of acetylcholine, hemoglobin caused contraction of the denuded aortic strips in suspension of porcine endothelial cells, demonstrating spontaneous EDRF release. Hemoglobin had no effect in cell-free medium. Endothelial-cell-dependent relaxation occurred without attachment of endothelial cells to the endothelium-deprived aortic strips: when the cell suspension was replaced by cell-free medium, relaxation did not occur after acetylcholine. Scanning electron microscopy showed no attachment of endothelial cells to the subendothelial layer. It can be concluded that freshly harvested endothelial cells produce endothelium-derived relaxing factor with an without stimulation by acetylcholine.
Explore the source record for details and available documents.