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Biomedical subjects

R Dietz

Publications and source records attributed to R Dietz.

At least 253 records · Page 14Linked to original sources
PubMed1985

[Radiotherapy of paraplegia caused by extramedullary hematopoietic tissue].

The presentation by computed tomography of an extramedullar epidural intraspinal hemopoisis has only been described sporadically. It has been possible to visualize by CT-scans the regression under radiotherapy of a sensory and motor paraplegia in a 17 years old patient with beta-thalassemia major. The central nervous system (thoracic and lumbar zone as well as os sacrum) was exposed to a total reference dose of 30 Gy which was administered within twenty days by a 60Co unit in single doses of 2 Gy each. From 4 Gy on, the paraplegic symptoms regressed continuously. The control CT taken after 26 Gy- the paraplegia had completely disappeared at this time-showed a significant regression of the intraspinal soft tissue masses. Radiotherapy is very important in the treatment of this disease. A direct correlation is found between clinical symptoms and CT-presentation.

Adolescent↗
PubMed1985

[Experience in the use of face masks for radiotherapy of head and neck tumors].

By means of positioning and fixation aids, the precision and reproducibility of irradiation fields in radiotherapy of malignant tumors of the head and neck can be considerably improved. Face masks made of different synthetic materials have proved to be a practicable solution of this problem. In our hospital we have developed and tested a simple and not expensive possibility of manufacturing the masks with "Baycast" (producer: Bayer AG Leverkusen). The material is generally well tolerated by the patients, and the head is sufficiently fixed. An increased incidence of radiogenic dermatitides is caused by the overlapping of the depth dose of the Co-60 gamma radiation due to additional secondary electrons emanating from the mask material. This effect can be partly prevented by cutting out the irradiation fields in the masks.

Cobalt Radioisotopes↗
PubMed1984

Modulation of sympathetic vasoconstriction by potassium.

A high-sodium diet accelerates the rise in blood pressure in stroke-prone spontaneously hypertensive rats (SHRSP). The blood pressure-increasing effect of sodium loading is associated with the following abnormalities in noradrenaline metabolism: (a) noradrenaline release from sympathetic nerve endings is facilitated (especially after stimulation, such as exposure to cold); (b) noradrenaline inactivation is reduced mainly as a consequence of diminished neuronal uptake of noradrenaline; and (c) the sensitivity of vascular smooth muscle to noradrenaline is enhanced. These changes in noradrenaline metabolism are partially reversed when the concentration of potassium in a high-sodium diet is increased from 100 to 250 mmol K+/kg diet. That is, the neuronal uptake of noradrenaline is improved, the sensitivity of vascular smooth muscle to noradrenaline is attenuated, and the release of noradrenaline into the plasma is reduced. The reversal of abnormalities in noradrenaline metabolism is accompanied by a substantial blood pressure reduction following potassium repletion in SHRSP. Hence, the addition of potassium to the diet may be regarded as an antihypertensive measure which affects noradrenaline metabolism in such a way that sympathetic vasoconstriction is attenuated.

Animals↗
PubMed1984

Effects of alpha- and beta-adrenoceptor blockade on the neurally evoked overflow of endogenous noradrenaline from the rat isolated heart.

beta-Adrenoceptor blockade by propranolol (4 X 10(-6)M) was without effect on the overflow of endogenous noradrenaline from the isolated heart of the rat induced by stimulation of sympathetic nerves for 1 min at 1 and at 4 Hz. The increase in heart rate in response to such stimulation was abolished by propranolol treatment. alpha 2-Adrenoceptor blockade by yohimbine (10(-6)M) induced approximately a two fold increase in the overflow of endogenous noradrenaline induced by stimulation of sympathetic nerves for 1 min at 1 and at 4 Hz. A combination of yohimbine (10(-6)M) and desipramine (10(-7)M) induced a more than 3 fold increase in the overflow of endogenous noradrenaline produced by sympathetic nerve stimulation at 1 and at 4 Hz. Heart rate increases produced by such stimulation were intensified. These results provide no evidence for the feedback stimulation of presynaptic beta-adrenoceptors in this preparation. The action of alpha-2-blockade was equipotent at stimulation frequencies of 1 and 4 Hz.

Animals↗
PubMed1984

Antihypertensive effect of the GABA receptor agonist muscimol in spontaneously hypertensive rats. Role of the sympathoadrenal axis.

The antihypertensive action of central GABA-ergic stimulation was investigated in conscious stroke prone spontaneously hypertensive rats. Injection of the potent GABA agonist muscimol (0.01-1 microgram) into the lateral brain ventricle (icv) lowered mean arterial blood pressure (192.1 +/- 8.4 mm Hg) dose-dependently in stroke prone spontaneously hypertensive rats with a maximal fall of -52.7 +/- 5 mm Hg lasting for about 90 minutes. This was accompanied by bradycardia and sedation. Pretreatment with atropine (2 mg/kg, ip, or 15 micrograms/kg, icv) did not significantly influence the muscimol-induced fall in mean arterial pressure. In normotensive (109.3 +/- 1.9 mm Hg) Wistar-Kyoto controls, the maximal decrease in mean arterial pressure was -12.1 +/- 1.6 mm Hg from 109.3 +/- 1.9 mm Hg, and the duration of the effect was much less than in stroke prone spontaneously hypertensive rats, Following 1 microgram muscimol, icv, plasma noradrenaline did not fall significantly in stroke prone spontaneously hypertensive and Wistar-Kyoto rats, but in stroke prone spontaneously hypertensive rats, plasma adrenaline was fully suppressed (from 118.1 +/- 24.2 to 22.8 +/- 5.7 pg/ml) throughout the depressor response. The efferent sympathetic nervous activity as directly recorded from the n. splanchnicus was similar in conscious stroke prone spontaneously hypertensive and Wistar-Kyoto rats, and was moderately reduced in both strains by 1 microgram muscimol, icv.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1984

Release of endogenous catecholamines in the ischemic myocardium of the rat. Part A: Locally mediated release.

The accumulation of endogenous catecholamines within the extracellular space of the ischemic myocardium has been studied in the isolated perfused (Langendorff) heart of the rat subjected to various periods of complete ischemia, with subsequent collection of the reperfusate. Catecholamines and deaminated metabolites were measured by radioenzymatic methods, or high pressure liquid chromatography. Ischemic periods of less than 10 minutes are not associated with an increased overflow of catecholamines or metabolites. Longer periods of ischemia are accompanied by the overflow of noradrenaline and its deaminated metabolite 3,4-dihydroxyphenylglycol. This overflow increases with lengthening of the preceding ischemic period (10 minutes: 2.5 +/- 0.6, 20 minutes: 209.8 +/- 17.2, 60 minutes: 1270.5 +/- 148.1 pmol noradrenaline/g heart). Noradrenaline concentration is highest during the first minute of reperfusion, suggesting that the noradrenaline detected during reperfusion is released into the extracellular space of the myocardium during ischemia and is subsequently eluted. Experiments with variation of extracellular calcium concentration and with neuronal uptake (uptake1) blocking agents suggest that different mechanisms of catecholamine release are acting during the course of ischemia. A calcium-independent carrier-mediated efflux of noradrenaline from the nerve terminals is of major importance, using the same carrier as is normally responsible for transporting noradrenaline from the synaptic clefts into the neuronal varicosities. Thus, various uptake1-blocking agents diminish the noradrenaline overflow following ischemic periods of between 10 and 40 minutes. The noradrenaline overflow following longer periods of ischemia is unaffected by uptake1-blocking agents, and additional noradrenaline release at this time is probably consequent upon dissolution of cell membranes. Overflow of adrenaline and dopamine occurs to a minor degree (less than 5% of the corresponding noradrenaline overflow), and only after ischemic periods of more than 15 minutes.

Animals↗
PubMed1984

Release of endogenous catecholamines in the ischemic myocardium of the rat. Part B: Effect of sympathetic nerve stimulation.

The contribution of centrally originating sympathetic activity to the myocardial extracellular accumulation of noradrenaline during the early phase of ischemia has been assessed in a perfused (Langendorff) rat heart preparation isolated except for its sympathetic innervation. A 10-minute electrical stimulation (4 Hz, 5 V) of the left cervicothoracic ganglion during normal perfusion causes the overflow of 177.5 +/- 13.7 pmol noradrenaline/g heart, whereas such stimulation during ischemia liberates only 21.5 +/- 3.6 pmol/g (collected during reperfusion). When neuronal reuptake is blocked by desipramine, corresponding values are 321.5 +/- 22.5 pmol/g (normal flow) and 151.8 +/- 22.4 pmol/g (ischemia). After combined blockade of neuronal uptake, extraneuronal uptake, and alpha 2-receptors, nerve stimulation liberates 674 +/- 22 pmol/g during normal flow and 206 +/- 24.3 pmol/g during ischemia. These results suggest that, in vivo, centrally originating neural activity would not lead to substantial accumulation of noradrenaline within the extracellular space of the ischemic myocardium. This failure of accumulation is due to both a functioning neuronal uptake of noradrenaline and a failure of neurotransmission.

Animals↗
PubMed1984

[Left ventricular function and activity of vasoconstrictor systems in patients with chronic heart insufficiency].

An increased activity of vasoconstrictor mechanisms may play an important role in circulatory adjustments to heart failure. Thus, hemodynamic data and the plasma hormones epinephrine (E), norepinephrine (NE) and arginin vasopressin (AVP) as well as the plasma renin activity (PRA) were assessed in 50 patients undergoing coronary angiography and right heart catheterization. Patients were classified into three groups according to severity of left ventricular (LV) dysfunction as assessed by ejection fraction (LVEF): those with normal left ventricular function (group 1 (n = 12): LVEF greater than or equal to 55%, mean 70 +/- 3%) and those with moderate (group 2 (n = 16): LVEF 54-35%, mean 43 +/- 2%) or severe LV dysfunction (group 3 (n = 22): LVEF less than 35%, mean 22 +/- 1%). At rest plasma NE concentrations in patients with heart failure (group 2: 187 +/- 17 pg/ml; group 3: 299 +/- 27 pg/ml) did not differ significantly from control values (199 +/- 26 pg/ml). During exercise, NE concentrations increased in all patients (p less than 0.001). This increase in plasma NE was more pronounced in group 3 (753 +/- 71 pg/ml) than in group 1 (262 +/- 37) and group 2 (388 +/- 64). A significant inverse correlation was found between plasma NE and stroke index at rest (r = -0.592, p less than 0.001) as well as during exercise (r = -0.659, p less than 0.001). PRA was elevated at rest and during exercise in patients of group 3 but not of group 2 as compared with control patients (p less than 0.05). Plasma E and AVP were similar in all groups. Patients of group 3 were subdivided according to exercise capacity into patients who tolerated a maximum work load of 50 watts or more (group 3A) and those who did not tolerate a work load exceeding 25 watts (group 3B). At rest and during exercise, patients of group 3A had a higher stroke index than patients of group 3B. In contrast, there was no significant difference in LVEF between group 3A and 3B (22 +/- 2 vs 20 +/- 1%). During exercise patients with low exercise capacity (group 3B) had higher NE levels than patients with less impaired exercise capacity (group 3A) (948 +/- 86 vs 590 +/- 65 pg/ml, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1984

[Possible mechanisms of action of potassium in arterial hypertension].

Potassium supplementation of the diet attenuates the rise in blood pressure in stroke prone spontaneously hypertensive rats (SHRSP) without a concomitant contraction of intravascular volume. This finding favours a resistance-mediated, but not a volume-mediated hypotensive action of potassium. A possible site of effect is modulation of sympathetically mediated vasoconstriction by potassium. Sympathetic vascular tone, which is enhanced in SHRSP on a high sodium diet because of a reduced noradrenaline inactivation, a facilitated noradrenaline release and an increased sensitivity of vascular smooth muscle to noradrenaline, tends to normalize when the potassium content of the diet is augmented. All three parameters of sympathetically mediated vasoconstriction are altered by potassium in a way to attenuate the enhanced sympathetic vasoconstriction.

Animals↗
PubMed1984

Vasopressor systems during smoking in humans.

In this study we correlated the effects of cigarette smoking on the activity of vasopressor systems in humans with changes in heart rate and blood pressure and compared them with changes observed after physical exercise or graded norepinephrine infusion. No relationship was established between changes in either plasma angiotensin II or vasopressin concentration and the hemodynamic parameters, although there was a small increase in both hormones during smoking. In contrast, heart rate (r = -0.245, p less than 0.01, n = 136) was negatively related to plasma norepinephrine concentration during the smoking of five cigarettes. A comparable, negative correlation, although much closer, was found during graded norepinephrine infusion between heart rate and norepinephrine concentration (r = -0.682, p less than 0.001), whereas both parameters were positively related under conditions of physical exercise (r = 0.866, p less than 0.001). In an attempt to block the assumed nicotine-induced sympathetic stimulation, smoking experiments were carried out after acute beta blockade (200 mg metoprolol orally). There was a parallel shift of heart rate and blood pressure to lower values. However, beta blockade did not abolish the smoking-induced rise in blood pressure and heart rate. At the present time no direct evidence is available for a nicotine-induced increase of norepinephrine concentration at postsynaptic receptors during smoking in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Metabolic aspects of compensatory mechanisms in cardiac failure.

Three metabolic adaptive or compensatory mechanisms of heart failure were discussed: Adaptation of energy production and of energy availability in the myocardial cell. With increased myocardial oxygen demands this is achieved by a progressive displacement of the mass action ratio of the creatine phosphokinase reaction, so that pronounced changes in the creatine phosphate-ratio, related to myocardial oxygen consumption, are accompanied by only small changes in adenosine-5'-triphosphate adenosine-5'-diphosphate and hence in free energy of the adenine-nucleotide system. Adjustment of the oxygen availability by adaptation of the hemoglobin dissociation curve due to an increase in the erythrocyte content of 2, 3-diphosphoglycerate. This is accompanied by a swelling of erythrocytes as a consequence of an increase in the Gibbs-Donnan potential. In patients with congestive heart failure 2,3-diphosphoglycerate-synthesis is augmented due to respiratory alkalosis and increased concentrations of deoxygenated hemoglobin. Increase in the sympathetic drive of the heart due to increased net discharge of the neurotransmitter caused by reduced neuronal reuptake of norepinephrine. The diminished myocardial norepinephrine content in heart failure is due to the diminished neuronal uptake and to insufficient de novo catecholamine synthesis in the heart. Rather than tyrosine-hydroxylase the transformation of dopamine to norepinephrine seems to be the rate limiting step for catecholamine synthesis in heart failure.

Adenosine Diphosphate↗
PubMed1983

Different antagonist potency of saralasin in acute and chronic angiotensin-dependent hypertension.

We investigated the antagonistic properties of saralasin in acute and chronic angiotension II (ANG II)-dependent hypertension. Two models of experimental hypertension were studied: (a) Rats acutely infused i.v. with ANG II to raise the blood pressure (BP) by about 35 mmHg. (b) One-clip, two-kidney renal hypertensive rats. In both experimental models increasing doses of saralasin were infused i.v., and three parameters were evaluated at each dose level: (1) fall of BP, (2) plasma concentration of saralasin, and (3) plasma concentration of ANG II. It was found that saralasin led to a more pronounced fall of BP in malignant than in benign renal hypertension. To reduce BP by about 20 mmHg, saralasin plasma concentrations had to exceed those of ANG II about 2000-fold in renal hypertension and about 7-fold in rats infused with ANG II. It is concluded that saralasin antagonises ANG II more effectively in acute than in chronic hypertension.

Acute Disease↗
PubMed1983

Evidence for the presence of enkephalins in the heart.

Extracts of guinea pig hearts were subjected to high performance liquid chromatography (HPLC) and the eluted fractions monitored by radioimmunoassays (RIA) for their content of leucine5-enkephalin (Leu-ENK) and methionine5 enkephalin (Met-ENK). Distinct peaks of both Leu-ENK and Met-ENK immunoreactivity were found corresponding to the position of synthetic Leu-ENK and Met-ENK respectively. The ratio of Leu-ENK to Met-ENK content was about 1:4. Chemical sympathectomy with 5-hydroxydopamine (6-OH-DA) produced a dramatic fall in noradrenaline content of the heart by more than 99%, whereas the concentration in Leu-ENK was reduced by only 70%. The Leu-ENK content of the adrenal glands was not affected by this treatment. These observations point to an enkephalinergic innervation of the heart which appears to be mainly of sympathetic origin. The results suggest the participation of enkephalins in cardiac reflex mechanisms.

Animals↗
PubMed1983

Comparative synergistic activity of ceftriaxone-piperacillin versus ceftriaxone-netilmicin.

The effect of combination of ceftriaxone with piperacillin or netilmicin was studied in a total of 119 clinical isolates using the checkerboard titration technique. The isolates included Pseudomonas aeruginosa, Staphylococcus aureus, enterococci and various Enterobacteriaceae. Synergy was observed in all Streptococcus faecalis strains with both combinations. Whereas the ceftriaxone/netilmicin combination showed a higher rate of synergy against Pseudomonas aeruginosa, the rate of synergy against Enterobacteriaceae was the same for the two combinations. In no instance was antagonism encountered.

Cefotaxime↗
PubMed1983

Experimental studies on the effect of duodenal contents on the epithelium of the esophagus.

10 male BD IX rats and 15 male and female Wistar rats weighing between 250 and 300 g had an esophago-jejunostomy according to the method described by Levrat et al. (1962). Four weeks after surgery all 40 animals were sacrificed and examined macroscopically as well as histologically. All animals had deep ulcerative lesions in the lower half of the esophagus associated with hyperplasia, hyperkeratosis and akanthosis.

Animals↗