[Effects of a nucleotide-nucleoside mixture on ischemic muscle metabolism in patients with stage II peripheral arterial occlusive disease. MR spectroscopic and biochemical analytic results]. / Effekte eines Nukleotid-Nukleosid-Gemisches auf den ischämischen Muskelstoffwechsel bei Patienten mit peripherer arterieller Verschlusskrankheit Stadium II. Mr-spektroskopische und analytisch-biochemische Ergebnisse.

In order to assess the acute metabolic effects of an intra-arterial infusion of nucleotide-nucleoside-mixture (NNM), 31P-mr-spectroscopy at the site of m. gastrocnemius and metabolite determinations from blood of the femoral artery and vein were carried out in 10 patients with PAOD stage II during ergometric calf exercise to the claudication pain limit. The spectroscopic measurements revealed a greater exercise-induced fall of PCr and a higher increase of Pi in calf muscles during supply of NNM compared with control ergometry. Post-exercise recovery of PCr was distinctly delayed during infusion of NNM. The anaerobic production of energy, however, was sufficient to maintain the ATP concentration to the same extent as under control ergometry. On the other hand, intramuscular lactate acidosis developed to a lower degree with NNM infusion than without NNM. A reduced muscular release of lactate, pyruvate, ammonia and alanine followed from the evaluation of the arteriovenous balance of these metabolites in the femoral vessels indicating a favourable global metabolic effect of NNM infusion in the extremity. The apparent contradiction in the spectroscopic and analytic-biochemical findings can be explained by local blood shunts induced by maximum vasodilation. Noninvasive mr-spectroscopy allows to detect directly and continuously the metabolic impact of ischemia in the calf muscles afflicted by arterial occlusion, whereas the metabolite concentrations in femoral blood are altered by afflux from non-ischemic areas. The known clinical benefit of frequently repeated intra-arterial infusions of NNM is thought to be due to an expansion of collateral circulation and to a favourable influence on endothelial functions.

Sympathetic neuronal activity in diabetic and non-diabetic subjects with peripheral arterial occlusive disease.

Despite the vasoconstrictory influence of the alpha-adrenergic system on the peripheral blood circulation the results of the sympathectomy were not satisfying in the therapy of peripheral arterial occlusive disease (PAOD). The aim of the present investigation was to clarify the pathophysiologic mechanisms of this clinical observation. Free and sulfoconjugated catecholamines were determined in the femoral artery, vein, and cubital vein of 19 healthy controls, 21 non-diabetic patients with PAOD stage II, 8 non-diabetic (PAOD IV) and 20 diabetic patients (D IV) with PAOD stage IV. In comparison with controls and group PAOD II an increased sympathoneuronal tone in group PAOD IV was evident at rest. Sympathetic activation was not restricted to the affected limb, since femoral and cubital venous norepinephrine levels were not different and plasma epinephrine fractional extraction (PEFE) was not altered by angiopathy. The lower sympathoneuronal activation in the group D IV may be attributed to an impaired pain perception or a reduced dopamine beta-hydroxylase activity indicated by a lower ratio of norepinephrine to dopamine. The failing long-term efficacy of lumbar sympathectomy in critical arterial limb disease may be explained by marked spontaneous sympathicolysis in diabetics, whereas in non-diabetics with sympathetic activation other mechanisms like development of unilateral Mönckeberg sclerosis, progression of proximal arterial occlusion or induction of steal effects have to be discussed.

[Comparison of 3 latest-generation glucose micro-reflectometers]. / Vergleich von drei Glucose-Kleinreflektometern der neuesten Generation.

Three glucose reflectance meters (Reflolux II = Accu-Chek II, Glucometer II and Hypocount GA) were tested for precision and accuracy when used by medical personnel of a diabetic outpatient department and for self-monitoring at home. In addition, the visual readability of the appropriate reagent strip was checked. All three systems were sufficiently valid for reflectometric reading, while visual evaluation showed a higher deviation. The precision of Accu-Chek II under optimal conditions in the outpatient department was comparable to the precision of laboratory examinations (CV 3.3%). When used by patients themselves, Accu-Chek II and Glucometer II were sufficiently precise (CV 4.8% [corrected] and 5.3% respectively). These devices are recommended for blood glucose self-monitoring.

Humoral regulation of the orthostatic reaction.

A tilt-table test was performed on 12 untrained subjects to evaluate the humoral adaptation to postural change. The observed peripheral reaction with a reversible short-term rise of norepinephrine (NE) and plasma renin activity (PRA) allowed us to divide the syndrome of the orthostatic dysregulation into a hyponoradrenergic and hypernoradrenergic type. This classification can be helpful for the clinical evaluation and therapy of orthostatic lability. The central excessive stimulation of the antidiuretic (ADH) and adrenocorticotropic hormone (ACTH) follow-ing orthostatic symptoms such as weakness or dizziness was not completely reversible within the observation period of 30 min. The ADH and ACTH increase was not different between the hypo- and the hypernoradrenergic type of dysregulation but was the most sensitive indicator of orthostatic lability: 41% of all subjects showed a hypernoradrenergic orthostatic dysregulation with pronounced NE response and alpha 2-adrenoceptor down-regulation. By use of antiembolism stockings (AES) or dihydroergotamine (DHE) this rate decreased to 16%. This was associated with a significantly reduced NE and PRA response and a diminished alpha 2-adrenoceptor number.

Determinants of plasma arginine-vasopressin in children.

Plasma concentration of arginine-vasopressin (AVP) was measured in 145 healthy subjects aged one day to 18 years of age. AVP decreased with age immediately after birth. Above one year of age values of children did not significantly differ from those in adults. AVP significantly correlated with plasma and urine osmolality after water deprivation during 16 h. Plasma AVP rose during exercise and fell after volume expansion. Nausea and vomiting are potent nonosmotic determinants of AVP release in children. Nonosmotic factors of AVP release should be controlled when sampling blood for measuring AVP in children for diagnostic and investigational purposes.