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Biomedical subjects

G Dietze

Publications and source records attributed to G Dietze.

At least 73 records · Page 4Linked to original sources

Substrate balances across the forearm during the early postoperative period.

The substrate metabolism of skeletal muscle has been studied by the forearm technique in 23 patients after abdominal operation. The data were compared to those of 55 healthy volunteers after an overnight fast. While the uptake of glucose into forearm muscle tissue was increased in relation to its elevated arterial concentration, its rate of oxidation was clearly reduced and the muscle extraction of ketone bodies was increased. Simultaneously, the production of lactate was doubled and the output of glycerol and alanine significantly enhanced. From these data one may conclude that 3 hours after abdominal surgery the energy requirements of skeletal muscle tissue are adequately met by the substrates provided that glucose sparing occurs in association with a rising arterial concentration of KB, and that the release of alanine is accelerated in spite of abundant caloric supply.

Journal Article↗

Dose-dependent effect of bradykinin on muscular blood flow and glucose uptake in man.

Using the forearm technique, the effect of bradykinin on muscular blood flow and glucose uptake in healthy man in the postabsorptive state (n = 8) was studied at different doses of an intra-arterial infusion of bradykinin (2.5-150 ng/min). The blood flow of the forearm was increased dose-dependently from basal 2.8 +/- 0.3 up to 14.7 +/- 2.8 ml/(100 g X min). At lower bradykinin concentrations (2.5-25 ng/min), muscular glucose uptake was raised parallel to the increased blood flow from basal 0.71 +/- 0.30 to 2.93 +/- 0.50 mumol/(100 g X min). However, at higher doses (50-150 ng/min) glucose uptake was decreased again. Thus, the greatest metabolic effect of bradykinin was seen at a calculated bradykinin concentration of approximately 1 X 10(-9)M in the blood.

Bradykinin↗

The kallikrein-kinin-prostaglandin system: involvement in the control of capillary blood flow and substrate metabolism in skeletal muscle tissue.

In spite of numerous work done in this field it is not clarified so far how the acceleration of the capillary blood flow, of glucose uptake, and of muscle growth occurring during work and after ischemia is controlled in muscle tissue. Since the signal for the induction of these responses stems from inside the cell, tissue factors have been postulated which should be responsible for the enlargement of the capillary net and the improvement of the tissue's insulin sensitivity. The accumulation of new evidences during the last few years points to an involvement of the kallikrein-kinin-prostaglandin system.

Blood Flow Velocity↗

[New aspects of the blood flow-augmenting and insulin-like activity of muscle exercise: possible involvement of the kallikrein-kinin-prostaglandin system (author's transl)].

Adaptations of energy metabolism, as they occur during contractions of skeletal muscle besides by anaerobic glycolysis are achieved via changes in capillary blood flow providing substrates and oxygen for combustion. Since, initially, oxygen supply is restricted in the working muscle, glucose would seem to be the adequate fuel as it may be used anaerobically and yields more energy per mole of oxygen than fatty acids under such circumstances. Besides glucose, amino acids are also required for accelerated proteosynthesis according to the work load. Therefore, an enlargement of the capillary net has to be accompanied by an amplification of the action of insulin, which is often present in only small amounts, e.g., after an overnight fast. This aim is met in three ways: (1) enlargement of the capillary net with accelerated blood flow increasing the supply of insulin and the number of receptor sites for insulin binding; (2) accelerated transport of insulin through the capillary wall, providing more insulin in the interstitial space and at the plasma membranes; (3) a molecular mechanism directly involving the insulin-receptor-messenger complex, localized at the plasma membrane of the working muscle cell. These mechanisms resemble a self-regulatory process, set in motion by the release of metabolites from the working tissue. From recent studies there is accumulating evidence that kinins liberated from their precursors are involved as tissue hormones by carrying the signal across the interstitial space to the smooth muscle cells of the capillary vessels. Concomitantly, prostaglandins are released intracellularly to bring about, in cooperation with kinins, the various adaptive mechanisms. Amplifying systems of this kind may play a role not only in muscle but also in other tissues where adequate kinin or prostaglandin release would appear beneficial under several clinical conditions such as shock, coronary infarction, wound healing, etc.

Bradykinin↗

Insulin-like activity of bradykinin on amino acid balances across the human forearm.

In order to investigate whether bradykinin which has been shown to improve carbohydrate metabolism of skeletal muscle exhibits also insulin-like activity on amino acid metabolism, balances of oxygen and 13 amino acids across the forearm and forearm blood flow were determined in normal subjects during the arterial infusion of insulin (n = 9, 250 mu-units x kg-1 x min-1), bradykinin (n = 7, 0.2 ng x kg-1 x min-1) and papverine (n = 5, 2 microgram x kg-1 x min-1). As expected, the infusion of insulin exhibited significant reduction of the release of glycine, proline, valine, phenylalanine, leucine, threonine and isoleucine. As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine. On the contrary, papaverine which exhibited almost identical accelerationof forearm blood flow as bradykinin, did not influence the amino acid release from forearm muscle. These findings further support the notion that kinins liberated during muscle work might be involved in the work-induced insulin-like action on carbohydrate- and also on amino acid metabolism.

Adult↗

Effect of metaproterenol on ketone body metabolism of the forearm in healthy and diabetic subjects.

Muscular ketone body metabolism was studied by the registration of arterial-deepvenous concentration differences of glycerol, beta-hydroxybutyrate and acetoacetate, and of muscular blood flow in 53 healthy volunteers and 23 juvenile diabetics. In six subjects of each group substrate metabolism was also investigated during the intrabrachial arterial infusion of metaproterenol (0.4 microgram/min). Identical rates of muscular glycerol release and ketone's fractional extraction were obtained in healthy and diabetic subjects during the basal period. A significant correlation between muscular ketone extraction and arterial ketone concentration was calculated in both groups. During the infusion of metaproterenol the diabetics, unlike the controls, revealed enhanced muscular glycerol output and reduced fractional extraction of beta-hydroxybutyrate. These findings are in line with the present view that the impairment of muscular ketone body utilisation in diabetic ketoacidosis may at least partly be due to enhanced muscular lipolysis.

Acetoacetates↗

[Improvement of pathological glucose tolerance by bradykinin in diabetics and in surgical patients (author's transl)].

Intravenous glucose tolerance tests (GTT) were performed in 13 metabolically healthy patients at the first and second day after abdominal surgery. GTT were carried out during an additional infusion of bradykinin (BK) (80 microgram/h) in six of these patients at the first day (group A) and in seven patients at the second day (group B). Furthermore, GTT were performed in six patients with chemical diabetes with and without BK-infusion. In addition, the effect of BK on blood glucose concentration in the postabsorptive state was investigated in nine maturity onset diabetics and in five healthy volunteers. As a control, another nine diabetics received physiological saline. In both groups of surgical patients BK improved glucose tolerance (k-values: group A without BK 1.03 +/- 0.12, with BK 1.31 +/- 0.07; group B without BK 0.85 +/- 0.18, with BK 1.25 +/- 0.21). This was also true in chemical diabetics (without BK 0.81 +/- 0.03, with BK 1.08 +/- 0.04). While BK did not change blood glucose concentration in healthy volunteers, it reduced that of diabetics by 12.2 +/- 1.4% continuously during 100 min. No spontaneous drop of blood glucose was observed in diabetics receiving saline. These results are in good accord with the present view that kinins may play a role within the regulation of carbohydrate metabolism.

Blood Glucose↗