Lundholm, L., E. Mohme‐Lundholm and N. Vamos. Lactic acid assay with L(+)lactic acid dehydrogenase from rabbit muscle. Acta physiol. scand. 1963. 58. 243–249. — Lactate assay with L(+)lactic acid dehydrogenase from rabbit muscle and with DPN involved the problem of quantitatively reducing lactate to pyruvate. The problem was overcome by use of a solution with a high pH, by an excess of DPN, and by addition of a carbonyl reagent e.g. semicarbazide or hydrazine, which trapped the formed pyruvate. Hydrazine was found to be preferable to semicarbazide since it appeared to bind pyruvate more effectively. It was thus possible to carry out the reaction, with a 100 per cent recovery, at pH = 9.0. This was advantageous because, at pH > 9.0, hydrazine and semicarbazide rapidly formed products with DPN that absorbed at 340 mμ, giving a high blank value that varied greatly with the pH of the solution and seriously affected the precision of the method. Unlike hydrazine, moreover, semicarbazide reacted with formed DPNH in the presence of atmospheric oxygen, so that the extinction of DPNH decreased.

L. Lundholm and E. Mohme-Lundholm. Length at inactivated contractile elements, length-tension diagram, active state and tone of vascular smooth muscle. Acta physiol. scand. 1966. 68. 347-359. Analysis of the mechanical properties of vascular muscle is complicated by the fact that normally it is contracted to a certain degree and has no constant resting length. By total blockade of the energy production of the muscle with monoiodoacetic acid under anaerobic conditions the vessel length a t inactivated contractile elements could be measured. With the aid of this length the length-tension diagram of the vascular muscle in untreated and adrenaline-treated vessels was studied. The muscle developed a maximal tension (2.100 gwt/cmY cross section) a t this length, which therefore probably corresponded to Lo in skeletal muscle. The vascular muscle shortened maximally to 25 per cent of the relaxed length. Both the development of maximal isometric tension and the maximal isotonic shortening were of the same magnitude in vascular as in skeletal muscle. The series-elastic component (15-20 per cent) was, on the other hand, greater in vascular than in skeletal muscle. No rigor mortis was noted in the vascular muscle. The spontaneous tension of the vascular muscle and tension increase induced by adrenaline could be largely ascribed to a n active state. T h e question of whether a "tonic" or "catch" mechanism is present in vascular muscle, independent of the active state, is discussed.

Summary. The effects of adrenaline. noradrenaline. lactic acid and sodium lactate. in intravenous infusion. upon the cardiac output. blood pressure. oxygen consumption. heart and respiration rates, and lactic, acid content of the blood were investigated in unanesthetized rabbits. Control experiments were performed with infusion of saline alone. Both adrenaline and lactic acid infusions were followed by a rise in the cardiac output but no change in blood pressure, which finding indicated a reduction of the total peripheral resistance. The increase in cardiac output was greater than the rise in oxygen consumption. After sodium lactate the cardiac output rose only to the same degree as the oxygen consumption. Noradrenaline elevated the cardiac output. oxygen consumption and lactic. acid production very slightly. concurrently with a pressor effect. The stimulating action of adrenaline in a low‐ concentration on the cardiac output is thought to be largely of reflex origin. resulting from a primary vasodilator effect. caused by adrenaline's stimulation of the lactic acid production in skeletal muscle. Lactic acid induces vasodilatation in the following ways: (1) Through the rise in the lactic acid content of skeletal muscle, CO, is liberated from the tissue bicarbonate and vasodilatation is produced via the increased CO2 tension. (2) When the lactic acid content rises in the blood, the latter's CO2 transporting capacity is impaired, and this also tends to raise the CO2 tension in the tissues. (3) With oxidation of the lactate the blood flow increases, chiefly in the liver. The discrepancies in the hemodynamic effects of adrenaline and noradrenaline are attributed to the fact that the former hormone, even in low concentrations, has a powerful stimulatory action on the lactic acid production, but the latter almost none. The lactic acid producing effect of adrenaline in muscle is assumed to be a phase of the mechanism by which it elicits an emergency reaction in the organism.

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