PROTEIN METABOLISM AND AMINO ACID ACCUMULATION IN THE RAT SUBMAXILLARY GLAND DURING REDUCED SYMPATHETIC ACTIVITY

Abstract— Unilateral sympathetic decentralization of the superior cervical ganglion of rats was performed 3 days prior to the experiments. A two-compartment kinetic model was proposed to describe the effect of decentralization on (1) the uptake of a nonphysiological amino acid from plasma to the submaxillary gland and (2) the incorporation of a physiological amino acid from precursor pool into protein. The calculations based on the model showed that the fractional rate constant for efflux of the nonphysiological amino acid, α-[3-¹⁴C] aminoisobutyric acid, was greater in the decentralized than in the normal gland. However, efflux rate was equal in the two glands because the extrapolated zero time value of the initial concentration was greater in the normal gland.
The labelled physiological amino acid, [¹⁴C]leucine, was used in initial experiments to assess turnover rate of the gland proteins but it was rapidly metabolized to many other radioactive compounds. Therefore, arginine[¹⁴C]guanido was employed-arginine being the only labelled amino acid found after injection. Since the steady state content of submaxillary gland proteins was not changed but the fractional rate constant of conversion of free arginine into protein (k_p) was greater in the decentralized gland (k_p= 0-40 h^_l) than in the normal (k_p= 0-27 h⁻¹), we can conclude that decentralization increases protein turnover rate; thus, assuming that arginine[¹⁴C]guanido is homogeneously distributed in the tissue pools of free arginine, the rate of protein turnover is greater in the sympathetically decentralized gland than in the normal.     

The relationship between the size of yellow water traps and catches of aphids

Yellow water traps are often used for sampling populations of flying aphids. This note suggests that the size and probably the shape of traps should be standardised, because trapping efficiency (nos. caught/unit area), and the relative attractiveness of traps to different species, depends on trap size. Aphidologists using water traps to compare mixed populations of flying aphids, should therefore compare catches from different traps with caution.Traps of three sizes were made up from individual trays, each 29×21.5×5cm, and painted Hansa yellow inside; 1 tray alone, 4 arranged in a 2×2 rectangle, and 9 in a 3×3 rectangle, gave trapping surfaces of approx. 625, 2500 and 5700 cm² respectively. The traps were half-filled with water plus a drop of detergent, placed on bare land and daily catches collected on 19 days in June and July 1966.     

Endogenous Benzodiazepine Receptor Ligands in Human and Animal Hepatic Encephalopathy

The role of endogenous benzodiazepine receptor ligands in the pathogenesis of hepatic encephalopathy was studied in humans and in rat models of hepatic encephalopathy. Endogenous benzodiazepine ligands were extracted from rat brain and human CSF by acid treatment and purification by HPLC. Detection and partial characterization of these endogenous benzodiazepine ligands were carried out using both radioreceptor binding assays and radioimmunoassays with anti-benzodiazepine antibodies. Four different benzodiazepine receptor ligands were identified in human and rat tissue, two of which may be diazepam and desmethyldiazepam, based on elution profiles and anti-benzo-diazepine antibody reactivity. Human CSF and serum from patients with hepatic encephalopathy contained approximately 10 times more endogenous benzodiazepine receptor ligand than CSF from controls or nonencephalopathic patients with liver disease. The levels of brain benzodiazepine receptor ligand compounds were also increased approximately 10-fold in rats suffering from fulminant hepatic failure, but not in rats with portacaval shunts, a model of chronic hepatic disease. The increased concentrations of these substances could be behaviorally significant and may contribute to the pathogenesis of hepatic encephalopathy.     

ATP hydrolysis by ischemic mitochondria

Cellular ATP levels are determined by the rates of ATP production and ATP hydrolysis. Both phenomena are affected by ischemia. Mitochondrial enzymes are damaged, inhibiting this organelle's ability to make ATP. Mitochondria are also uncoupled by ischemia and have the ability to hydrolyze ATP. We designed a series of experiments to determine whether decreased production or increased hydrolysis of ATP was the primary effect of mitochondrial damage. Rat hearts were subjected to 45 min of warm ischemia in order to induce irreversible cell damage. ATP or ADP was injected into cuvettes containing mitochondria isolated from normal myocardium or myocardium damaged by ischemia. Luciferin-luciferase, which fluoresces in the presence of ATP, was also added to the tubes as an indicator of ATP levels. Mixtures of uncoupled and coupled mitochondria were made and compared with the mitochondria damaged by ischemia. The results showed that mitochondria damaged by prolonged ischemia hydrolyze ATP more rapidly than normal mitochondria; however, normal mitochondria can easily compensate for increased ATP hydrolysis when in mixture with equal amounts of uncoupled mitochondria. These data suggests that the low cellular levels of ATP following irreversible ischemia are primarily due to decreased ATP synthesis and not to increased hydrolysis.