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Biomedical subjects

M Rundgren

Publications and source records attributed to M Rundgren.

87 records · Page 5Linked to original sources
PubMed1978

Delayed drinking in response to electrical and thermal stimulation of the medial forebrain.

Water intake in response to electrical and thermal stimulation of the medial forebrain was studied in the goat. When the frontal wall of the third cerebral ventricle was included in a field of bipolar electrical stimulation a dipsogenic response was obtained after discontinuation of the stimulation. Release of antidiuretic hormone (ADH) was apparently also elicited. The water intake was roughtly proportional to the amount of current which had been applied during the stimulation period. Water consumption in response to stimulation attenuated the dipsogenic effect of subsequent stimulation, as did also pre-stimulatory hydration by stomach tube. A 2 degrees C elevation of the temperature of parts of the preoptic/anterior hypothalamic region for 40 min periods incuded cumulative drinking starting after 2.5 to 18 min. There were great interindividual differences in the amount of water consumed in response to the thermal stimulation, possibly due to variations in thermo-couple electrode placement. The dipsogenic effect of forebrain warming was inhibited by pre-hydration, and by lowering of the environmental temperature. The delayed thirst responses are discussed in relation to stimulus-bound drinking previously observed in the same and other species. It appears possible that the delayed drinking was a manifestation of artificially induced excitation of juxtaventricular "thirst" receptors.

Animals↗
PubMed1978

Transient water diuresis and syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by forebrain lesions of different location.

Inhibition of ADH-secretion and transient water diuresis was observed as acute effects of radio-frequency lesions in the septal region of goats. The water diuresis was not compensated for by drinking and therefore rapidly induced pronounced hypernatremia and hypovolemia. The development of hypovolemia was accompanied by a rise in plasma renin activity. Lesions of the same kind, but extending into the preoptic region near the medial portion of the supraoptic nuclei induced the inability to excrete excessive water characteristic of SIADH. Determinations of plasma arginine vasopressin suggested that the lesions causing SIADH did not produce any noticeable increase in basic ADH-secretion. The results suggest that impulses from juxtaventricular receptors regulating ADH-release and water intake to a considerable extent are transmitted via the septal region, and that elimination of this impulse traffic is sufficient to turn water balance to the negative side. However, reflex volumetric inhibition of the ADH-secretion does not seem to be mediated by pathways passing through the septal region.

Animals↗
PubMed1978

A study of permanent adipsia induced by medial forebrain lesions.

Cerebral lesions involving most of the anterior wall of the ventricle, and the medial part of the septal region, induced a permanent loss of thirst in two goats. The ventral part of the lamina terminalis remained intact in one of the animals. Pronounced dehydration (10--13% loss of b.wt.) developed during periods (3--7 days) when water supplementation was omitted. Determinations of plasma arginine vasopressin in one of the animals revealed that the dehydration did not cause any significant increase in the secretion of antidiuretic hormone. However, the water deficit induced a considerable rise in plasma renin activity and tachycardia. If anything, the caroitid blood pressure became slightly elevated towards the end of 7 d dehydration periods. The lesions obviously inactivated a cerebral sensory mechanism controlling water balance. It may have been due mainly to destruction of juxtaventricular receptors in the anterior hypothalamic region, but perhaps also to a disruption of afferents from such receptors located posterior to this cerebral level.

Animals↗
PubMed1977

Steady state kinetics of 4-hydroxyphenylpyruvate dioxygenase from human liver (III).

Kinetic experiments have been made with an apparently homogenous preparation of human liver 4-hydroxyphenylpyruvate dioxygenase Form 3 (4-hydroxyphenylpyruvate: oxygen oxidoreductase (hydroxylating, decarboxylating), EC 1.13.11.27) at 37 degrees in 0.2 M Tris/HCL, pH 7.5, by measuring the evolved carbon dioxide from the 1-14C-labeled substrate or the formation of homogentisate from the U-14C-labeled substrate. The effect of variations in the concentrations of substrates, products, and metal chelators on the velocity of the forward reaction was studied. The results agree with an Ordered Bi Bi kinetic mechanism (Cleland, W. W. (1963) Biochim. Biophys. Acta 67, 104--137), where 4-hydroxyphenylpyruvate is added prior to oxygen and CO2 released before homogentisate. A Theorell-Chance mechanism has not been excluded.

4-Hydroxyphenylpyruvate Dioxygenase↗
PubMed1977

Deuterium induced extinction of ADH-release in response to intracerebroventricular infusions of hypertonic NaCl and angiotensin.

Infusions (20 microliter/min) of hypertonic (0.3 M) NaCl and angiotensin II (1 ng/kg min-1) in isotonic (0.15 M) NaCl were made for 1 h in the hydrated goat during fully developed water diruesis. Either H2O or deuterium (D2O) WAS USED AS SOLVENT. A pronounced antidiuretic response, outlasting the infusion period by 30 min or more, was seen when the substances were dissolved in H2O. Only a weak inhibition of the water diuresis, which was extinguished during the infusion period, was obtained when D2O was used as the solvent. The infusion of 0.3 M NaCl/H2O invariably induced drinking in one of the goats, which, however, showed no drinking response to the infusions of 0.3 M NaCl/D2O. The possibility is discussed that D2O (perhaps by its inhibitory effect on (Na+-K+)-ATPase activity) reduced the sensitivity of juxtaventricular receptors regulating ADH-release and water intake.

Angiotensin II↗
PubMed1975

Duration of central action of angiotensin II estimated by its interaction with csf Na+.

In pre-hydrated goats, an urge to drink persisted for approximately half an hour after combined infusions of angiotensin II and hypertonic (0.5 M) NaCl into the lateral or third cerebral ventricle. The intraventricular infusion of angiotensin/glucose solution, having no dipsogenic action of its own, markedly accentuated the dipsogenic and antidiuretic effects of the subsequent intraventricular infusion of hypertonic NaCl. The possibility is discussed that angiotensin may be bound at periventricular receptor sites where it continues to interact with Na+ in eliciting thirst and ADH release for about half an hour.

Angiotensin II↗
PubMed1975

Inefficiency of isoprenaline to induce drinking in the goat.

Isoprenaline, which acts as a potent dipsogen in water-satiated rats and dogs, did not elicit water intake when infused intravenously at 0.1 or 0.3 mu/kg min-1 in non-hydrated goats. Even the low dose of the drug caused a marked reduction of parotid salivary flow. The possibility is discussed that reduced salivary secretion might be the particular effect which makes isoprenaline dipsogenic in prandially drinking species. The intravenous infusion of isoprenaline at the high dose level caused an inhibition of the water diuresis of hydrated goats, concomitant with reduced renal Na+ excretion and a marked, sustained fall in the arterial blood pressure. Significant amounts of ADH were recovered from the urine secreted during the antidiuresis. This ADH-release was apparently not due to central beta-adrenergic stimulation since no inhibition of the water diuresis was observed during intraventricular infusions of isoprenaline. Rather, the ADH-release appears to have been secondary to the isoprenaline-induced fall in arterial blood pressure.

Animals↗
PubMedDate not supplied

On the role of Ca2+ in the toxicity of alkylating and oxidizing quinone imines in isolated hepatocytes.

The cytotoxicity of acetaminophen (paracetamol) has been shown to be associated with a disruption of intracellular Ca2+ homeostasis caused by the interaction of its metabolite N-acetyl-p-benzoquinone imine (NAPQI) with hepatocyte thiols [Moore, M., et al. (1985) J. Biol. Chem. 260, 13035-13040]. Inasmuch as NAPQI can both covalently bind to thiols and oxidize thiols, we investigated the effects of two dimethylated analogues of NAPQI, one of which (2,6-dimethyl-NAPQI) primarily binds to thiols and the other of which (3,5-dimethyl-NAPQI) primarily oxidizes thiols. Of the three compounds, 2,6-dimethyl-NAPQI decreased protein thiols to the greatest extent and also inhibited hepatocyte plasma membrane Ca(2+)-ATPase to the greatest extent. The 3,5-dimethylated analogue decreased protein thiols to the least extent and inhibited the plasma membrane Ca(2+)-ATPase to a lesser extent. The cytotoxicity of all three compounds was preceded by a sustained elevation in cytosolic Ca2+ as compared to the transient rise caused by the alpha-agonist phenylephrine. Again, the 2,6-dimethyl analogue was the most potent of the three compounds. The thiol reagent dithiothreitol (DTT), which reversed the inhibition of the Ca(2+)-ATPase and the rise in cytosolic Ca2+, also protected against cytotoxicity. Agents that are known to inhibit either Ca(2+)-dependent proteases or phospholipases significantly delayed the onset of cytotoxicity caused by NAPQI and its analogues. Our results suggest that both arylation and oxidation of protein thiols may result in the elevation of cytosolic Ca2+ and in cytotoxicity and that arylation of critical thiol groups appears to be the more lethal reaction.

Alkylation↗