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Biomedical subjects

K Olsson

Publications and source records attributed to K Olsson.

At least 127 records · Page 7Linked to original sources
PubMed1980

Transient vasopressin release and thirst in response to prolonged intracerebroventricular infusions of hypertonic mannitol in saline.

In the conscious goat infusions of 0.4 M mannitol in 0.15 M NaCl into the lateral cerebral ventricle (40 or 100 min, 0.02 ml/min) caused slight, transient vasopressin release and temporary thirst, whereas infusions or pure, hypertonic (0.7 M) mannitol did not elicit thirst and inhibited the basic vasopressin release in the nonhydrated animal. In contrast, infusions of equiosmolal (0.35 M) NaCl induced persistent thirst and pronounced elevation of the plasma vasopressin concentration throughout the infusion period. The cerebrospinal fluid (CSF) osmolality was raised by the same order of magnitude (= 13%) after the mannitol/NaCl and the hypertonic NaCl infusions. The CSF Na+ concentration was elevated by greater than 10% at 5 min after hypertonic NaCl infusions, but it was reduced by approximately 10% at 5 min after the mannitol/NaCl infusions. There was no appreciable difference in the CSF K+ concentration after the infusions. The results are discussed with regard to the possible importance of CSF Na+-concentration as opposed to strict osmotic factors for the excitation of receptors involved in the control of water balance.

Animals↗
PubMed1978

Inhibition of vasopressin-release during developing hypernatremia and plasma hyperosmolality: an effect of intracerebroventricular glycerol.

In non-hydrated goats prolonged (3 h, 0.02 ml/min) intracerebroventricular (IVT) infusion of 0.35 M glycerol depressed the plasma vasopressin level during the entire infusion period which resulted in a conspicuous water diuresis outlasting the infusion by about 20 min. Since no compensatory drinking occurred during this sustained water diuresis it gradually induced pronounced dehydration (loss of greater than 1 liter of total body water causing 5% increase in plasma [Na+] and osmolality). The same degree of dehydration was in other experiments induced by water deprivation. It then caused a 5-fold increase in plasma vasopressin level. Corresponding IVT infusions of 0.35 M d-glucose depressed plasma vasopressin level only during the first half of the 3 h infusion period. Consequently, the resulting water diuresis was transient and subsided before the glucose infusion was finished. Plasma renin activity increased during the IVT glycerol infusion and during water deprivation, but was largely unaffected by IVT glucose. Both IVT glycerol and glucose decreased renal sodium excretion. The possibility is discussed that the pronounced ability of IVT glycerol to depress the vasopressin release and thirst is not only due to dilution induced reduction of CSF [Na+], but also to an influence of glycerol on choroidal and/or transependymal Na+-transporting mechanisms.

Animals↗
PubMed1977

1H-N.M.R., 13C-N.M.R., and mass spectra of glucosinolates and related compounds.

The mass spectra of per(trimethylsilyl) ethers of desulfated glucosinolates are dominated by ions derived from the glucose moiety. The ions at m/e 271 and 361 are much more abundant than in the spectra shown by the corresponding derivatives of hexoses and their simple glycosides. The individual glucosinolates are distinguished by a few ions originating from their respective aglycon groups. The 1H- and 13C-n.m.r. spectra of sinigrin and some closely related compounds have been analyzed.

Glucose↗
PubMed1976

Influence of altered CSF solute composition on parotid salivary secretion in goats.

Infusions of hypertonic NaCl solution into the CSF of the lateral cerebral ventricle of the goat caused a marked reduction in parotid salivary flow concomitant with a rise in salivary [Na+]. Corresponding infusions of iso- or hypertonic glucose and glycerol solutions affected salivary secretion in the opposite direction. The possibility is discussed that a periventricular sodium-sensitive mechanism, which is of importance in the central control of fluid balance, also may participate in the regulation of parotid secretion in the goat. This interpretation of the results is to some extent obscured by the observation of a high incidence of intermittent rumination during the intraventricular infusions of glucose and glycerol solution.

Animals↗
PubMed1976

Intracerebroventricular glycerol: a potent inhibitor of ADH-release and thirst.

Infusions of isotonic or hypertonic (0.3 or 0.5 M) glycerol into the lateral cerebral ventricle (60 min, 0.02 ml/min) of non-hydrated goats invariably induced a conspicuous and sustained water diuresis. Corresponding infusions of 0.3 M glycerol/0.16 M NaCl were almost equally efficient in this respect. A more short-lasting and less pronounced water diuresis was obtained in response to equivalent infusions of pure d-glucose, and the response to 0.3 M glucose/0.16 M NaCl was variable. Intravenous injections of vasopressin blocked the glucose-induced diuresis, but only postponed the glycerol-induced diuresis. Intracerebroventricular (IVT) infusions of 0.5 M glycerol caused a sustained, complete inhibition of the urge to drink in the 48 h dehydrated goat, whereas IVT glucose only attenuated dehydrative drinking. Twenty min after the infusions of glycerol the CSF [Na+] in the lateral ventricle was about 15% below normal. About 10% reduction of CSF [Na+] was obtained 20 min after the IVT infusion of glycerol/NaCl. The corresponding infusion of pure d-glucose reduced the CSF [Na+] by less than 5%. The glycerol and glycerol/NaCl infusions caused a moderate reduction of renal Na+ + K+ excretion. The possibility is discussed that the observed effects of IVT glycerol is a manifestation of its efficiency to inhibit choroidal and/or juxtaventricular (Na+-K+)-ATPase activity.

Animals↗
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↗