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R Stalder

Publications and source records attributed to R Stalder.

26 records · Page 2Linked to original sources
PubMed1983

Renal vascular effects of angiotensin II, arginine-vasopressin and bradykinin in rats: interactions with prostaglandins.

1. The renal vascular responses to the peptide hormones angiotensin II (ANG II), arginine-vasopressin (AVP) and bradykinin (BK) were studied in anaesthetized rats with flow-meter techniques. The contribution of prostaglandins (PG) to their renal vascular effects was assessed with the aid of the PG-synthesis inhibitor indomethacin. 2. ANG II and AVP induced a dose-dependent increase in renal vascular resistance (RVR). The renal vasoconstrictor effects of both peptides were significantly augmented in rats pretreated with indomethacin. Indomethacin alone induced an increase in RVR, but not in mesenteric vascular resistance (MVR). 3. BK in low doses (1 micrograms/kg . min) tended to decrease RVR but increased RVR in high doses (20 micrograms/kg . min). MVR was reduced after all doses. The renal vasoconstrictor effect of BK was not affected by the ANG II-antagonist saralasin but almost completely blocked by indomethacin. 4. These results suggest that in the rat, as in other animal species and in man, renal PG's attenuate the renal effects of vasoconstrictor hormones such as ANG II and AVP. Although it has no such effect in other species. BK in high doses induces renal vasoconstriction in the rat, which appears also to be mediated by PG's. This response might be peculiar to the rat, since PG's act as renal vasodilators in other species.

Angiotensin II↗
PubMed1983

Haemodynamic effects of bradykinin in rats.

The intravenous infusion of bradykinin (20 micrograms/kg X min) induced an initial fall in blood pressure and total peripheral resistance in anaesthetized rats. These changes were accompanied with an increase in cardiac output and stroke volume. These effects were transient and after 20 min of infusion blood pressure and total peripheral resistance were much less decreased than initially. Cardiac output and stroke volume had completely normalized. Lower doses of bradykinin (1 microgram/kg X min), which did not affect blood pressure, induced a reduction in mesenteric and renal vascular resistance. After higher doses (4 or 20 micrograms/kg X min) mesenteric vascular resistance was further decreased but renal vascular resistance was unchanged or markedly increased. This renal vasoconstrictor response was almost absent in rats which were pretreated with indomethacin (4 mg/kg i.v.). Hence the increase in renal vascular resistance was most probably due to the stimulation of the synthesis of prostaglandins, which act as renal vasoconstrictors in the rat.

Animals↗
PubMed1981

Evidence against the reported antithiamine effect of caffeic and chlorogenic acids.

Contrary to earlier literature reports, chlorogenic acid (I) is shown to have little or no deleterious effect on thiamine (II) when the 2 compounds are codissolved in aqueous solution. Evidence from nmr spectroscopy and from t. l. c. determination demonstrate that when II is heated at 60 degrees C and at pH 7.8 for 24h, about 10% is destroyed. This result is the same whether I is present or not. Incubating II with I or with caffeic acid (III) in a phosphate buffer at pH 7 or in thiamine assay medium at pH 6 for up to 24h at 37 degrees C did not reduce the growth activity of II or Lactobacillus viridescens. We conclude that I and III are not antithiamine agents.

Caffeic Acids↗
PubMed1976

A nomogram to obtain pulmonary shuntflow (Qs/Qt).

A nomogram to simplify the determination of pulmonary shunt is presented. It is based on Leigh's et al. shunt-equation (1969). The nomogram aggregates the factors which contribute most to the pulmonary shunt in acute respiratory failure. Arterial and venous oxygen saturation, Hb content, arterial oxygen tension and barometric pressure do influence strongly the result of calculated shuntflow. For the factors with little importance in the calculation (vapor pressure, mixed venous oxygen tension, alveolar-CO2 tension), international mean values are used. The shunt determined with the nomogram deviates less than 1% from the calculated values, if the range of PCO2 is between 32 and 52 mm Hg and the error does not exceed 1,5% with a PCO2 up to 82 mm Hg unless it is combined with a very low Hb and a high mixed venous saturation. By the nomogram the effect of the different parameters on the shunt can be very well illustrated. Especially mistakes in determination of the mixed venous saturation and of arterial O2 tension result in errors. Too high saturation values in mixed venous blood occur in distally located catheters due to pulmonary capillary admixtures. This contamination can be easily detected if the relationship between PVO2 and PACO2 is examined. The other source of error lies in the technical problems of PO2 determination in high ranges and is caused by escape of O2 into the PO2-electrode and O2-consumption of the blood. The end effect which the factors of O2 escape have on the accuracy of PO2 determination in high ranges is demonstrated with blood samples which have been equilibrated with different gas mixtures at different temperatures and had their PO2 measured at regular intervals. The error in PaO2 measurement can be reduced if blood-gas analyses are performed immediately or on cooled samples.

Carbon Dioxide↗
PubMedDate not supplied

The value of serum magnesium estimations in the diagnosis of acute perioperative myocardial infarction after coronary artery surgery.

Serum magnesium levels fall significantly after acute myocardial infarction. Even greater decreases have been found in all patients undergoing aorto-coronary bypass surgery. This is probably related to the use of cardiopulmonary bypass. No significant difference in serum magnesium levels was found between those patients who had a well documented peri-operative infarct and those who had an uncomplicated course. Thus determination of serum magnesium levels if of no use in the diagnosis of peri-operative myocardial infarction.

Coronary Artery Bypass↗