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Biomedical subjects

P Olsson

Publications and source records attributed to P Olsson.

At least 127 records · Page 7Linked to original sources
PubMed1984

Leukotriene D4 increases nasal blood flow in humans.

The effect of leukotriene D4 on the nasal mucosal blood flow in humans was measured using a laser doppler flow meter. The leukotriene solution was applied topically to the nasal mucosa in 9 healthy subjects, and changes in blood flow were measured non-traumatically by the laser doppler instrument. The response showed a consistent increase in blood flow. A dose-response was found in the range of 0.063 - 4.0 nanomole. These results confirm an earlier study on the human skin, implicating leukotriene D4 as an important vasodilator in humans. No increase in nasal secretion was noted by the subjects tested.

Administration, Topical↗
PubMed1984

Effect on the uptake kinetics of serotonin (5-hydroxytryptamine) in platelets from workers with long-term exposure to organic solvents. A pilot study.

Six workers from a paint industry were examined concerning the concentration of solvents in the breathing zone, the platelet count and kinetic uptake of serotonin [5-hydroxytryptamine (5-HT)], the serum concentration of calcium, potassium and sodium, and pH. The degree of exposure was found to be moderate. The results showed a decrease in platelet count in whole blood and platelet-rich plasma. The maximum uptake rate for serotonin in platelets (Vmax) was significantly increased compared to that of nonexposed subjects. No changes in the ionic concentration and pH of serum were observed. One worker was reexamined after a six-week period of nonexposure. Though the measured platelet variables were still aberrant, the values approached normal.

Adult↗
PubMed1983

Effect of glycosaminoglycans and antithrombin III on uptake and inhibition of thrombin by the vascular wall.

Thrombin binds to and is inactivated by the endothelium. The inactivation is potentiated by plasma. The present investigation was designed to clarify the role of vessel wall glycosaminoglycans (GAG) and plasma antithrombin III (AT III) in the inactivation and binding of thrombin by endothelium. Thrombin was shown to bind to vascular endothelium and artificial surfaces containing GAG:s. The binding could be inhibited on both types of surfaces by pretreating them with protamine. Thrombin bound to endothelium was rapidly inactivated in the presence of plasma but only slowly if the plasma was replaced by AT III, AT III-depleted plasma or a balanced salt solution. It is concluded that thrombin binds to vessel wall GAG:s and is inactivated by the endothelium. Potentiation of the inhibition of the endothelially bound thrombin by plasma is dependent upon presence of AT III but an additional plasma factor is also required.

Animals↗
PubMed1983

Inactivation of thrombin by the aortic endothelium.

The aim of the investigation was to clarify the uptake of thrombin on vascular endothelium and the inhibition of thrombin on the endothelium in the presence or absence of plasma. Segments of porcine aorta were used. Thrombin was labelled with 125I and its enzymatic activity was assayed amidolytically using a specific chromogenic substrate. After exposure to the endothelium both enzymatic activity and radioactivity disappeared from the thrombin solution and were recovered as surface bound activities. The enzyme activity confined to the endothelium rapidly disappeared in the presence of plasma but no activity was recovered in the plasma. The surface confined radioactivity, however, decreased slowly and was quantitatively recovered in the plasma. In the absence of plasma, i.e. in the presence of a balanced Ringer's solution, only slow disappearance of thrombin enzymatic activity occurred although the rate of disappearance was higher than that of release of radioactivity. It is concluded that thrombin, taken up on the endothelium, is almost instantaneously inhibited by an interaction mechanism with plasma and then released in an inactive state. The endothelium itself, however, seems to slowly inhibit bound thrombin and then release it.

Animals↗
PubMed1983

Effects of dietary protein-tryptophan restriction upon 5-HT uptake by platelets and clinical symptoms in migraine-like headache.

Ten women with recurrent migraine-like headache, flush, urticaria and itching excoriations were put on a protein/tryptophan reduced diet. The 5-HT uptake kinetics in platelets, the frequency of headache attacks and skin symptoms were recorded. On customary food the 5-HT uptake kinetics were severely disturbed. On diet, the platelet 5-HT uptake was normalized and, in parallel, the migraine-like symptoms and skin manifestations were reduced. The parallel between the improvement in active 5-HT uptake by platelets and clinical symptoms during dietary protein/tryptophan restriction supports the idea that impairment of the 5-HT uptake in platelets is a contributory factor in the pathogenesis of migraine-like headache and other 5-HT related symptoms.

Adult↗
PubMed1983

A new non-thrombogenic surface prepared by selective covalent binding of heparin via a modified reducing terminal residue.

A new method for the covalent binding of heparin to artificial surfaces has been developed. The heparinized surface releases insignificant amounts of heparin and can be regarded as stable. The blood contact properties as studied in vitro revealed that the surface was highly thromboresistant in terms of reduced platelet adhesion, surface catalyzed adsorption and inhibition of thrombin and capacity to prevent clotting of nonanticoagulated blood.

Blood Coagulation↗
PubMed1983

Increased uptake of serotonin in platelets from car painters occupationally exposed to mixtures of solvents and organic isocyanates.

Twelve car painters occupationally exposed to mixtures of solvents and organic isocyanates were investigated concerning serotonin uptake in platelets. The data from the exposed workers were compared to data from a reference group consisting of 50 nonexposed volunteers. The mean platelet count in whole blood of the exposed workers was markedly lower than the corresponding value of the reference group. Three workers had values below the lower limit of the 95% tolerance interval of the referents. In both groups the serotonin transport strictly obeyed Michaelis-Menten's simple saturation kinetics. Nine of the twelve exposed workers had uptake rates which were significantly higher (p = 0.05) than those of the referents. The obtained data suggest that the present method may be used to reveal early organ damage, prior to the appearance of clinical symptoms, due to intermittent exposure to organic solvents and isocyanates.

Adult↗
PubMed1983

The vascular endothelium as an inhibitor of thrombin.

Uptake and inhibition of thrombin on the endothelium of porcine aorta was studied in vitro. The thrombin was labelled with 125J and its enzyme activity was measured with an amidolytic assay. After exposure to the aorta both the enzyme activity and radioactivity disappeared from the solution and were recovered as surface bound activities. The rate of inhibition of the surface bound thrombin was determined in presence or absence of plasma. In presence of plasma the endothelially confined enzymatic activity was rapidly inhibited, no enzymatic activity was recovered in plasma. The surface bound radioactivity, however, decreased slowly and was recovered in plasma. In absence of plasma only slow inhibition took place. It is concluded that thrombin taken up on the endothelium is rapidly inhibited there by an interaction with plasma and then released in an inactivated state. An alternative conclusion, based on the anticoagulant and antithrombotic actions of the endothelial fibrin lining is briefly discussed.

Animals↗
PubMed1983

The vascular endothelium as an inhibitor of thrombin.

Uptake and inhibition of thrombin on the endothelium of porcine aorta was studied in vitro. The thrombin was labelled with 125J and its enzyme activity was measured with an amidolytic assay. After exposure to the aorta both the enzyme activity and radioactivity disappeared from the solution and were recovered as surface bound activities. The rate of inhibition of the surface bound thrombin was determined in presence or absence of plasma. In presence of plasma the endothelially confined enzymatic activity was rapidly inhibited, no enzymatic activity was recovered in plasma. The surface bound radioactivity, however, decreased slowly and was recovered in plasma. In absence of plasma only slow inhibition took place. It is concluded that thrombin taken up on the endothelium is rapidly inhibited there by an interaction with plasma and then released in an inactivated state. An alternative conclusion, based on the anticoagulant and antithrombotic actions of the endothelial fibrin lining is briefly discussed.

Adsorption↗
PubMed1982

Uptake and inhibition of thrombin by the vascular wall.

Thrombin activity and inhibition were assayed on the aortic surface of dogs and pigs. After sacrifice, the aortae were excised and thrombin activity was measured with an amidolytic assay. A small thrombin activity was found on the endothelium. Heparinization of the animals lowered endothelial thrombin activity. After exposure of the aortic endothelium to a thrombin/albumin solution in vitro, thrombin activity disappeared from the solution and was recovered on the surface. De-endothelialized vessels took up more thrombin than those with intact endothelium. Endothelium confined thrombin was rapidly inactivated when exposed to plasma. A slow inactivation was seen upon exposure to a modified Ringer's solution. Thrombin confined to de-endothelialized aortae, i.e. to medial structures, was always inactivated at a slow rate irrespective as to whether it was exposed to plasma or Ringer's solution. It is concluded that endothelium and subendothelium bind thrombin and subsequently inactivate it. The inactivation proceeds faster on endothelium when exposed to plasma. The possible role of glycosaminoglycans is discussed.

Animals↗
PubMed1982

Defective serotonin (5-HT) transport mechanism in platelets from patients with endogenous and allergic asthma.

The kinetics of the 5-HT-uptake by platelets in platelet-rich plasma (PRP) and PRP diluted with autologous platelet-poor plasma (PRP/PPP) were determined in normal subjects, patients with asymptomatic exogenous asthma and those with symptomatic endogenous asthma. In normal subjects the 5-HT-uptake by platelets strictly obeyed Michaelis-Menten's kinetics. In patients with asymptomatic exogenous asthma, the active 5-HT-transport was moderately distorted in PRP and severely altered in PRP/PPP. Patients with symptomatic endogenous asthma exhibited already in PRP a dramatic transport disturbance. The alteration of the active 5-HT-transport was characterized by increasing uptake inhibition by rising 5-HT concentrations in plasma. This phenomenon could be due to changes in the platelet environment, defects in the platelet membrane or intrinsic platelet disorders. It is concluded that asthmatics have genetically or later acquired platelet disorder, which is more clearly observed in patients with symptomatic endogenous asthma than in those with asymptomatic exogenous asthma.

Adolescent↗
PubMed1982

Continuous intra-arterial PO2 monitoring with a surface heparinized catheter electrode. A study of conformity in conventional blood gas analysis and of long-term electrode function in the non-heparinized dog.

Surface-heparinized catheter PO2 electrodes were used for continuous intra-arterial monitoring in non-heparinized dogs. During one-day experiments the read-out of the electrode monitoring unit was compared with that of conventional blood gas analysis. Furthermore, the electrodes were studied after long-term implantation. The intra-arterial PO2 electrodes have previously been reported to be linear in the gas phase, water phase and in heparinized blood. The present study demonstrates that the catheter electrodes remain linear after surface heparinization. As compared with the conventional blood gas analysis it was found that the desk analyser in the range PaO2 greater than 18 kPa underestimated the actual PaO2 as compared to the invasively monitored PaO2, but in the range below 7 kPa the desk analyser overestimated the PaO2. Surface-heparinized PO2 catheter electrodes were studied after up to 23 days of implantation. No coagulation phenomenon was found around the catheters, neither macroscopically nor by scanning electron microscopy. The electrical function withstood 7 days of implantation. After more extended periods the electrical leads were broken without any damage to the catheter itself. When compared with acutely implanted surface-heparinized electrodes, there was no difference in monitoring characteristics between the acutely implanted and the long-term implanted PO2 electrodes.

Animals↗