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Biomedical subjects

C Mattsson

Publications and source records attributed to C Mattsson.

50 records · Page 3Linked to original sources
PubMed1984

Inhibition of the human tissue plasminogen activator in plasma from different species.

The rate and extent of complex formation between protease inhibitors present in plasma from different species and a human plasminogen activator purified to homogeneity from the supernatant of a human melanoma cell line was studied in vitro. The fibrinolytic activity of the one-chain plasminogen activator disappeared form human, cat and rabbit plasma with a half-life of 100 minutes. By means of antibodies directed against purified protease inhibitors the main inhibitor in human, cat, dog and rabbit plasma was identified as alpha 2-antiplasmin. Alpha 2-macroglobulin and C1-esterase-inhibitor functioned as inhibitors to a lesser extent. The main inhibitor in rat plasma was alpha 2-macroglobulin. The plasma half-life was 3 (rabbit and human) to 10 (dog and rat) times shorter for the two-chain form than for the one-chain form of the plasminogen activator molecule. It is also concluded that, with respect to plasma elimination of the fibrinolytic activity, among the common laboratory animals, the rabbit is the most suitable animal available for the study of fibrinolysis.

Animals↗
PubMed1983

Effect on haemostasis of intravenous injection of alpha 2-antiplasmin in cats treated with streptokinase.

The effect in cats of an intravenous injection of purified human alpha 2-antiplasmin on changes in the haemostatic system, caused by administration of streptokinase was investigated. The decrease in fibrinogen and plasminogen caused by streptokinase infusion was immediately inhibited by the alpha 2-antiplasmin infusion. The increase in vascular permeability and the prolongation of coagulation times were efficiently inhibited.

Animals↗
PubMed1983

Human extrinsic plasminogen activator fibrinolytic properties and neutralization in vivo.

The thrombolytic activity and elimination rate in vivo of a plasminogen activator purified from a melanoma cell line was examined in a rabbit thrombus model. Following an intravenous injection of 125I labelled plasminogen activator, its biological activity disappeared very rapidly from the plasma (t1/2 = 1.5 min) and radioactivity immediately accumulated in the liver. After a two-hour infusion with a total amount of 0.5 mg plasminogen activator a 60 per cent reduction in the weight of partially occluding thrombi was noted. No significant thrombolysis was seen in totally occluded vessels. Treatment with 0.5 mg plasminogen activator caused no depletion of fibrinogen or alpha 2-antiplasmin. No significant thrombolysis occurred after infusion of 0.5 mg streptokinase, but total lysis of occluding and non-occluding thrombi was obtained after a two-hour infusion of 1 mg streptokinase, without any reduction of fibrinogen. A marked reduction of alpha 2-antiplasmin was seen after both 0.5 and 1 mg of streptokinase treatment but were not seen in rabbits infused with plasminogen activator.

Animals↗
PubMed1982

Anticoagulant and antithrombotic effects of heparin and low molecular weight heparin fragments in rabbits.

Heparin and heparin fragments of different molecular weight and with different anti-factor Xa/APTT activity ratios were studied with respect to their ability to inhibit thrombus formation in an animal model. It is concluded that: a) Neither anti-factor Xa nor the APTT activity alone is a good reflector of the antithrombotic activity. b) Anti-factor Xa active fragments must have a minimum molecular weight in order to elicit good antithrombotic activity. c) High affinity for antithrombin III is important for good antithrombotic activity. d) A heparin fragment of molecular weight 4 000 has the same antithrombotic activity as heparin but less effect on the clotting time.

Animals↗
PubMed1977

Acetylcholine receptor protein. Neuromuscular transmission in immunized rabbits.

Rabbits injected with purified acetylcholine (ACh) receptor protein produce antibodies against the receptor and develop generalized muscle weakness. The compound muscle action potentials show a decremental fall in amplitude with repetitive nerve stimulation. Both the weakness and the decrement is counteracted by reversible cholinesterase inhibitors. Intracellular recordings from muscle endplates show that the amplitude of the miniature end-plate potentials is considerably reduced. A reduced binding of neurotoxin to muscles from immunized rabbits was observed. Nerve impulses release a normal number of ACh packages (quanta) from the motor nerve terminals. The muscle weakness in immunized rabbits thus has the same features as the muscle weakness in myasthenia gravis and may be a good animal model of myasthenia gravis.

Acetylcholine↗
PubMed1975

Antibodies against nicotinic acetylcholine receptor and skeletal muscle in human and experimental myasthenia gravis.

Using rocket immunoelectrophoresis and indirect haemagglutination tests, antibodies to nicotinic acetylcholine receptor (n-AChR) from Torpedo marmorata were detected in sera from rabbits with experimental myasthenia but not in sera from patients with myasthenia gravis or in rabbit antisera to a partly purified skeletal muscle antigen. Antibodies to this antigen were demonstrated in sera from patients with myasthenia gravis but not in sera from rabbits with experimental myasthenia. The results indicate that there is no immunological cross-reaction between the muscle antigen and n-AChR from Torpedo marmorata, and little or no cross-reactivity between these n-AChR antibodies and possible muscle n-AChR antibodies in myasthenia gravis patients.

Acetylcholine↗
PubMedDate not supplied

Myringosclerosis develops within 9h of myringotomy.

The aim of the present experimental study was to elucidate the temporal development of myringosclerosis. Twenty-four Sprague-Dawley rats were myringotomized bilaterally. At 3, 6, 9, 12, 18, 24, 30, 36, 48, 60, 72 and 84 h after the myringotomy, 2 animals at each time were examined otomicroscopically and thereafter sacrificed. The pars flaccida and pars tensa were excised and prepared for light- and electron-microscopic studies. Otomicroscopically, myringosclerosis was visible in the pars tensa 24 h after myringotomy, whereas no sclerotic lesions were noted in the pars flaccida. Histologically, sclerotic lesions were present in the pars tensa and pars flaccida 9 and 12 h, respectively, after myringotomy. The pars flaccida responds promptly with an inflammatory reaction characterized by abundant macrophages. Myringosclerosis develops promptly after myringotomy and its establishment is related to an inflammatory reaction.

Animals↗