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T Gustafsson

Publications and source records attributed to T Gustafsson.

At least 55 records · Page 3Linked to original sources
PubMed1994

In vitro effect of D-myo-inositol 1,2,6-trisphosphate (PP-56) on aggregation of platelets from normal and diabetic rats: relationship to malondialdehyde release and phosphoinositide pathway.

In the present study, we investigated the in vitro effects of D-myo-inositol 1,2,6-trisphosphate (PP-56) on platelets from normal and streptozotocin-induced diabetic rats. PP-56 markedly inhibited aggregation, in a dose-related manner, when added in vitro, more efficiently with thrombin- than with ADP-induced aggregation and, after 90 min incubation, more in diabetic than in normal platelets. The PP-56 platelet inhibitory effect seems to be related to its phosphate content. PP-56 blocked the release of malondialdehyde from erythrocytes, but to the same extent in normal and diabetic rats. PP-56, after 20 min incubation, restored the platelet phosphoinositide turnover, which was significantly modified in diabetic rats. This last observation could explain at least part of the specificity of PP-56 for normalizing platelet aggregation in diabetic animals after long-term administration in vivo.

Animals↗
PubMed1994

[A harmonious and hierarchic order].

As is well known, biologists in Darwin's own life-time were sceptical to the mechanism he proposed as the driving force behind evolution. In this essay it is argued that one reason for this scepticism was the idealistic structure of 19th century thought. Scientists in the 19th century saw perfection as the ultimate goal for history, society and mankind. A concept of evolution that emphasized random selection of individuals was unacceptable as long as there were other theories that could support the scientist's idealism. It is argued that the embryological concept of evolution was such a theory. By studying evolution on the model of the stages of the embryo's growth to maturity, life's history on earth described an evolution with an ultimate goal. From the anatomist Anders Retzius (1796-1860) to the zoologist Vilhelm Leche (1850-1927) it is shown how different scientists in Sweden were studying this growth process and how their idealistic frame of mind made the embryological conception of evolution an acceptable alternative to the mechanical process described by Darwin.

Biological Evolution↗
PubMed1993

Effects of treatment with myo-inositol or its 1,2,6-trisphosphate (PP56) on nerve conduction in streptozotocin-diabetes.

Nerve conduction abnormalities in peripheral nerves from diabetic patients may be early indicators for the future development of symptomatic neuropathy. In this study, three weeks of experimental diabetes in the rat caused a significant decrease in motor nerve conduction velocity measured in vivo (45.3 +/- 3.6 m/s; mean +/- S.D.) compared to controls (57.7 +/- 4.5 m/s). myo-Inositol administration to diabetic rats (500 mg/rat per day) for the duration of the study, partially prevented this decrease (50 +/- 4.4 m/s). An analogue of myo-inositol, PP56 (D-myo-inositol-1,2,6-trisphosphate), at a dose of 24 mg/rat per day completely prevented this reduction in diabetic rats (53.4 +/- 5.8 m/s). Resistance to hypoxic conduction block was determined in vitro in endoneurial preparations and was assessed as the decline in compound action potential amplitude over a 40 min period of hypoxia. Compound action potential amplitude (as % of initial value +/- S.D.) was significantly greater in diabetic preparations compared with controls at 40 min of hypoxia (76.1 +/- 9.1 vs. 54.8 +/- 14.7 respectively). Treatment to diabetic rats with myo-inositol did not significantly affect this value (79.9 +/- 16.6) but PP56 treatment partially prevented the increased resistance to hypoxic conduction block (69.4 +/- 16.0). This study demonstrates that these acute abnormalities of nerve function in early experimental diabetes may be attenuated by the administration of PP56, possibly acting via a vascular mechanism.

Action Potentials↗
PubMed1992

Antagonism of pre- and postjunctional responses to neuropeptide Y and sympathetic stimulation by D-myo-inositol-1,2,6-trisphosphate in the anaesthetised dog.

Pre- and postjunctional responses to nerve released or exogenous neuropeptide Y (NPY) were measured in the anaesthetised dog before and after administration of D-myo-inositol-1,2,6-trisphosphate (PP56) a putative NPY antagonist. The inhibition of the increase in pulse interval evoked by vagal stimulation was used as a measure of prejunctional action of NPY and the magnitude of increase in blood pressure was used as a measure of postjunctional action of NPY (direct action or constrictor potentiating). Elevated plasma levels of PP56 were maintained throughout the course of the experiment. PP56 significantly reversed the inhibitory effect of NPY (nerve released or exogenous) on cardiac vagal action, and significantly inhibited the pressor response to exogenous NPY. PP56 did not affect the pressor response to intravenous phenylephrine, a selective alpha-adrenoceptor agonist. PP56 therefore significantly antagonises both pre- and postjunctional effects of NPY (nerve released and exogenous) and, with respect to its postjunctional antagonism, this action is selective for NPY.

Anesthesia↗
PubMed1992

Effect of D-myo-inositol on platelet function and composition and on cataract development in streptozotocin-induced diabetic rats.

Diabetes is known to be associated with an increase in aldose reductase activity, platelet hyperaggregability, lipid peroxidation, and cataract formation. A molecule, D-myo-inositol 1,2,6-trisphosphate (PP-56), derived from phytic acid, could in principle, by supplying myoinositol to tissues and acting as an antioxidant, counteract some of the manifestations of diabetes. Thus, the effects of PP-56 on platelet aggregation, fatty acids, and polyols were investigated in uncontrolled streptozotocin-induced diabetes in rat in relation to cataract and lipid peroxidation. A decrease in the response of platelet aggregation to thrombin and ADP (P less than 0.05, P less than 0.001) and in the level of sorbitol and the ratio sorbitol/myo-inositol (P less than 0.01) in platelets was observed in the rats treated by PP-56 for 7-8 weeks. These beneficial effects were associated with an incidence of cataract reduced by 26 to 44% (P less than 0.05 to P less than 0.001) depending on the duration of treatment. They were also accompanied by a significant lower plasma level of malondialdehyde (P less than 0.05), and, more markedly, of conjugated dienes (P less than 0.001) as well as an increase in platelet lipids of the 20:4(n-6)/20:3(n-6) ratio, an index of delta 5 desaturase activity. PP-56 appears to modulate fatty acid desaturases and aldose reductase in platelets and delay by a few weeks the development of cataract in this acute model of diabetes.

Animals↗
PubMed1991

Effects of PP-56 and vitamin E on platelet hyperaggregability, fatty acid abnormalities, and clinical manifestations in streptozocin-induced diabetic rats.

The effects of vitamin E and D-myo-inositol 1,2,6-trisphosphate (PP-56) were investigated in long-term studies in streptozocin-induced diabetic rats fed a purified diet with 33% lipids and a polyunsaturated-to -saturated fatty acid ratio of 1. A supplement of vitamin E decreased plasma triglycerides, platelet lipid biosynthesis, some of the delta 6- and delta 5-desaturase abnormalities, and urine ketone bodies but did not affect the response of platelets to aggregation. PP-56 completely normalized the platelet reactivity to ADP and thrombin. This was accompanied by normalization of platelet lipid biosynthesis and diabetes-induced abnormalities in delta 6- and delta 5-desaturases. PP-56 treatment also reduced the mortality rate and to a certain extent urinary ketone bodies. The protective effect of PP-56 on platelet aggregation and mortality rate were dose related. PP-56, a molecule derived from phytic acid, seems to exert potent protective effects on some of the manifestations associated with diabetes in rats.

Adenosine Diphosphate↗