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Biomedical subjects

R Reneman

Publications and source records attributed to R Reneman.

10 recordsLinked to original sources
PubMed1988

In vivo demonstration of microvascular pathology by intravital microscopy in experimental chronic graft-versus-host disease: analogy with scleroderma.

Experimental models of chronic graft-versus-host disease have been advocated for studying the pathogenesis of scleroderma. However, microvascular abnormalities have not been documented in these models, whereas in man, cutaneous microvascular pathology (demonstrable by intravital microscopy) is a common feature of scleroderma. In our study scleroderma-like skin disease was evoked by allogeneic bone marrow transplantation in rats. Intravital microscopy of the skin of these animals showed strongly dilated capillaries, resembling the dilated loops in patients. This finding demonstrates that chronic graft-versus-host (scleroderma-like) disease may be pertinent to study the pathogenesis of microvascular injury in scleroderma.

Animals↗
PubMed1979

Comparative study of cardiovascular, neurological and metabolic side effects of 8 narcotics in dogs. Pethidine, piritramide, morphine, phenoperidine, fentanyl, R 39 209, sufentanil, R 34 995. III. Comparative study of the acute metabolic toxicity of the narcotics used in high and massive doses in curarised and mechanically ventilated dogs.

The I.V. administration in dogs of high and massive doses of narcotics produced an acute rise in CO2 consumption, a rise of plasma catecholamines and other slight biochemical and metabolic perturbances. A general trend towards metabolic acidosis and hypermetabolism was noticed but important differences appeared according the drugs and doses chosen. The safety margin for metabolic toxicity (ratio between IV doses producing severe metabolic side-effects and doses necessary for deep surgical analgesia) were calculated for each narcotic and found as follows: 1 for pethidine, 3.3 for piritramide, 13 for morphine and phenoperidine, 12.5 for R 39 209, 60 for fentanyl, 800 for sufentanil and 4 000 for R 34 995. Drug associations may decrease or increase the metabolic safety margin of the narcotics. Beneficial associations with morphinomimetics are found with droperidol, etomidate and flunitrazepam.

Acidosis↗
PubMed1979

Comparative study of cardiovascular, neurological and metabolic side effects of 8 narcotics in dogs. Pethidine, piritramide, morphine, phenoperidine, fentanyl, R 39 209, sufentanil, R 34 995. II. Comparative study on the epileptoid activity of the narcotics used in high and massive doses in curarised and mechanically ventilated dogs.

The experimental design, described in part I, was again used here. The electrocortical activity was registered with an EEG amplifier using a bipolar derivation of needle electrodes fixed in the scalp of a dog in the fronto-occipital position. In this situation the convlusion threshold for the 8 substances is as follows: pethidine 20 mg.kg-1 I.V., piritramide 30, morphine 180, phenoperidine 4, R 39 209 5, fentanyl 4, sufentanil 4 and R 34 995 10 mg.kg-1 I.V. Comparing the I.V. doses producing severe convulsions with the doses necessary for deep surgical analgesia a safety margin of neurological toxicity was calculated. This was for pethidine 2.2, for piritramide 6.6, for phenoperidine 16, for R 39 209 62.5, for morphine 72, for fentanyl 160, for sufentanil 1 000 and for R 34 995 10 000. It is concluded that for pure narcotics there exists an inverse relationship between analgesic potency and neurological toxicity which is always accompanied by a hyperactivity of the automatic nervous system. Factors modifying the convulsive level of the narcotics are still under investigation. In the meanwhile it can be stated that the association of a strong narcotic with flunitrazepam, droperidol or etomidate will increase the convulsion threshold of the morphinomimetics.

Acidosis↗
PubMed1976

Electrophysiological effects of droperidol in different cardiac tissues.

The effect of droperidol in concentrations between 0.05 and 5 mg/I was evaluated on different electrophysiological variables in auricular preparations of the guinea-pig, papillary muscles of dog and cat, Purkinje fibres of the dog, cow and sheep. At low concentration (0.25 to 0.5mg/I) droperidol decreased pacemaker activity and prolonged the effective refractroy period. The inhibition of pacemaker activity was not accompanied by a reduction in the rate of early diastolic depolarization, but was related to an inhibition of the depolarization process during late diastole. At high concentrations (5mg/I) resting potential, action potential amplitude, (dV/dt)max and conduction velocity were reduced. Reduction of dV/dt during the upstroke was more pronounced at lower membrane potentials, the inactivation curve was shifted to more negative membrane potentials. The action potential was lengthened or shortened, the effect being dependent on the frequency, dose, exposure time and animal species. Droperidol had no deleterious effect on Ca-mediated action potentials. The antiarrhythmic activity of droperidol in therapeutic concentrations (0.25 and 0.5mg/I) can be explained by the reduction of pacemaker activity and the lengthening of the effective refractory period. In terms of changes in ion conductance most effects can be explained by a reduction in Na conductance. No simple explanation can be offered for the complex changes in action potential duration.

Action Potentials↗
PubMed1975

Activated reptilase clot retraction of dog platelet-rich plasma: differences with human platelet-rich plasma.

The retraction of dog platelet-rich plasma (PRP) clotted with Reptilase in the presence of inducers and inhibitors of the platelet adhesion-aggregation reaction was studied. In contrast to human cells, dog platelets fail to support retraction in an ADP-Reptilase system. With Thrombofax as aggregation inducer, slight (without additional CaCl2-MgCl2) to moderate (with additional CaCl2-MgCl2) retraction occurs. In contrast to human samples, such retraction is inhibited by platelet release inhibitors. Electron-microscopic examinations show that Thrombofax, but not ADP, induces the formation of large cytoplasmic protrusions from dog platelets. Such formation is inhibited by release-inhibitors. The results of the study support the concept that platelet pseudopod formation, rather than the release reaction, is a prerequisite for clot retraction.

Adenosine Diphosphate↗
PubMed1975

Effects of suprofen, an inhibitor of prostaglandin biosynthesis, on platelet function, plasma coagulation and fibrinolysis. I. In vitro experiments.

?The effects of suprofen, an inhibitor of prostaglandin biosynthesis, on human platelet function, fibrinolysis, proteolysis and coagulation in vitro were compared to those of reference compounds. Platelet aggregation induced by collagen, adrenaline and arachidonic acid was inhibited by suprofen depending on its concentration. Suprofen and indomethacin proved to have an equally inhibitory effect on platelet aggregation induced by collagen. Thrombin-induced aggregation was more inhibited by suprofen than by indomethacin. While the primary wave of A.D.P.-induced aggregation remained unchanged, the rate of disaggregation was enhanced by both compounds. Experiments on platelet factor-4 and 14C-serotonin release showed that suprofen and indomethacin reduced the platelet release reaction. Based upon results from experiments on synergism of suprofen with other compounds, on inhibition of arachidonic acid-induced platelet reactions and of prostaglandin E2-release, it is suggested that suprofen by inhibiting the prostaglandin biosynthesis in platelets also inhibits the platelet release reaction. In contrast to indomethacin and flufenamic acid, suprofen did not affect fibrinolysis or thrombin clotting activity. Tryptic proteolysis of albumin, however, was reduced by suprofen in a concentration-dependent and a substrate-competitive way. Tryptic decompisition of a synthetic substrate, on the other hand, was not reduced by either suprofen, indomethacin or flufenamic acid. These findings suggest that the observed reduction of albumin proteolysis by suprofen is related to an effect on the protein substrate rather than on the proteolytic enzyme itself.

Adenosine Diphosphate↗
PubMed1975

Effects of suprofen, an inhibitor of prostaglandin biosynthesis, on platelet function, plasma coagulation and fibrinolysis II. In vivo experiments.

Suprofen, an inhibitor of prostaglandin biosynthesis, was found to affect certain aspects of platelet function after in vivo administration in various species. In guinea-pigs, platelet aggregation induced by collagen and Thrombofax, and secondary A.D.P. aggregation were reduced in a dose-dependent way by suprofen (single oral administration) from 0.08 mg/kg on. In dogs, the effect of a single oral dose of 2.5 mg/kg of suprofen on collagen-induced aggregation started 30 min after administration, lasted for at least 8 h and had disappeared after 24 h. Plasma coagulation parameters were not affected by the compound in this species. In rats, suprofen prolonged tail bleeding times, but did not modify fibrinolysis, platelet adhesion to glass beads or plasma coagulation. Sub-chronic administration of comparatively high doses of the compound resulted in potentiation of the anti-coagulant effect of warfarin in this species.

Adenosine Diphosphate↗