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Biomedical subjects

D Joseph

Publications and source records attributed to D Joseph.

At least 127 records · Page 7Linked to original sources
PubMed1982

Platelet-activating factor (PAF-acether): thromboxane-independent synergism with adrenaline on human platelets and recent insights into its mode of action.

The mode of action of PAF-acether on human and rabbit plasma-free platelets is reviewed. PAF-acether and adrenaline synergize to trigger aggregation of human platelets, and this synergism is refractory to aspirin. When degranulated rabbit platelets are stimulated with PAF-acether, with thrombin or with the snake venom component convulxin, aggregation is obtained in the absence of detectable secretion. Collagen-induced aggregation is reduced, and is suppressed when aspirin is applied to the degranulated platelets. The formation of PAF-acether by platelets, and their stimulation by PAF-acether itself, should be added to the newly recognized pathways for platelet stimulation.

Animals↗
PubMed1981

Experimental myocardial infarction in the rat as a quantitative model for the study of anti-ischemic interventions.

The identification of metabolic and drug interventions able to reduce myocardial injury after coronary artery occlusion requires experimental models. The rat model of ischemic injury is technically simple, unexpensive, informative and accessible to quantitative studies. In this present study, 41 rats underwent temporary myocardial ischemia of variable duration using left coronary artery ligation. They were sacrificed at 48 hours, and the heart was immediately frozen in liquid nitrogen. Serial 8 micrometer sections of known intervals were tested for succinodehydrogenase (NBT stain). Gross sectional areas measured planimetrically were utilized to calculate total myocardial volume (Vmyocardium) and infarcted myocardial volume (Vinfarct) with the aid of a programmable calculator. The data showed a linear regression for Vinfarct/Vmyocardium according to the time of ischemia (p 0,001). We suggest to test the efficiency of metabolic and drug interventions on the regression curve of the necrotic tissue using a multiple linear analysis. Since ischemic changes evolve more rapidly in this model, the intervention under study should be set up at the time of coronary artery occlusion.

Animals↗
PubMed1980

Impaired sarcolemmal membrane permeability in reperfused ischemic myocardium. Ultrastructural tracer study.

Sarcolemmal membrane permeability to intravenously injected horseradish peroxidase HRP (MW = 40,000) was examined in 8 Wistar rats which had temporary ischaemia produced by left coronary artery ligation. HRP reaction product was identified following 6 min of circulation time by light and electron microscopy. Controls included 4 uninjected animals with coronary ligation, 2 uninjected animals without myocardial ischaemia and 2 injected non operated rats. In normal myocardium, the tracer permeated endothelial plasmalemmal vesicles, intercellular spaces and intracellular vesicle of the T-tubule system, but never permeated the cytoplasm of myocardium cells. As early as 15 min after coronary artery ligation followed by 6 min of reperfusion with circulation of the tracer, HRP product could be seen in the cytoplasm of muscle cells randomly distributed in the subendocardial area. The quantity of permeated cells increased when the ischaemic myocardium is reperfused during 10 min before injecting the tracer. These data indicate that sarcolemmal membrane alteration is an early event in myocardial ischaemic injury and precede the irreversible cellular degenerative changes.

Animals↗
PubMed1980

The pH and titratable acidity of stored CPD blood.

Blood stored in citrate-phosphate-dextrose (CPD) solution for periods up to 20 days had a mean pH 6.71. The mean metabolic hydrogen ion excess was 32 mmol/litre and the mean respiratory hydrogen ion excess was 80 mmol/litre. These results for CPD blood are compared with those obtained on acid-citrate-dextrose blood. A prediction is made that clnically, only small variations in metabolic and respiratory acid-base balance would be produced directly due to the acid and base loads in transfused blood.

Acid-Base Equilibrium↗
PubMed1980

[Pathological patterns of reperfused myocardial infarction. Experimental study (author's transl)].

The effect of the reperfusion on the pathological appearance of experimental myocardial infarction has been studied in the rat (87 animals). Following permanent ischemia (33 animals sacrified after 1, 6, 24 and 48 hours), there appeared a reproducible extended transversal infarction marked by a uniform sequence of histologic, histoenzymatic and ultrastructural changes. Following temporary ischemia (54 animals), the pathological patterns were marked by myofibrillar degeneration (contraction band necrosis), cellular edema, calcium deposits and interstitial hemorrhages. These changes appeared after reperfusion of short duration (10 minutes). Sarcolemmal and capillary permeability alterations could be the main factor involved in the reperfusion injury. Similar tissue damage have been found in clinical conditions in subendocardial hemorrhagic necrosis after cardiopulmonary by-pass, and in reperfused infarction.

Animals↗
PubMed1979

Mechanisms of bronchoconstriction and of thrombocytopenia induced by collagen in the guinea pig.

Collagen injected to guinea pigs i.v. increased the pulmonary resistance to inflation (bronchoconstriction) and induced thrombocytopenia. Immune platelet depletion protected against the effects of collagen, and has been shown not to prevent bronchoconstriction induced by the prostaglandin/thromboxane A2 precursor arachidonic acid. Use of inhibitors demonstrated that histamine, serotonin, acetylcholine and bradykinin were not involved with the effects of collagen in the guinea pig. Aspirin and indomethacin inhibited collagen-induced bronchoconstriction completely and thrombocytopenia partly, supporting the hypothesis that the former is prostaglandin cyclo-oxygenase dependent, whereas the latter has a thromboxane A2-independent mechanism as well. Carrageenan, heparin and reserpine inhibited the in vivo effects of collagen to various extents, but their precise mechanism of action could not be discovered. Collagen-induced bronchoconstriction is strictly platelet and thromboxane A2-dependent.

Airway Resistance↗
PubMed1977

The effect of coronary artery reperfusion on the extent of myocardial infarction.

The effect of the reperfusion on myocardial infarction has been studied in the rat in order to assess the possible reversibility of myocardial damage. The present study deals with reperfusion of experimental myocardial infarction in the rat. Two groups of animals were compared: one was subjected to permanent ischemia and the other was subjected to ischemia of variable duration 1) hour to 24 hours). The differences between infarction caused by permanent ischemia and the evolution of infarction following reperfusion were studied by means of histologic (121 specimens) histoenzymatic (56 specimens), ECG (100 specimens), techniques and study of the mcirocirculation (70 specimens). The size of the infarctions caused by temporary ischemia was found to be significantly smaller in 60% of the cases as compared to the infarctions caused by permanent ischemia. Histoenzymatic study (phosphorylase activity and succinodehydrogenase activity) confirmed the existance of a marginal zone extending over one third of the surface of the ischemic myocardium: reperfusion permitted the salvage of this zone and thereby diminished the extent of necrosis. The latter findings were further confirmed by the ECG study showing earlier regression of ischemic ST changes following early reperfusion. Microcirculatory changes secondary to anoxia may account for the fact that, in a certain percentage of the cases, early reperfusion does not prevent extension of infarction.

Animals↗
PubMed1976

Microcirculatory changes following early reperfusion in experimental myocardial infarction.

69 rats underwent temporary or permanent ligation of the left coronary artery and were studied by the injection of colloidal carbon following fixation-perfusion. 10 rats were using the same protocol and served as controls. Localized myocardial ischemia was accompanied by microvascular changes which produced capillary obstruction when blood flow was reestablished. This phenomenon of "no-reflow" was characterized by the presence of large non perfused areas seen after brief periods of ischemia (15 min). These areas were increased when the period of ischemia was lengthened. After 30 to 60 min of interruption of blood flow the non perfused area extended over the major portion of the ischemic area. During reperfusion the "no-reflow" phenomenon displayed during the first hour showing a transitory improvement in capillary perfusion which was soon followed by a progressive reexpansion of the non injected zones. After 24 hours of reperfusion, the latter zones were identical in their extent to those cases showing tissue necrosis following permanent ischemia. This "no-reflow" phenomenon appears to play a role in the evolution of the reperfused ischemic area by excluding certain areas from the benefits of reperfusion. The most probable factors involved in this process are: increased blood viscosity, endothelial changes peri-capillary edema and the contractile state of the myocardium. The incidence of these microvascular changes, using various methods of myocardial preservation during open heart surgery operations, as well as the present attempts directed towards metabolic therapy of myocardial anoxia, are under investigation.

Animals↗
PubMed1975

[Basic phospholipase of Naja nigricollis venom].

It is confirmed that N. nigricollis venom contains several phospholipases one of these is a basic phospholipase A. This enzyme is toxic for mice when injected intravenously. In vitro it reacts on egg yolk lecithin producing lysolecithin and prevents the phenomenon of blood clotting. An immunological identity has been established between this basic phospholipase and two acidic phospholipases present in the same venom.

Amino Acids↗