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E Jennische

Publications and source records attributed to E Jennische.

82 records · Page 5Linked to original sources
PubMed1980

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock.

Skeletal muscle reactions to hemorrhagic shock were investigated in anesthetized cats (n = 23). The tenuissimus muscle was exposed for vital microscopy and shock was induced by single-withdrawal of 45% of the blood volume. Muscle microcirculation, energy metabolism and cell membrane potentials were followed over a 2 h period along with blood pressure, hematocrit and blood leukocyte, platelet, glucose, pyruvate and lactate contents. Bleeding usually caused complete cessation of muscle blood flow for 5--20 min, while the animal compensated the blood pressure. Reflex constriction occurred in medium-sized but not in terminal arterioles. When flow reappeared a marked maldistribution was evident in the capillary bed. Flow remained in 30--50% of the capillaries, permanently or intermittedly. Leukocytes could be found lodged in many arrested capillaries and also adhering to venules in large numbers. Erythrocyte or platelet plugs were not seen in the muscle microvasculature. Glucose and G6-P contents doubled and lactate increased 5-fold in muscle tissue during shock. CP was reduced by about 25% while the ATP-level remained unchanged. Membrane potentials declined 12% in shock and the spread in potentials from adjacent fibers increased.

Animals↗
PubMed1979

Metabolic responses in feline "red" and "white" skeletal muscle to shock and ischemia.

In order to investigate possible differences in the reaction to hypoxic conditions between "red" and "white" skeletal muscle, cats were subjected to a 2 h period of either hemorrhagic shock or hind limb tourniquet ischemia, and the hypoxia induced changes were studied in the soleus and lateral gastrocnemius muscles. Muscle biopsies were analysed for ATP, CP, glucose, G 6-P and lactate. Using microelectrodes, the resting membrane potential was repeatedly measured. Both experimental models resulted in increased tissue lactate levels and a successive decrease in the membrane potential of both muscles studied. No reduction of the high energy phosphagen content (ATP + CP) occurred in any of the muscles during shock. The tourniquet ischemia resulted in a 40% reduction of the ATP + CP content in the soleus muscle, whereas in the gastrocnemius muscle no significant reduction occurred. A significant correlation was found between the tissue lactate content and the membrane potential under both conditions and in both muscles studied. It is concluded that "red" muscles are more susceptible to metabolic derangement than "white" muscles during total ischemia, whereas during hypovolemia "red" muscles appear to be protected from early hypoxic damage, probably due to a redistribution of skeletal muscle blood flow.

Adenosine Triphosphate↗
PubMed1978

Cellulr restitution after 3 h of complete tourniquet ischemia.

The refinement of techniques for extremity surgery makes it urgent to get more information at cell level of the effects of tourniquet times exceeding the usually accepted 90--120 min. Therefore, in the present experiments, the cellular metabolic and functional restitution of canine skeletal muscle after 3 h of complete tourniquet ischemia was studied. During the ischemia and after recirculation, repeated skeletal muscle samples were taken for ATP, CP and lactate analyses. At the same time periods, blood from a regional vein and vena cava was drawn for pH, pyruvate and lactate analyses. Cellular function was evaluated from repeated measurements of transmembrane potentials. The tourniquet ischemia resulted in a rapid decrease of CP to 40% of the initial level within 1 h and a continuous decrease of ATP. The lactate levels increased continuously. The transmembrane potentials decreased from an initial level of --90 to --54 mV. The release of the tourniquet resulted in a hyperemic reaction and a rapid regain of tissue CP and ATP levels within 5 min of recirculation. There was a continuous washout of lactate up to about 1 h after the release and the transmembrane potentials were normalized after about the same time period. The latter parameters indicate that areas of no-reflow persisted for up to 1 h after restored circulation. The results indicate that after a 3-hour tourniquet ischema, the cellular energy metabolism as well as the membrane function are completely normalized after about 1 h of recirculation.

Adenosine Triphosphate↗
PubMed1978

Correlation between tissue pH, cellular transmembrane potentials, and cellular energy metabolism during shock and during ischemia.

The relevance of two direct techniques for monitoring of cellular function during tissue hypoxia has been evaluated. Tissue pH and cellular transmembrane potentials were registered in canine skeletal muscle during intestinal exteriorization shock and during prolonged local tourniquet ischemia. The obtained pH and transmembrane potential changes were correlated to simultaneous changes in high-energy phosphagen (ATP + CP) and lactate levels in skeletal muscle. In control dogs no significant changes in either of the studied variables occurred. Intestinal exteriorization shock as well as local tourniquet ischemia resulted in a gradual increase in tissue lactate and a concomitant decrease in tissue pH and transmembrane potentials. In both experimental situations there was a close correlation between the transmembrane potential reduction and the tissue lactate increase. Tissue pH registrations, on the other hand, did not similarly reveal the full extent of the tissue lactate increase under the two experimental conditions. Possible reasons for this discrepancy are discussed. On the basis of the present results it may therefore be concluded that the transmembrane potential seems to be a better variable for revealing the full extent of cellular metabolic deterioration during various situations with tissue hypoxia.

Adenosine Triphosphate↗