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Biomedical subjects

H Haljamäe

Publications and source records attributed to H Haljamäe.

At least 91 records · Page 5Linked to original sources
PubMed1982

Effects of commercial (pH approximately 3.5) and freshly prepared (pH approximately 6.5) lidocaine-adrenaline solutions on tissue pH.

Differences in the effects of commercially available, sodium bisulfite-containing (pH 3.5-4), and freshly prepared (pH 6.5) lidocaine-adrenaline solutions on tissue pH and tissue oxygenation were studied experimentally. In rabbits, a 5 x 5 cm area under the panniculum was infiltrated with 0.9% NaCl, plain lidocaine, plain adrenaline or one of the two lidocaine-adrenaline solutions. Tissue pH was measured continuously as well as intermittently in the infiltrated area with monocrystalline antimony needle electrodes. Infiltration of the tissue with the 4 ml volume of a test solution did not seem to induce any significant tissue injury. Tissue pH was decreased for 30 min following plain lidocaine and for 90 min or more following lidocaine-adrenaline infiltration. With the exception of the first few minutes, no significant differences in the effects on tissue pH between commercial and freshly prepared lidocaine-adrenaline solutions could be seen. Tissue hypoxia occurred only following infiltration with plain adrenaline. It may thus be concluded that in spite of the low pH and the O2-reducing properties of commercial lidocaine-adrenaline solutions, a rapid buffering occurs in the tissues. The use of commercial lidocaine-adrenaline solution for local infiltration thus seems as safe as that of freshly prepared lidocaine-adrenaline solutions.

Animals↗
PubMed1981

Vascular and metabolic effects of methylprednisolone and phenoxybenzamine during controlled hypotension in the dog.

The relationship between central haemodynamics and vascular and metabolic parameters in skeletal muscle was studied in dogs subjected to controlled haemorrhagic hypotension and treated with cumulative doses of methylprednisolone (4-32 mg x kg-1), (or saline in the control group), followed by phenoxybenzamine. There were no significant haemodynamic or metabolic changes between the groups during the injections of steroid or saline. The alpha-adrenergic receptor blockade caused, as found earlier, a pronounced vasodilation in the steroid group, which was parallelled by an increase in muscle blood flow in the same order of magnitude. There was no clearcut relationship between metabolic and vascular effects in the groups. Despite the significant difference in blood flow between the groups after phenoxybenzamine, only small and insignificant differences were seen in muscle metabolites, with the exception of muscle lactate which showed higher values in the steroid group. The study provides further evidence in support of the hypothesis that the haemodynamic effects of the combination of methylprednisolone and phenoxybenzamine are of neurogenic origin.

Animals↗
PubMed1980

Control of tissue environment during vital microscopy of the microcirculation in the m. tenuissimus in cat.

The physiological preservation of the tenuissimus muscle preparation in cat during vital microscopy of the microcirculation is assessed, comparing the originally described technique with a modified approach. Differences in the compared techniques include modes of dissection and transillumination, room-air exposure and moisturizing procedures. The original technique involves extensive dissection, inadequate temperature control and irrigation in open air. The modified technique involves less surgery due to a new illumination system, controlled heating and a Mylar foil cover on the preparation to minimize room-air influences. Temperature measurements and analyses of energy metabolism (ATP, CP, glucose, G6-P and lactate) are used as objective criteria of tissue normalcy. The microcirculation and metabolism are evaluated during anesthesia (alpha-chloralose) at rest as well as in hemorrhagic shock. In the resting state, muscle temperature drops to 28 degrees C with the irrigation technique, whereas the Mylar technique keeps the temperature at 34--35 degrees C. Neither technique causes deviations in normal metabolism. In shock, however, the temperature in the irrigated tenuissimus muscle fall 8--9 degrees C below deep muscle temperature and there is a significantly attenuated metabolic response to ischemia, while the Mylar preparation follows the changes of unexposed muscle, both in temperature and metabolism.

Animals↗
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

Effect of calcium on brain metabolism in vitro.

In attempts to distinguish between direct and indirect effects of Ca on brain cell metabolism, respiration, glycolysis, ATP, phosphocreatine, incorporation of [14C] leucine into protein, and accumulation of 45Ca was determined in brain slices. Incubation was carried out in normal salt-balanced medium, in high-potassium-or ouabain-containing medium under aerobic and anaerobic conditions. Calcium ions inhibited slightly glycolysis and respiration in normal medium and activated amino acid incorporation into proteins. Levels of ATP and phosphocreatine remained normal. The effects were interpreted as due to a stabilization of plasma membranes by Ca ions to prevent their spontaneous depolarization. Incubation of slices in high-potassium and ouabain media in aerobic conditions in the presence of Ca resulted in activation of respiration and glycolysis, decrease of ATP and phosphocreatine levels, and inhibition of amino acid incorporation into proteins. The disturbances in energy metabolism, caused by the respiration-linked Ca uptake in brain mitochondria and concomitant inhibition of oxidative phosphorylation, may lead to the inhibition of amino acid incorporation into proteins. An increase in Ca levels in the cytoplasm may only be expected in anaerobic conditions during the incubation in high-potassium and ouabain media. This is manifested by a direct inhibition of glycolysis by Ca ions and a drastic decrease of ATP and phosphocreatine in slices. The results suggest that stimulation of aerobic glycolysis and inhibition of anaerobic glycolysis by Ca may explain the unknown mechanism of the so-called "reversed Pasteur effect" of brain slices incubated in high-potassium media.

Aerobiosis↗
PubMed1978

Effect of glucagon and blood transfusion on liver metabolism in hemorrhagic shock.

Treatment with glucagon in addition to blood transfusion was compared with blood transfusion alone after one hour of hemorrhagic shock in the rat. In liver tissue Na+ increased and K+ decreased during haemorrhagic shock. After treatment the initial values were restored equally in both groups within ten minutes. Incubation of liver slices in cold Krebs' solution resulted in a pronounced increase in Na+ and decrease in K+, the values being partially restored to initial levels after subsequent incubation at 37 degrees. Thirty minutes after treatment the liver slices obtained from rats given glucagon showed a more normal ion composition after leaching and rewarming than slices from rats not given glucagon. ATP decreased and glucose and lactate increased in liver tissue during hemorrhagic shock. These variables were partially restored 30 minutes after treatment. No difference between the treatment groups was noted. Animals trreated with glucagon were, however, more efficient in reducing the elevated blood lactate level. The results suggest that the use of glucagon in the treatment of hemorrhagic shock might be of benefit for cellular function in the liver.

Adenosine Triphosphate↗
PubMed1978

Pressure-induced ischemia. II. A metabolic study in hamster cheek pouch.

The effects of pressure-induced ischemia on energy metabolism, measured as ATP and glucose content, is studied in hamster cheek pouch. Metabolic deterioration during ischaemia is studied and after 2 h the glucose content was significantly reduced but not the ATP content, which was significantly reduced after 4 h of ischemia. Restoration of glucose levels in the cheek pouch tissue was achieved within 30 min of recirculation after release of pressure. The cellular energy metabolism is unable after 4 h of ischemia to restore ATP levels in the tissue during the 120-min of postischemic observation time. There is a difference in ability to resume normal energy metabolism after 2 and 4 h of pressure-induced ischemia.

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↗
PubMed1977

Pressure-induced ischemia. I. An experimental model for intravital microscopic studies in hamster cheek pouch.

A model to study pressure-induced ischemia by intravital microscopy is presented. A hamster cheek pouch is prepared to get a single layer of epithelium, together with vessels and connective tissue. Pressure, which can be varied, is transmitted to the tissue by a pressure chamber with a rubber membrane. Microcirculatory reactions may be studied while the pressure is applied, when the pressure is released and as the tissue is regaining circulation. The local environment is controlled by irrigating the test tissue with a solution approximating the composition of interstitial fluid. Local oxygen and carbon dioxide tensions are controlled. There is a marked difference in restoration of blood flow to the tissue after 2- and 4-hour ischemia. After 2-hour ischemia the tissue regained circulation rapidly. Microbleedings developed during the postpressure observation time. After 4-hour ischemia, on the other hand, the tissue regained circulation slowly and only in one third of the microvessels. Extensive white blood cells sticking to the vessel walls were seen indicating endothelial damage. In the 4-hour experiments there were very few microbleedings compared to the 2-hour experiments.

Animals↗