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Biomedical subjects

L Mela

Publications and source records attributed to L Mela.

At least 19 recordsLinked to original sources
PubMed2005

Primary and secondary closure of the surgical wound after removal of impacted mandibular third molars: a comparative study.

Primary and secondary closure techniques after removal of impacted third molars were compared in terms of post-operative pain and swelling. Two hundred patients with impacted third molars were randomly divided into two groups of 100. Panoramic radiographs were taken to assess degree of eruption and angulation of third molars. Teeth were extracted, and in Group 1 the socket was closed by hermetically suturing the flap. In Group 2 a 5-6 mm wedge of mucosa adjacent to the second molar was removed to obtain secondary healing. Swelling and pain were evaluated for 7 days after surgery with the VAS scale. The statistical analysis (*analysis of variance for repeated measures, P < 0.05) showed that pain was greater in Group 1, although it decreased over time similarly in the two groups (P = 0.081, F(6,198) = 3.073*). Swelling was significantly worse in Group 1 (P < 0.001, F(6,198) = 44.30*). In Group 1, dehiscence of the mucosa was present in 33% of patients at day 7, and 2% showed signs of re-infection with suppurative alveolitis at 30 days. Pain and swelling were less severe with secondary healing than with primary healing.

Adult↗
PubMed1983

Efficacy of glucocorticoids in preventing mitochondrial metabolic failure in endotoxemia.

Endotoxemia was induced in rats and guinea pigs by an intraperitoneal injection of E coli endotoxin. In the rat, the dose used (3 mg/100 g body weight) resulted in a 60% mortality in 24 h. The same dose in the guinea pig resulted in a similar mortality at 24 h, and a 100% mortality by 3 days. Methylprednisolone Na-succinate, a glucocorticoid, given simultaneously with the endotoxin, prevented mortality in the rats. No animals died during the observation period. In the guinea pigs the same treatment protected all animals for 24 h, and resulted in an 80% survival rate over a 6-day observation period. Administration of glucocorticoids 1 or 2 h after endotoxin showed diminished efficacy. About 60% of the guinea pigs died during the 6-day observation period. Rat kidney and guinea pig brain and kidney mitochondria were isolated and analyzed for their function in untreated and treated animals 24 h after the injection of endotoxin. Rat kidney mitochondrial O2 utilization and ATP synthesis function, as well as Ca++ transport activity, were significantly below normal in the untreated animals, but did not differ from normal in glucocorticoid-treated animals. In untreated and at zero time treated guinea pigs similar results were found in brain and kidney mitochondrial functions. If treatment was delayed for 1 or 2 h, however, brain mitochondrial O2 utilization and ATP synthesis rates were significantly below normal, and both brain and kidney mitochondrial Ca++ transport capacities remained significantly lowered. The data support the efficacy of early glucocorticoid treatment in endotoxemia. Early glucocorticoid treatment prevents the deterioration of brain and kidney mitochondrial function.

Animals↗
PubMed1982

Alterations of mitochondrial metabolism and protein concentrations in subacute septicemia.

Male Sprague-Dawley rats were made septic by cecal ligation for a period of 6 days. Sham-operated rats were used as control animals. Septic rats developed gram-negative bacteremia within 18 to 24 h. Blood cultures were positive for Escherichia coli, Proteus spp., and Klebsiella spp. in all cases. Significant loss of body weight was observed in septic rats during the 6-day period, whereas control rats exhibited a steady gain in body weight after the second postoperative day. Liver and muscle mitochondria were isolated and analyzed 6 days after the operation in control and septic rats. Liver mitochondrial cytochrome a(a3), b, and c concentrations were normal in septic rats. Oxygen utilization rates in state 3 (during ATP synthesis) were also within the normal range. State 4 respiratory rates, however, were increased with glutamate and pyruvate as substrates, resulting in low respiratory control ratios in septic rats. Muscle mitochondria from septic rats exhibited several abnormalities: the yield of cytochromes b, c, and a(a3) per gram of tissue was 34% below normal in septic rats. ATP synthesis rates declined significantly with pyruvate as substrate. Respiratory control ratios were below normal with all substrates studied except glutamate. These data are in agreement with previous reports on loss of muscle proteins and abnormalities in energy fuel utilization in septic patients.

Adenosine Triphosphate↗
PubMed1981

Ion transport and energy metabolism in brain.

The kinetics of extracellular K+ activity was compared to the availability of energy in the cortex of rats and gerbils exposed to anoxia, hypoxia, spreading depression, and ischemia. A combined K+/DC surface electrode was used alone or together with a fiber optic light guide in various experiments. All experiments were done on slightly anesthetized animals that were practically awake. The results can be summarized in the following conclusions: (1) Under conditions such as hypoxia or ischemia, K+0 showed a two-phase efflux kinetics, and a transition or critical point was reached where the response proceeds at a higher rate. This critical point was in the range of 10-16 mEq/1 potassium. (2) Availability of oxygen is necessary but not sufficient for a full rate of recovery from a long-term oxygen-deprivation insult. (3) There is an energy debt or energy-transduction bottleneck formed during a prolonged O2 insufficiency. This debt is reversed slowly during the recovery phase even when full restitution of O2 supply and blood flow has occurred.

Animals↗
PubMed1980

Mitochondrial carbonic anhydrase.

We have assayed carbonic anhydrase activity (carbonate dehydratase, carbonate hydro-lyase, EC 4.2.1.1) and bicarbonate permeability in suspensions of broken and intact guinea pig mitochondria by monitoring the disappearance of C16O18O. We found significant activity in preparations from liver and skeletal muscle, but not in preparations from heart muscle, brain, and kidney. Intact mitochondria containing carbonic anhydrase produce a two-phase acceleration of the disappearance of the labeled CO2, which indicates that the enzyme is located in a region more accessible to CO2 than to HCO3-. Acetazolamide inhibits the enzyme activity instantly in broken mitochondria but only after a delay in intact mitochondria, indicating that the enzyme is in a region not immediately accessible to the inhibitor. Sonication of mitochondria containing carbonic anhydrase activity releases the enzyme, which remains in the supernatant after sedimentation of the submitochondrial particles. This shows that mitochondrial carbonic anhydrase is in the matrix compartment and not in, or bound to, the inner membrane. The activity of the enzyme increases markedly with increasing pH. The enzyme activity of intact mitochondria is greater than that of the broken mitochondria at the same pH of the suspending fluid, corresponding to an intramitochondrial pH that is 0.2-0.5 unit more alkaline.

Animals↗
PubMed1980

The interrelation between brain oxidative metabolism and extracellular potassium in the unanesthetized gerbil.

The unanesthetized gerbil model was used to study the interrelation between metabolic, electrical and ionic activities in the brain. A combined K+DC surface electrode with a fiber optic light guide was implanted above the parietal cortex and cemented to the skull. The subjects were exposed to various pathological and physiological conditions such as anoxia, hypoxia, spreading cortical depression, and ischemia. During anoxia a leakage of cellular K+e was detected simultaneously with an increased level of NADH. The recovery phase in a few animals was followed by a spreading depression phenomenon. Exposing the brain to spreading depression led to a typical oxidation cycle of NADH, and the shape of this cycle was affected by hypoxia. Unilateral carotid artery ligation induced localized ischemia that affected cellular and K+e responses to spreading depression. Bilateral carotid artery occlusion increased NADH concentration to its maximum level; as a result, K+e also accumulated. Complete restoration of NADH and K+e to normoxic levels occurred after a few minutes, depending on the duration of the occlusion.

Animals↗
PubMed1980

High pressure oxygenation in unanesthetized brain: mitochondrial activity, pyridinenucleotide redox state, and electrical activity.

The effects of hyperbaric oxygenation (HPO) on mitochondrial activity, NADH oxidation-reduction state, and electrical activity were studied in the unanesthetized rat brain. Mitochondrial activity was measured in vitro after isolation of the mitochondria from brains exposed to HPO in mitochondria from brains exposed to HPO in vivo for various time intervals. The results showed that exposure of the brain to HPO in vivo decreased state 3 respiration of the mitochondria within 5-10 min of exposure. The level of respiration remained low until the final step of exposure. Despite this low respiration rate in vitro, the brain from which the mitochondria were isolated showed an oxidized state that, in comparison to the normoxic level of NADH, suggested a higher rate of respiration had occurred as a response to the convulsion appearing in vivo.

Animals↗
PubMed1979

Mitochondrial function in cerebral ischemia and hypoxia: comparison of inhibitory and adaptive responses.

In cerebral ischemia, brain oxygen supply is totally exhausted within seconds. This necessitates cessation of mitochondrial electron transfer and energy (ATP) production. After certain periods of ATP deficiency of from 5 to 90 min, irreversible damage of mitochondrial membranes occurs. This results in decreased mitochondrial function, characterized by inhibited State 3 respiratory rates, low respiratory control ratios, and inhibited Ca2+ transport activities. A 30-min recirculation period of the ischemic brain tissue induces total restitution of mitochondrial respiratory capacity after complete ischemia, but not after incomplete ischemia. Regional in situ measurements of brain pyridine nucleotide redox levels, tissue ATP, and lactate concentrations indicate variable metabolic responses of different brain regions to oligemia. Macroheterogeneity from region to region, as well as microheterogeneity within a region are demonstrated. Contrary to the effect of tissue ischemia involving reduced or zero cerebral blood flow and tissue oxygenation, sublethal hypoxia alone at normal or increased levels of blood flow induces adaptation of the mitochondrial enzyme system to a new level of respiratory capacity, without any indications of inhibited mitochondrial energy production. Acute hypoxia induces increased respiratory capacities within 30-60 min. Under chronic conditions, alterations of mitochondrial cytochrome concentrations accompany the increased respiratory capacities. Instead of the decreased efficiency of mitochondrial energy-producing mechanisms induced by ischemia, hypoxia induces increased efficiency of energy production.

Adenosine Triphosphate↗
PubMed1979

Cerebral energy state, mitochondrial function, and redox state measurements in transient ischemia.

Earlier results are reviewed suggesting that transient pronounced, incomplete cerebral ischemia could be more deleterious for the recovery of brain tissue energy state than a complete interruption of the blood flow. Measurements of respiratory function of brain mitochondria, isolated after 30 min of either complete or incomplete ischemia, demonstrated a similar inhibition of respiratory activity and maximal phosphorylation rates in both situations. This inhibition was totally normalized during recirculation after complete ischemia while a further deterioration was found after incomplete ischemia. The in vivo alterations of the cortical tissue distribution of redox states during transient, incomplete ischemia (15--60 min) were measured using a flying spot fluorometer, which gives a real-time and on-line display of the tissue distribution of NADH and oxidized flavoprotein. A reoxidation in both systems was demonstrated during the recirculation period and the distribution of redox states showed no further heterogeneity in the postischemic period as compared to the preischemic distribution. It is concluded that reoxygenation of the brain tissue is possible even after long periods of incomplete ischemia. The normal distribution of redox states during recirculation suggests that mechanisms other than an impaired or inhomogeneous oxygen delivery during the postischemic period are responsible for the failure in recovery of mitochondrial function and tissue energy state.

Animals↗
PubMed1978

The dynamics of K+ leakage and recovery in cerebral ischemia.

A combination of K+/DC surface electrode and a fiberoptic fluorometric probe are applied to measurements in brain during cerebral ischemia. The kinetics of the responses of extracellular K+ activity and intracellular NADH fluorescence in the gerbil cerebrum following reversible carotid ligation are measured. K+e shows a two-phase response to carotid occlusion and an extended recovery phase following recirculation. The length of the recovery phase is dependent on the duration and severity of the ischemic period. In the gerbil model the degree of communication in the anterior circulation is variable, whereas a bilateral carotid occlusion is presumed to give complete cerebral ischemia. Pyridine nucleotide fluorescence serves as an indicator of the degree of ischemia. Bilateral carotid occlusions of up to 35 minutes in duration were performed. K+e reaches 30--50 mEq/liter in the extracellular space within the first two minutes. This represents cell depolarization and equilibration of K+ activity levels. Recovery appears to be complete in terms of the ability of the system to clear raised levels of K+e from the extracellular space.

Animals↗