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Biomedical subjects

T Ida

Publications and source records attributed to T Ida.

At least 145 records · Page 8Linked to original sources
PubMed1981

Four stages of mitochondrial deterioration in hemorrhagic shock.

It is of great importance to define the manner in which cells are damaged and how intracellular derangement becomes irreversible during shock. When supply of both oxygen and substrates to cells is limited during shock, cellular energy metabolism of vital organs is severely depressed. In this experiment, the relationship was clarified between the reversibility of shock and the cellular energy status, from the viewpoint of hepatic energy change, mitochondrial redox state, ATP synthesis of isolated mitochondria, and fragility of mitochondrial membrane in rat livers. The derangement of energy metabolism passed through a series of four stages during hemorrhagic shock. At Stage I (initial stage), the cellular energy level decreased greatly due to marked energy consumption, without any organic damages in the mitochondria. Stage II (cell distress stage) showed that cellular energy imbalance occurred due to the depressed mitochondrial activity in vivo, although it was reversible when the blood supply was restored. Stage III (transitional stage) was the phase at which mitochondrial fragility increased severely. At Stage IV (terminal stage), mitochondria were markedly damaged organically and cellular energy metabolism was not remedied by any intensive therapies, which inevitably meant the death of vital organs.

Adenosine Diphosphate↗
PubMed1979

Renal vein fibrin degradation products (FDP's) in glomerulonephritis.

In order to determine the role of intrarenal vascular coagulation (IVC) in chronic glomerulonephritis, coagulant parameters in renal blood (RVB), urine FDP's and renal histology were examined in 70 patients with chronic glomerulonephritis (CGN). RVB was obtained by Seldinger's technique. A correlation was obtained between an increase of fibrinogen, FDP and soluble fibrin monomer complexes (SFMC) in RVB and the degree of intraglomerular fibrin deposition shown on immunofluorescence. An increase of FDP's, SFMC and a slight decrease of fibrinolytic activity in RVB were observed in patients with CGN with decreased renal function or with the nephrotic syndrome. Daily excretion of FDP in the urine and the extent of intraglomerular fibrin deposition were greater in nephrotics than in non-nephrotics. We conclude that measurement of coagulation parameters in RVB is a reliable and sensitive method of assessing IVC, and that IVC plays an important role in aggravation of chronic glomerulonephritis, particularly when the nephrotic syndrome is present.

Chronic Disease↗
PubMed1978

Stimulatory effect of adenosine on hepatic adenine nucleotide and energy charge levels in shocked rats.

In hemorrhagic shocked rats, the hepatic energy charge (ATP+1/2ADP)/(ATP+ADP+AMP) fell rapidly from 0.857 to 0.542 within 2 hours and was rapidly restored to normal levels after completing the reinfusion of shed blood. The total adenine nucleotide levels decreased slowly from 3.83 to 2.57 mumoles per g wet liver 2 hours after shock, and increased to normal levels 2 hours after reinfusion of shed blood. The intraperitoneal injection of 2 mg adenosine/100g body weight, 85 mg glucose/100 g body weight and 3.3 units insulin/100 g body weight, simultaneously with the reinfusion of shed blood, enhanced the recovery of energy charge and adenine nucleotide levels. The injection of 2 mg adenosine alone was ineffective in restoring the energy charge. However, administration of more than 6.7 mg adenosine/100 g body weight enhanced recovery of energy charge and adenine nucleotide levels, whether insulin was added or not.

Adenine Nucleotides↗