Biomedical subjects

V L Kinnula

Publications and source records attributed to V L Kinnula.

77 records · Page 5Linked to original sources

PubMed1976

Mitochondrial cytochrome concentrations in rat heart and liver as a consequence of different hypoxic periods.

Rat heart and liver cytochrome concentrations were determined after three hypoxic conditions (atmospheric pressure 50.5 kPa, 40.8 kPa and 38.0 kPa) lasting one week and two weeks. The heart showed clear hypertrophy which was 38% in most severe hypoxia (38 kPa, 2 weeks). A small decline in the liver weight to body weight ratio was observed, this decrease being 21% in the most severe case. During the hypoxic periods the mitochondrial cytochrome concentration decreased. This phenomenon was more obvious when the degree of hypoxia was increased and more pronounced after 2 weeks than one week. The heart and liver showed quite similar patterns in this respect. In most severe hypoxia the decreases in the liver were 29% for cytochrome aa3, 30% for cytochrome b, 20% for cytochrome c and 15% for cytochrome c1, with the concentrations expressed on mitochondrial protein basis. The corresponding values in the heart were 31%, 43%, 28%, and 22%. It can be concluded that in mammals the mitochondrial cytochrome content probably varies according to the amount of oxygen available.

Animals↗

PubMed1976

Liver and heart mitochondrial succinate dehydrogenase activity of newborn rats in anoxic hypoxia and starvation.

Succinate dehydrogenase activity was determined in the liver and heart of newborn rats after 3 and 48 hours' exposure to anoxic hypoxia (10% O2) and after 48 hours' starvation. Control determinations were made on newborn animals of corresponding ages, full term foetuses (21 days), infantile (1 and 2 weeks) and full grown animals. Hypoxia for 3 h had no influence on succinate dehydrogenase activity at all in either the heart or liver mitochondria of the newborn animals. After 48 h no difference was observed in the liver between the hypoxic animals and the starved controls of the same age, though starvation itself had resulted in a significant increase in activity, as much as 42%. When liver mitochondrial succinate dehydrogenase in normal mitochondria was activated by preincubation mitochondria with the substrate, the activity increase obtained was greater than that resulting from starvation. The increase in activity in the heart of the hypoxic or starved animals was not significant (less than 10%).

Age Factors↗

PubMed1975

Rat liver mitochondrial enzyme activities in hypoxia.

Rat liver mitochondrial enzyme activities were measured after exposing the animals to the atmospheric pressure of 380 mm Hg for 5 h and 14 days. Succinate dehydrogenase and succinate oxidase activities increased significantly during the hypoxic period of 14 days. No change was observed in cytochrome oxidase activity. Malate dehydrogenase and glutamate dehydrogenase activities increased somewhat, but not significantly. The efficiency of oxidative phosphorylation (the ADP:O ratio) in the isolated mitochondria remained unchanged. The exact mitochondrial protein values showed a 15% decrease as compared with the control group. The concentrations of cytochromes did not change significantly in the hypoxic group. During the short hypoxic period succinate dehydrogenase, succinate oxidase and cytochrome oxidase activities increased as compared with those in the control group.

Animals↗

PubMedDate not supplied

Hydrogen peroxide release from alveolar macrophages and alveolar type II cells during adaptation to hyperoxia in vivo.

The effect of hyperoxia (1-14 days, 85% O2) on rat alveolar macrophage and alveolar type II cell oxidant and antioxidant characteristics was investigated. Unstimulated control macrophages (2 h ex vivo) released hydrogen peroxide at a rate of 3.5 +/- 1.3 nmol/min mg protein-1, which was a cyanide-sensitive process. H2O2 release from alveolar macrophages decreased slightly but not significantly after 1 day in hyperoxia and increased significantly after 3 days (180%, p less than .05) and 14 days (380%, p less than .01). When H2O2 release was expressed as nmol from total macrophages per animal, the increase after 14 days in hyperoxia was 760%. H2O2 generation by hyperoxic macrophages was cyanide resistant, indicating the involvement of active NADPH oxidase. In both control and hyperoxic macrophages H2O2 release could be significantly stimulated with phorbol myristate acetate (PMA). Comparisons of H2O2 release by freshly isolated alveolar macrophages and alveolar type II cells must be cautiously interpreted because some cell functions may change during the isolation procedure. Freshly isolated (6 h ex vivo) control alveolar type II cells were found to generate H2O2 at a rate of 0.26 +/- 0.05 nmol/min mg protein-1. In type II cells H2O2 release, calculated as nmol/mg protein, decreased during the first 7 days of hyperoxia to 10% (p less than .01) of the control value and then returned back up to the control level after 14 days. A similar decrease was observed if H2O2 release was calculated as nmol/cell number. H2O2 release from control and hyperoxic type II cells was cyanide sensitive. The decrease in H2O2 release in type II cells was associated with cell membrane injury (as assessed by electron microscopy), while biochemical markers of cellular injury (trypan blue exclusion and cellular high-energy phosphates ATP, ADP) were unchanged. The ability of type II cells to scavenge extracellular H2O2 did not change in acute hyperoxia, but it increased significantly during the second week in hyperoxia. These results indicate that macrophages but not type II cells are stimulated to produce H2O2 during prolonged exposure to hyperoxia.

Adaptation, Physiological↗

PubMedDate not supplied

Assessment of forced expiratory volume in one second-fraction of the engrafted lung with 133-Xe radiospirometry improves the diagnosis of bronchiolitis obliterans syndrome in single lung transplant recipients.

BACKGROUND: Staging of bronchiolitis obliterans syndrome is based on the decline of forced expiratory volume in 1 second, a measure of overall ventilatory capacity. A single staging system is applied to all lung recipients, regardless of the bias which can be caused by the native lung after single lung transplantation. METHODS: We determined the decline of graft function in single lung recipients by a combination of two methods: 133-Xe radiospirometry and dynamic spirometry. The forced expiratory volume in 1 second fraction of the transplant (FEV1tx) was calculated from the proportion of ventilation of the transplant (Vtx) and forced expiratory volume in 1 second. Eight single lung recipients were followed up for a median observation period of 17 months; bronchiolitis obliterans syndrome developed in four of them. RESULTS: The fractional decline of forced expiratory volume in 1 second of the transplant was significantly greater than the decline of forced expiratory volume in 1 second (p = 0.016) in all patients during the follow-up. In the patients with bronchiolitis obliterans syndrome, the mean decline in forced expiratory volume in 1 second was 1.1 L (39.5%), and in forced expiratory volume in 1 second of the transplant it was 0.9 L (55.8%). The measurement of forced expiratory volume in 1 second of the transplant suggested stage 2a and 3a dysfunction in two grafts in which the assessment of forced expiratory volume in 1 second indicated stage 1a bronchiolitis obliterans syndrome. In one patient, decrease of forced expiratory volume in 1 second of the transplant was suggestive of chronic dysfunction 4 months before it was diagnosed by biopsy and declined lung function. CONCLUSIONS: The assessment of forced expiratory volume in 1 second seems to underestimate the severity of chronic dysfunction in single lung grafts. Instead, the determination of forced expiratory volume in 1 second of the transplant with radioactive tracers provides selective information of the graft function, which could be used for clinical evaluation of bronchiolitis obliterans syndrome in single lung recipients.

Adult↗