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Biomedical subjects

Yehuda Arieli

Publications and source records attributed to Yehuda Arieli.

10 recordsLinked to original sources

Acute tobacco smoke exposure promotes mitochondrial permeability transition in rat heart.

Chronic exposure to tobacco smoke is known to impair mitochondrial function. However, the effect of acute tobacco smoke exposure (ATSE) in vivo, as might occur in social settings, on mitochondrial function and calcium handling of cardiac cells has not been examined. It was hypothesized that ATSE might adversely modify mitochondrial function as reflected in mitochondrial energetics, membrane potential, and calcium transport. Mitochondria were isolated from the hearts of adult rats either exposed to 6 h of environmental tobacco smoke ( approximately 60 mg/mm3 tobacco smoke particles) or sham exposure. To model a calcium stress similar to ischemia/reperfusion, mitochondria were exposed to a Ca2+ bolus with measurement of membrane potential, energetics, Ca2+uptake and release, and redox state. ATSE mitochondria were characterized by significantly higher ADP-stimulated ATP production and a more reduced redox state (NADH ratio) under basal conditions without observed changes in resting Psim. Exposure of ATSE mitochondria to Ca2+stress resulted in significantly more rapid depolarization of Psim. The initial rate of Ca2+uptake was not altered in ATSE mitochondria, but CsA-sensitive Ca2+ release was significantly increased. ATSE does not significantly alter resting mitochondrial function. However, ATSE modifies the response of cardiac mitochondria to calcium stress, resulting in a more rapid depolarization and subsequent release of Ca2+ via the mitochondrial permeability transition (MPT).

Animals↗

The effect of alpha2-adrenergic receptors on cutaneous water evaporation in the rock pigeon (Columba livia).

The role of beta-adrenergic receptors in regulating cutaneous water evaporation (CWE) in the rock pigeon (Columba livia) is well documented. Here, we studied the involvement of the alpha2-adrenergic receptors in this cooling mechanism of the heat-acclimated (HAc) pigeon. Systemic alpha2-adrenergic activation [clonidine, 50 microg kg(-1), intramuscular (i.m.)] was found to increase CWE in heat-acclimated pigeons at an ambient temperature (T(a)) of 25 degrees C. Subcutaneous administration of the drug had no significant effect. Preinjection of an alpha2-adrenergic antagonist (yohimbine, 10 mg kg(-1), i.m.) completely prevented clonidine-induced CWE and attenuated propranolol-induced CWE by 53%. Pretreatment with a beta-adrenergic agonist (isoproterenol, 4 mg kg(-1), i.m.) abolished the effect of clonidine. None of the above treatments was found to elicit significant CWE in nonacclimated (NAc) pigeons. These findings, in addition to previously reported data, indicate a complex regulatory pathway of CWE in the heat-acclimated pigeon consisting of alpha2- and beta2-adrenergic receptors. The possible hierarchical pattern of these receptors is discussed.

Adrenergic alpha-2 Receptor Antagonists↗

Gender modulation of Ca(2+) uptake in cardiac mitochondria.

BACKGROUND: Mitochondrial calcium overload is an important factor in defining ischemia/reperfusion injury. Since pre-menopausal women are relatively protected from ischemia and heart disease, we tested the hypothesis that gender differences alter Ca(2+) handling in rat cardiac mitochondria. METHODS: Using cardiac mitochondria isolated from male, female, and ovariectomized Sprague-Dawley rats, we measured mitochondrial calcium transport, redox state, and membrane potential (Deltapsi(m)) during exposure to a calcium bolus. Redox state was modulated using either succinate (S) or succinate and pyruvate (SP) as substrates. RESULTS: Net Ca(2+) uptake rates were significantly lower in female than male mitochondria using SP, substrate conditions that resulted in a lower redox state (NADH/NAD(+)). Inhibition of the mitochondrial transition pore (MTP) using cyclosporin A showed significantly lower net Ca(2+) uptake in both substrate solutions when mitochondria from female and ovariectomized animals were compared to males, a finding consistent with gender modulation of the mitochondrial uniporter. Blockade of the Ca(2+) uniporter by ruthenium red abolished gender or substrate solution differences in calcium release. While there were no significant differences in resting Deltapsi(m), or Deltapsi(m) following Ca(2+) addition, 80% of female samples recovered from Ca(2+)-induced depolarization compared to 57% and 43% of male and ovariectomized animals, respectively. CONCLUSIONS: Mitochondria from female hearts have lower Ca(2+) uptake rates under physiologic substrate solutions (succinate/pyruvate) and are able to appropriately maintain DeltaYm under conditions of high [Ca(2+)]. These differences are consistent with gender modulation of the Ca(2+) uniporter and may be a mechanism by which female myocardium suffers less injury with ischemia/reperfusion.

Animals↗

Heat acclimation prolongs the time to central nervous system oxygen toxicity in the rat. Possible involvement of HSP72.

Oxygen toxicity of the central nervous system (CNS-OT) can occur during diving with oxygen-enriched gas mixtures, or during hyperbaric medical treatment. CNS-OT is characterised by convulsions and sudden loss of consciousness, which may be fatal in diving. Heat acclimation is known to provide cross-tolerance to various forms of stress in different organs, including the brain. We hypothesised that heat acclimation may delay the onset of CNS-OT in the rat. Male Sprague-Dawley rats were acclimated to an ambient temperature of 32 degrees C for 4 weeks. Rats in the control group were kept at 24 degrees C. Both groups were exposed to oxygen at 608 kPa. EEG was recorded continuously until the appearance of the first electrical discharge preceding clinical convulsions. CO(2) production was measured simultaneously with the EEG. Latency to CNS-OT was measured and brain samples were taken for evaluation of heat shock protein 72 (HSP72) levels by Western blot analysis at the end of the acclimation period and during 4 weeks of deacclimation. Latency to CNS-OT was twice as long in the heat-acclimated rat, with insignificant changes in CO(2) production. This prolongation continued for 2 weeks during deacclimation. There was a significant increase in the level of HSP72 following heat acclimation, with a subsequent decrease during deacclimation. We conclude that heat acclimation prolongs latency to CNS-OT in a way that does not involve changes in metabolic rate. During deacclimation there was a linear relationship between latency to CNS oxygen toxicity and the level of HSP72. A possible beneficial effect of HSP72 is discussed.

Acclimatization↗

High-frequency sound transmissions under water and risk of decompression sickness.

We tested the possible occurrence of a neurological insult secondary to high-frequency sound exposure. Immersed, anesthetized rats were subjected to a simulated diving profile designed to induce decompression sickness, while exposed to the transmission of an acoustic beacon. Intermittent sound at a pressure level of 184.5 dB re 1 microPa at 1 m (1.7 kPa), a frequency of 37 kHz, and with a duration of 4 ms, was transmitted in a duty cycle of 0.26%. Four groups, each containing nine animals, were included in the study as follows: group 1, immersion only, no sound exposure; group 2, immersion with sound exposure; group 3, diving simulation when immersed, no sound exposure; group 4, diving simulation when immersed, with sound exposure. Somatosensory evoked potentials (SSEPs) were recorded the day before the study, and a second recording was made 30 min after immersion. Some of the SSEP components disappeared after the dive in 3 rats from group 3 and 2 rats from group 4. SSEP components could not be identified in a significantly larger number of animals from groups 3 and 4, compared with groups 1 and 2. No differences were found in wave latency, amplitude or conduction time. Our data show that the high-frequency sound exposure employed did not contribute to the development of the neurological insult.

Animals↗

Training improves divers' ability to detect increased CO2.

BACKGROUND: Elevated arterial PCO2 (hypercapnia) is a known risk in diving with closed circuit breathing apparatus. In a retrospective study, we determined CO2 retention and the ability to detect CO2 in novice divers who were either CO2-recognition-trained subjects (TS) or untrained subjects (UTS). METHODS: Ventilatory and perceptual responses to variations in inspired CO2 (range 0-5.6 kPa, 0-42 mm Hg) during moderate exercise were assessed in novice Israeli Navy divers on active duty. Tests were carried out on 231 TS and 213 UTS. RESULTS: The minimal mean inspired PCO2 that could be detected was 4.8 +/- 1.6 kPa (36 +/- 12 mm Hg) in UTS and 2.9 +/- 0.7 kPa (22 +/- 5 mm Hg) in TS (p < 0.0001). No significant changes were found in PETCO2 between the two groups during exposure to a PICO2 of 5.6 kPa (42 mm Hg). There were 46 TS who were found to be CO2 retainers (more than +1 SD above the mean) and 19 were classified as poor detectors (more than +1 SD above the mean). Seven subjects exhibited both traits. During actual oxygen diving performed later by this group, the only four cases of CNS-oxygen toxicity were among those seven subjects (p < 0.01). CONCLUSIONS: We conclude that CO2 recognition training improves the diver's capability to detect CO2. We suggest that a diver who is both a poor CO2 detector and a CO2 retainer will be prone to CNS-oxygen toxicity.

Adult↗

Hyperoxia may reduce energetic efficiency in the trained rat.

BACKGROUND: Several studies have been conducted in recent years in the attempt to improve running performance by the use of hyperbaric oxygen, but there is disagreement as to whether this has any beneficial effect. The purpose of this study was to measure the effect of 24 h breathing 100% O2 in normobaric conditions on energetic efficiency in the trained rat. METHODS: Experiments were carried out on trained rats whose oxygen consumption was evaluated during the training period and on its completion. At the end of the training period, the rats were divided into two groups: 1) rats exposed to air (21% O2) in normobaric conditions; and 2) rats exposed to 100% O2 in normobaric conditions. In addition, two groups of sedentary rats were used: 3) sedentary rats exposed to air (21% O2) in normobaric conditions; and 4) sedentary rats exposed to 100% O2 in normobaric conditions. Energetic efficiency was estimated by measuring O2 consumption at submaximal exercise (45 m.min-1, 10 degrees incline). RESULTS: Training alone reduced O2 consumption by 18% during submaximal exercise. Exposure to 100% oxygen for 24 h in normobaric conditions reversed the effect of complete training by elevating the O2 consumption by 17%, which was close to the oxygen consumption of the rats during the incomplete training period. CONCLUSIONS: Our results suggest that prolonged exposure to hyperoxia induces a reduction in the energetic efficiency of the trained rat. The relevance of these findings to sports and diving is discussed.

Animals↗

High-frequency sound field and bubble formation in a rat decompression model.

High-frequency sound might cause bubble enlargement by rectified diffusion. The purpose of the present study was to investigate gas bubble formation in the immersed diving animal during exposure to high-frequency sound. Anaesthetised rats were subjected to a simulated diving profile while immersed inside a hyperbaric chamber. An acoustic beacon (pinger) was placed ventral to the animal's abdomen, transmitting at an intensity of 208.9 dB re 1 micro Pa and a frequency of 37 kHz. Six groups of eight animals were included in the study as in Table 1, breathing air (n = 4) or Nitrox 72/28 (n = 2), at a depth of 0 m, 30 m or 40 m. Immediately after decompression, the intestinal mesenterium was imaged, and frames were acquired digitally. The number of bubbles and their radii were analysed and compared among the groups. The mean bubble density for group 1 was 1.35 +/- 0.18 bubbles/mm(2), significantly higher when compared with the other groups (p < 0.0001). The average bubble radius for groups 1 and 2 was similar (12.57 +/- 4.1 and 10.63 +/- 1.8 microm, respectively), but significantly larger than in the other groups (p < 0.0002). The percentage of bubbles with a radius greater than 50 microm was significantly higher in group 1 (p < 0.0001). The results suggest that commercially available underwater pingers might enhance bubble growth during deep air diving.

Acoustics↗

Cooling by cutaneous water evaporation in the heat-acclimated rock pigeon (Columba livia).

The present study provides an up-to-date overview of the cutaneous water-evaporation cooling mechanism in the rock pigeon. Cutaneous water evaporation fully replaces the classic respiratory cooling mechanism in the resting, heat-acclimated bird, and is more economical in terms of water conservation. It enables the pigeon to maintain homeostasis, and to breed successfully in harsh environments. Adrenergic signaling is involved in the initiation of this novel mechanism, either by deactivation of the beta-adrenergic receptors (ARs), or activation of the alpha-AR. The adrenergic signaling results in a marked increase in cutaneous blood flow and in the arterial-to-venous blood-flow ratio. This is associated with alterations in the cutaneous capillary wall ultrastructure, which increase its permeability to plasma proteins and water. The end result of this process might be an increase in water efflux from the capillary lumen. The properties of beta-ARs were measured in the cardiac muscle of thermal-acclimated pigeons. Significant down-regulation in the density of beta-ARs, associated with increased affinity of these receptors, was measured in the heat-acclimated pigeon. Concomitantly, changes in the skin ultrastructure and lipid composition were found in very well defined patches in the epidermis of heat-acclimated pigeons. These suppress the skin resistance to water transfer. We suggest that this cooling mechanism involves finely orchestrated adjustments in the ultrastructure of the skin and the cutaneous capillaries, and in skin blood flow. Adrenergic signals are among those factors that regulate this cooling mechanism during exposure to a hot environment.

Acclimatization↗

Hyperbaric oxygen may reduce gas bubbles in decompressed prawns by eliminating gas nuclei.

It is accepted that gas bubbles grow from preexisting gas nuclei in tissue. The possibility of eliminating gas nuclei may be of benefit in preventing decompression sickness. In the present study, we examined the hypothesis that hyperbaric oxygen may replace the resident gas in the nuclei with oxygen and, because of its metabolic role, eliminate the nuclei themselves. After pretreatment with oxygen, prawns were 98% saturated with nitrogen before explosive decompression at 30 m/min. Ten transparent prawns were exposed to four experimental profiles in a crossover design: 1) 10-min compression to 203 kPa with air; 2) 10-min compression with oxygen; 3) 10-min compression with oxygen to 203 kPa followed by 12 min air at 203 kPa; and 4) 10 min in normobaric oxygen followed by compression to 203 kPa with air. Bubbles were measured after explosive decompression. We found that pretreatment with hyperbaric oxygen (profile C) significantly reduces the number of bubbles and bubble volume. We suggest that hyperbaric oxygen eliminates bubble nuclei in the prawn.

Animals↗