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Biomedical subjects

D Torbati

Publications and source records attributed to D Torbati.

44 records · Page 3Linked to original sources
PubMed1979

Organ blood flow, cardiac output, arterial blood pressure, and vascular resistance in rats exposed to various oxygen pressures.

Blood flow in different organs, cardiac output, and arterial blood pressure were measured in unanesthetized rats under 1, 2, 3.5, 5, and 7 ATA O2, during first electrical discharge developed at 7 ATA O2 and following decompression. Brain, spinal cord, and hypophysis blood flow were reduced after 10 min of exposure to 2, 3.5, and 5 ATA O2 and were normal before and during first electrical discharge. Liver and muscle blood flow were significantly reduced under all investigated pressures, while myocardium, lung, kidney, and adrenal blood flow remained unchanged except for a significant increase in myocardium and lung blood flow under 1 ATA O2. Cardiac output was significantly decreased while arterial blood pressure was significantly decreased under all investigated pressures. The total peripheral resistance increased 36 to 81% at various oxygen pressures. These results are discussed in relation to the possible involvement of hemodynamic changes in awake animals, in the development of the adverse effects of HOP.

Adrenal Glands↗
PubMed1978

Blood flow in rat brain during exposure to high oxygen pressure.

Total cerebral blood flow and blood flow in 10 brain structures of unanesthetized rats were measured by the indicator fractionation technique under different oxygen pressures. The first electrical discharge seen under high oxygen pressure was considered as an early sign of brain oxygen toxicity. It was found that the effect of high oxygen pressure on cerebral blood flow was time- and pressure-dependent. Exposure to 2 and 3.5 ATA of O2 led to vasoconstriction. Exposure to 5 ATA of O2 produced an initial vasoconstriction followed by a secondary vasodilatation to normal level. Cerebral blood flow was not reduced during exposure to 7 ATA of oxygen. Non-decreased blood flow preceded the appearance of the first electrical discharge in all investigated structures of the brain. There was no change in electrical activity of the brain as long as a decrease in cerebral blood flow was maintained. It is suggested that changes in electrical activity of the brain may be produced by toxic levels of brain tissue PO2. Vasoconstriction resulting in decreased cerebral blood flow was considered as a protective mechanism against the toxic effects of high tissue PO2.

Action Potentials↗
PubMed1978

Capillary fragility during air exposure of man to 1-5 ATA and after decompression.

Capillary fragility in man during exposure to 1-5 ATA air and after decompression from these pressures was studied by means of a petechiometer. A significant increase in capillary fragility was observed at 4 and 5 ATA air and after decompression from 3, 4, and 5 ATA air to normal pressure. It is suggested that this phenomenon may be associated with impairment of neurophysiological functions detectable only by special tests.

Adult↗
PubMed1977

Changes in local brain tissue Po2 and electrocortical activity of unanesthetized rabbits under high oxygen pressure.

Po2 changes in the thalamus, hippocampus, reticular formation, and cortex, and cortical electrical activity, were recorded simultaneously in unanesthetized, unrestrained rabbits breathing air or hyperbaric oxygen. The average tissue Po2 of investigated brain structures during exposure to 100% oxygen at 7 ATA pressures, was two to three times greater than that during air breathing at 1 ATA. In seven out of 10 rabbits, successive myoclonic fits were observed before the appearance of the first electrical discharge or abnormal EEG. Postmortem examination of the lungs showed signs of edema and hemorrhage in all the animals. Because of the possibility that the lung damage took place before the development of brain oxygen toxicity, we concluded that the rabbits are not animals of choice for the investigation of brain oxygen toxicity. The possible interrelationship between cerebral metabolic rate-O2, cerebral blood flow, and lung pathology in determining the level of tissue Po2 and the appearance of oxygen toxicity in the brain under hyperbaric conditions are discussed.

Animals↗
PubMedDate not supplied

Reduction of rattlesnake-venom-induced myonecrosis in mice by hyperbaric oxygen therapy.

Hyperbaric oxygen therapy (HBOT) at 1, 2, and 2.75 atmospheres absolute (ATA) was used to treat rattlesnake (Crotalus atrox) venom-induced tissue damage and edema in thigh muscles of mice. Tissue damage was evaluated by double-blind histopathologic examination: tissue edema was determined by measuring tissue water content. A total of 10 intermittent exposures to oxygen over a period of 4 days at 2 and 2.75 ATA did not influence the resolution of venom-induced tissue edema, whereas tissue damage was significantly ameliorated as compared to air-treated envenomated controls. HBOT also promoted healing in the venom-injected mice as evidenced by the presence of regenerating muscle cells. It is concluded that HBOT may limit rattlesnake venom-induced myonecrosis and promote healing in a dose-response relationship without reducing venom-induced edema.

Animals↗
PubMedDate not supplied

Intratracheal pulmonary ventilation versus conventional mechanical ventilation: continuous carinal pressure monitoring at low and high flows and frequencies.

We continuously measured proximal and carinal pressures at low and high flow rates and frequencies during conventional mechanical ventilation (CMV) and intratracheal pulmonary ventilation (ITPV), using an artificial lung. The proximal peak inspiratory pressure (PIP), carinal PIP, proximal positive end expiratory pressure (PEEP), and carinal PEEP, or negative end expiratory pressure (NEEP), were measured during simulated CMV and ITPV. Two levels of frequency (30 and 90 per min) and two gas flow rates (3 and 6 L/min) were examined, in both dry and humid states (four combinations of gas flow and frequency at each state). The gas flow and inspiratory time were held constant throughout the CMV and ITPV trials. Humidification of the ventilatory circuit during ITPV prevented the accurate measurement of carinal pressures. This problem was solved by introducing a continuous "bias flow" of 11 ml/min into the pressure monitoring line. A combination of low gas flow and low frequency with CMV showed no significant differences between the proximal and carinal PIP, as well as the proximal and carinal PEEP. The same combination with ITPV, however, resulted in a significantly lower carinal PIP and PEEP, compared to proximal PIP and PEEP. Carinal PIP and PEEP during ITPV were also significantly lower than those observed during CMV with a low flow and low frequency rates. During both CMV and ITPV, using a combination of a high flow rate with a high breathing frequency, carinal PIPs were significantly lower than proximal PIPs. ITPV, however, generated much larger differences between proximal and carinal PIPs than the CMV. A significant NEEP was generated at the carinal level during ITPV with high flow rates, both with high and low frequencies. The NEEP did not occur with a low gas flow, in combination with either a low frequency or a high frequency. The "bias flow" had no significant effect on carinal pressures. In conclusion, ITPV, compared with CMV, generates a significantly lower carinal PIP, but it may also generate carinal NEEP. For safety reasons, therefore, it is essential to monitor carinal pressures continuously in patients treated with ITPV.

Artificial Organs↗