Ventilation of a fossorial mammal (Spalax ehrenbergi) in hypoxic and hypercapnic conditions.
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Animals↗
Biomedical subjects
R Arieli
Publications and source records attributed to R Arieli.
Blood-gas properties and function in the fossorial mole rat under normal and hypoxic-hypercapnic atmospheric conditions.
Blood and tissue gas exchange properties of mole rats in normoxic and hypoxic-hypercapnic conditions were compared to the common mammalian pattern. RBC count was 14.0 +/- 1.2-10(6)/microliter. Hb concentration was 15.0 +/- 0.4g/100 ml. P50 (at pH 7.4 and 37 degrees C) was 29.5 +/- 0.5 mm Hg. Oxygen capacity averaged 20.2 +/- 0.4 vol% and the Hill coefficient was 2.9 +/- 0.1. The Bohr effect was -0.53 +/- 0.02 (deltalog P/deltapH). The temperature coefficient was 0.0152 +/- 0.0014 (deltalog P/delta degrees C). The Haldane effect was 4.8 +/- 0.5 (deltaCCO2 vol%)at PCO2 =40 mm Hg. Steady-state partial pressures in gas pockets were PO2 = 15.1 +/- 1.4 mm Hg and PCO2 = 85.8 +/- 3.9 mm Hg in normoxia, and 11.5 +/- 3.0 and 101.8 +/- 3.5 repectively in hypoxia-hypercapnia (PIO2 congruent to 85 mm Hg). Under the same conditions 2,3-DPG dropped from 0.87 and 0.88 to 0.62 and 0.65 (mol/mol Hb) in the rat and in the white rat, respectively. Heart muscle myoglobin concentration of the mole rat (1.44 mg/g) did not differ significantly from that of the white rat (1.96 mg/g), whereas masseter myoglobin was 4.0 mg/g--significantly different from the rat (1.21 mg/g). Results indicate that the strategy used by the mole rat to maintain a normal metabolic rate under variable atmospheric conditions, besides having high oxygen affinity, is to expand the physiological range of the oxygen dissociation curve to very low oxygen tensions, at the expense of its acid-base regulation. The regulation of the shape of the oxygen dissociation curve is discussed.
Acid-Base Equilibrium↗
Latency to CNS oxygen toxicity in rats as a function of PCO(2) and PO(2).
Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness, without any premonitory symptoms. We have made a quantitative study of the effect of inspired carbon dioxide on sensitivity to oxygen toxicity in the rat. Rats were exposed to four oxygen pressures (PO(2); 456, 507, 608 and 709 kPa) and an inspired partial pressure of carbon dioxide (PCO(2)) in the range 0-12 kPa until the appearance of the electroencephalograph first electrical discharge (FED) that precedes the clinical convulsions. Exposures were conducted at a thermoneutral temperature of 27 degrees C. Latency to the FED decreased linearly with the increase in PCO(2) at all four PO(2) values studied. This decrease, which is probably related to the cerebral vasodilatory effect of carbon dioxide, reached a minimal value that remained constant on further elevation of PCO(2). The slopes (absolute value) and intercepts of latency to the FED as a function of carbon dioxide decreased with the increase in PO(2). This log-linear relationship made possible the derivation of equations that describe latency to the FED as a function of both PO(2) and PCO(2) in the PCO(2) - dependent range: Latency (min) = e((5.19-0.0040)(P)(O(2)))-e((2.77-0.0034)(P)(O(2))) x PCO(2) (kPa), and in the PCO(2)-independent range: Latency(min) = e((2.44-0. 0009)(P)(O(2))). A PCO(2) as low as 1 kPa significantly reduced the latency to the FED. It is suggested that in closed-circuit oxygen diving, any accumulation of carbon dioxide should be avoided in order to minimize the risk of CNS oxygen toxicity.
Animals↗
P-V characteristics in heart-pulsation affected and non-affected lung units: a model.
Elastic recoil pressure, pleural pressure and pressure pulsation of the heart (PHRT) control the expired flow from a small lung unit. Variability in each trait may affect the expirate. The same (SDPV) or different (DDPV) regional distribution of P-V characteristics, regional effects of PHRT-affected (O) and non-affected units (N) and regional differences in pleural pressure, were incorporated into a computer model. Output acceptability was judged by the alveolar slope of the N2 washout, cardiogenic oscillations (CO) and the phase shift between PHRT and CO. Can SDPV be in both O and N units? What causes CO and phase shift? With SDPV in O and N units, CO were negligibly small. The incorporation of the pleural pressure difference did not fulfill the three criteria, which were met when there was DDPV in the N and O units. We conclude that the distribution of P-V characteristics changes with the distance from a pulsating artery, and only DDPV, and not different time constants or pleural pressure difference, can explain CO.
Blood Pressure↗
Cyclic perfusion of the lung by dense gas breathing may reduce the (A-a)DO2.
The decrease in the alveolar-arterial O2 difference (A-a)Do2 in dense atmosphere could be the result of cyclic lung perfusion due to large swing in pleural pressure during breathing cycles /4/. Using a mathematical model of the lung to calculate (A-a)Do2, a slight decrease was demonstrated in (A-a)Do2 as perfusion changed from steady to cyclic. The present study incorporates variable vertical partitioning of perfusion in this model, as a function of instantaneous total blood flow. This demonstrated a reduction of the Po2 difference between the apex and the base of the lung, and a reduction of (A-a)Do2, when perfusion was assumed to be cyclic, of 4.1 to 5.0 torr when blood flow was continuous throughout the breath, and of 5.0 to 5.7 torr when perfusion was assumed to be pulsatile. The results agree with experimental findings: reduction of (A-a)Do2 when breathing dense gas and improved apical perfusion in pulsatile blood flow. Calculation of the spatial VA/Q inequality suggests there is no correlation with (A-a)Do2 reduction. The decrease in (A-a)Do2 is attributed to the mixing of lung capillary blood flows having different O2 saturations.
Models, Biological↗
Power equation for all-or-none effects of oxygen toxicity and cumulative oxygen toxicity.
Quantification of the level of O2 toxicity may provide a means of setting limits on various hyperoxic exposures. A previously suggested expression for quantitative oxygen toxicity, DMG = a x t2 x PO2c (t-time, DMG-measured level of O2 toxicity), has been adapted for the all-or-none phenomenon: K = t2 x PO2c. A symptom may appear when K reaches a threshold value Kc. Non-linear regression was successfully applied to all-or-none symptoms from the literature: survival, convulsions, substernal distress, reduction in short circuit current and nerve conduction blockade. The generality of these expressions enabled calculation of cumulative oxygen toxicity and a search for the mechanism of oxygen toxicity. Cumulative oxygen toxicity is calculated in three-step calculation loops in three suggested exposure profiles. For a possible recovery period between exposures the expressions took the form: DMGt = DMGc x e-rt, and Kt = Kc x e-rt, where r is the recovery constant. A possibly bimodal distribution of c close to the values of 1 and 4 could be attributed to systemic effects.
Animals↗
The effect of hypothermia on gas exchange in anaesthetized rats in a confined atmosphere.
Both hypothermia and anaesthesia are known to prolong hypoxic survival. The combined effect of anaesthesia and hypothermia on survival in a confined atmosphere was studied in rats whose O2 consumption (VO2) produced hypoxia. Blood gases and respiratory parameters were measured in either ambient temperature TA = 30 degrees C (final body temperature TB = 36 degrees C) or initial TA = 30 degrees C followed by TA = 0 degree C below 100 torr inspired O2 (final TB = 19 degrees C). Oxygen consumption, breathing frequency and heart frequency decreased in hypoxic hypothermia compared to hypoxic normothermia. Hypothermia did not affect blood pressure, blood gas tension of pH. Hypothermia in hypoxia: 1) reduced the demand for oxygen with respect to O2 transport; 2) abolished the normothermic elevation of lactate in the blood, and 3) maintained high arterial saturation of oxygen. In contrast with awake rats (our previous study), there was no difference in the terminal inspired PO2 and survival time for normothermia and hypothermia in the anaesthetized rat, but survival time was doubled by anaesthesia as compared to awake rats due to reduced VO2.
Animals↗