Atm Abs Research Articles

51. Control of crythropoiesis in the fetal and neonatal rat

Erythropoiesis in the fetal rat was studied by measuring the incorporation of Fe59 into red cells of fetuses following injection of the isotope into their mothers on the 18th day of gestation. Two days later the amount of radioactivity present in the fetuses was determined by whole body counting. From this value and from the radioactivity found in fetal blood, the percentage incorporation of Fe59 into red cells (PI) was calculated. About 60% of the injected dose was found in the fetuses. The PI in individual fetuses varied with fetal weight, showing a linear relationship. It was therefore concluded that the rate of erythropoiesis. When mothers were bled or subjected to hypoxia during the 3rd week of pregnancy, or given 75–100 units of erythropoietin, they showed, as expected, an increase in PI. The fetuses likewise showed a significant increase in PI, controlled for fetal weight. The PI was decreased in mothers made polycythemic or kept at 4 atm abs but not in their fetuses. It has therefore been shown that in the rat erythropietin can pass through the placenta and that the fetus responds to erythropoietin, either endogenously produced or transferred from the mother. Newborn rats hypertransfused during the 1st and 2nd postnatal weeks showed a marked decrease in PI and a good response to exogenous erythropoietin. Since the rat is born relatively immature and follows a fetal pattern of erythropoiesis for the first 2 postnatal weeks, these observations provide further evidence that erythropoiesis in the fetus is regulated through the hypoxia-erythropietin mechanism.

Stability of the normal flame front

We have investigated the instability of the normal flame in propane-air mixtures at initial pressures from 1 to 9 atm abs in a small chamber (volume 5 cc).

A closed-cycle Joule-Thomson liquefier and cryostat for He 3

A small closed-cycle liquefier and cryostat, liquefying He 3 by Joule-Thomson expansion, is described. Its characteristics, operation, and performance are discussed. The JT expansion takes place from pressures of 4 atm abs or less at flow rates up to 14 litres (s t p) min −1. The closed cycle character of the circulation is maintained by use of an oil-free diaphragm compressor. The coefficient of liquefaction at an input pressure of 4 atm is about 59%, which at the maximum flow of 14 litres (s t p) −1 corresponds to a refrigerative capacity at 3·2 K of 230 mW. When used as a cryostat, the liquid He 3 chamber has a capacity of 40 cm 3 and this can be filled in a few minutes. Using a built-in adsorption pump, temperatures down to 0·25 K can be maintained for periods up to 50 hours under conditions of minimal refrigerative loading. Using the quantitative results obtained with this liquefier, deductions are made regarding the inversion curve of He 3 and a design has been made for a cryostat covering the temperature range 0·25 K and upwards, which does not require any liquid refrigerants, such as liquid nitrogen, liquid hydrogen, or liquid helium.

The effect of hyperbaric helium-oxygen on the acute toxicity of several drugs

The effect of a hyperbaric helium-oxygen environment on drug toxicity was investigated in the following systems: (1) The intravenous lethal doses of pentobarbital, lidocaine, and ethanol in rats; (2) the intravenous LD50 for morphine in rats; and (3) the oral toxicity of an LD50 dose of aspirin in mice. Except for mice given aspirin, restrained, unanesthetized animals were equilibrated with the atmosphere (19.2 atm abs. helium-0.2 atm abs. oxygen, equivalent to the pressure at a depth of 600 feet) for 45 min in a hyperbaric chamber. Animals were then injected remotely via indwelling jugular vein catheters. The lethal dose of pentobarbital, lidocaine, or ethanol was determined by slow intravenous infusion to the point of respiratory arrest. The LD50 of morphine was determined from the mortality 2 hr after injection. Mice were injected orally with a suspension of aspirin in sodium alginate and pressurized rapidly; the mortality was determined 3 hr later. For each drug, control animals were treated in exactly the same manner as pressurized animals. In the case of every drug examined, the toxicity observed during exposure to the hyperbaric environment did not differ significantly from that under normal pressure.

Determination of the concentration limits of flame propagation in oxyhydrogen mixtures on the initial pressure interval from 1 to 100 ATM ABS

Determination of the concentration limits of flame propagation in oxyhydrogen mixtures on the initial pressure interval from 1 to 100 ATM ABS

Effect of increased oxygen of hydroxyproline synthesis in the cuticle and body wall of Ascaris lumbricoides

1. 1. Ascaris lumbricoides injected with [ 14C]proline were incubated for 24 h in 70% O 2 at normal pressure and in air at 1.6 atm abs. 2. 2. In Ascaris incubated at high O 2 concentration a substantial increase in collagenous proline hydroxylation occured (1.6–3 times) in the cuticle while little effect of perhaps a decrease in hydroxyproline synthesis was observed in the body wall. 3. 3. When incubating Ascaris at four varying concentrations of O 2 (0, 5, 20 and 70%) the hydroxylation of proline (given as ration specific activity hydroxyproline/specific activity proline) measured in purified cuticle collagen was maximal when the worms were under 70% O 2 and 4 times higher than when under N 2. In the case of muscle collagen, hydroxylation was maximal at 20% O 2; 70% O 2 was no better than N 2. 4. 4. The results are discussed in terms of two different protocollagen proline hydroxylases; one in the cuticle stimulated by O 2 and one in the body wall that is perhaps slightly inhibited by high O 2. Alternatively, the results may be due to differences mainly in the availability of O 2 to protocollagen hydroxylase in the two body layers. 5. 5. Data are presented on the distribution of various forms of collagenous hydroxyproline in Ascaris cuticle and body wall.

Hyperbaric Oxygen Toxicity Prevention With Succinate

Succinate protection against oxygen toxicity in rats was investigated at oxygen pressures of 5, 7, 9, and 11 atmospheres absolute (atm abs), and compared with protection given by dextrose and malate. Times to convulsions were used for comparison. Dextrose and malate gave no protection. Succinate provided relatively long-term protection at 5 and 7 atm abs oxygen exposures, but showed decreasing protection with increasing pressure. Succinate provided no protection at oxygen pressures of 12 atm abs or higher. A 3:1 sodium succinate:ammonium succinate mixture (0.4M, pH 7.4) solved the problem of alkalosis previously encountered with a sodium succinate solution. The infusion of the 3:1 mixture (6 millimols/kg/hr) in dogs exposed to 5 atm abs oxygen delayed convulsion 5 to 11 times longer than in controls. Intracellular localization and thin layer chromatography studies with succinate-2, 3 14 C showed that succinate readily penetrated the blood brain barrier.

Changes in electrical activity of the cerebral cortex and of some subcortical centers in hyperbaric oxygen

The electrical activities of the cerebral cortex and of some subcortical structures were recorded during hyperoxic seizures, in order to ascertain the structures first fired. Unrestrained, unanesthetized rats were subjected to hyperbaric oxygen by being placed in a hyperbaric chamber at 4 atm abs. for 2–4 h. In some experiments EMGs from the biceps muscle of the right forelimb and from posterior cervical muscles were recorded for the duration of the hyperbaric oxygen. A greater incidence of initial seizures was observed during the first hour from the beginning of hyperoxia. The seizures were usually preceded by pre-seizure activity, more evident in the subcortical centers, consisting in increase in voltage and discharge rate and in spindle-like waves. Two different patterns of seizure were observed characterized by different discharge rates and durations. The final part of long-duration seizures (type I) usually exhibited an opposite polarity compared with the initial one. The onset of hyperoxic seizures was simultaneous in all the cortical records. The subcortical leads were usually fired at the same time as the cortex and the process of seizure extinction was invariably simultaneous in the cortical and the subcortical leads. Hyperoxic seizures were also observed in decorticate rats in which the whole cerebral cortex had been removed by suction. This supports the view that the cerebral cortex is not necessary for starting and developing hyperoxic seizures.

Cortical CO2 and O2 at high pressures of argon, nitrogen, helium, and oxygen.

In 37 chloralosed cats (45–50 mg/kg) exposed to increased pressures of argon, nitrogen, or helium between 8.67 and 10.8 atm abs in the presence of either 0.2 or 2.34 atm abs oxygen or oxygen alone, the cortical carbon dioxide was measured with a modified Severinghaus electrode and the cortical oxygen polarographically. In mixtures with an oxygen partial pressure of 2.34 atm abs, the cortical oxygen increased above controls. The greater the density of the mixture then, the less was the increase. The cortical carbon dioxide also increased, but conversely, the greater the density of the mixture the greater the increase in carbon dioxide. In mixtures of low oxygen partial pressures, the cortical oxygen was below control values whereas the carbon dioxide showed little change except for a slight increase with the heavier argon mixture. Inert gas narcosis, as indicated by depression of auditory induced cortical spikes, did not correlate with the changes in cortical carbon dioxide but with the inert gas itself. Increasing the oxygen partial pressure and the density of the mixture respired caused retention of brain carbon dioxide, which synergistically potentiated the narcosis. nitrogen narcosis; inert gases; depth intoxication; tissue carbon dioxide; tissue oxygen; brain Submitted on August 10, 1964

Adrenergic effects in splenic pO2 of rats in air or oxygen at 5 atmospheres

Oxygen tensions have been measured in the spleens of rats breathing air and during exposure of the animals to 5 atm abs of oxygen (HPO). The response of splenic pO2 to compression was complex, usually reaching a peak value immediately after compression, then falling to a lower value. This form of response has been termed a hump response. After adrenalectomy or bretylium tosylate injection the hump response of pO2 after compression was almost abolished, and the values of splenic pO2 at 5 atm were considerably higher than in control animals. A combination of adrenalectomy and bretylium tosylate also markedly reduced the number of hump responses, but unexpectedly significantly lowered splenic oxygen tensions, both when the animals were under ambient conditions or at 5 atm of oxygen. Cardiac rate and blood pressure were studied in an attempt to find the explanation of this latter effect, and while blood pressure was the same in adrenalectomized rats and control rats after bretylium injection, adrenalectomy potentiated the bradycardia produced by bretylium tosylate. bretylium tosylate; compression in oxygen; cardiac rate; adrenalectomy; blood pressure Submitted on September 21, 1964

REDUCTION BY HYPERBARIC OXYGENATION OF THE MORTALITY FROM VENTRICULAR FIBRILLATION FOLLOWING CORONARY ARTERY LIGATION.

The effect of the inhalation of hyperbaric oxygen on the incidence of ventricular fibrillation following ligation of the circumflex coronary artery was studied in 151 dogs weighing 17 kg or more. Fifty-two per cent of the animals in the control group (room air, 1 atm abs) survived the challenge of this ligation. Survival increased to 60.4, 70, and 77.8% in the groups given 100% oxygen at an ambient pressure of 1, 2, and 4 atm abs, respectively. The orderly progression in the proportion of survivals is impressive but only approaches statistical significance. The results of these experiments are less dramatic than those previously reported by others. They do point out the need for cautious clinical trial in rigidly controlled series.

EFFECT OF O2 AT HIGH AMBIENT PRESSURE ON BLOOD FLOW AND O2 CONSUMPTION OF THE KIDNEY.

Renal blood flow of chloralosed dogs, measured while they breathed 100% O2 at ambient pressures of 1, 2, 3, and 4 atm abs (OHP), declined exponentially as an inverse function of PiOO2 until at 4 atm O2 it was 57% of control. Denervating the kidney did not affect the response, the mechanism of which remains unknown. Mean arterial blood pressure increased to 112% of control and heart rate decreased to 60% of control as O2 pressure increased from 1 to 3 atm abs, suggesting a generalized systemic vasoconstriction in which the kidney participated. We estimate that the measured decrease in renal blood flow during OHP would account for approximately 20% of the total decrease in peripheral blood flow. Renal O2 consumption was not affected by OHP. This can be accounted for in terms of a constant filtered and reabsorbed sodium load Note: (With the Technical Assistance of D. R. Wilson) hyperbaric oxygenation; kidney circulation; environmental pressure Submitted on February 20, 1964

RESPONSE TO HIGH PRESSURE OXYGEN OF CONSCIOUS VOLUNTEERS AND PATIENTS

A trial is described in which 19 fit volunteers and 49 patients with malignant tumors have breathed oxygen at a pressure of 3–4 atm abs for periods of from 21 to 67 min in a pressure chamber filled with oxygen. Subjects at complete rest will not safely tolerate 4 atm abs for frac12 hr but are unlikely to show signs of oxygen toxicity in a similar period at 3 atm abs. One patient convulsed during decompression after 46frac14 min at 3 atm pressure. A slow, even rate of pressurization did not prevent the occurrence of otitic barotrauma in nine of the volunteers. The patients had myringotomies performed. Temperature and pulse rate changes are described.

HYPERBARIC OXYGEN AND PERSISTENCE OF VISION IN RETINAL ISCHEMIA.

When retinal ischemia is produced by elevating the intraocular tension, normal vision persists for about 4 sec in healthy subjects breathing air at atmospheric pressure. Persistence times were determined at alveolar oxygen pressures up to 4 atm abs (3,000 mm Hg), obtained by oxygen breathing in a high-pressure chamber. Below an alveolar Po2 of 2 atm the rise in persistence time is relatively small. Above that level the time increases in direct proportion to the increase in alveolar Po2 and may exceed 50 sec at 4 atm. The rise of persistence time follows a pattern similar to that of computed blood oxygen pressure assuming an oxygen extraction of about 3 vol%. high pressure; blood oxygen tension; tissue oxygenation; intraocular tension; retinal circulation; visual blackout Submitted on February 7, 1964

Prevention in rats of narcosis produced by inert gases at high pressures.

A technique is described for quantitative evaluation of inert gas narcosis in animals. The response of 46 adult Wistar rats to minimal electroshock was used in 102 experiments to determine the narcotic effect of nitrogen at 12.6 and 13.5 atm abs and argon at 12.6 atm abs, before and after the oral, intraperitoneal, and intravenous administration of alpha-(4-piperidyl)benzhydrol hydrochloride. The drug controlled the narcotic effect produced by these inert gases at pressure without, so far as could be observed, the occurrence of undesirable side effects. The effective dose was 40 mg (130–150 mg/kg body wt). Lower doses were only partially effective. The maximum protective action of the drug was some 48 hr after its administration.

MEASUREMENT OF OXYGEN TENSIONS IN CEREBRAL TISSUES OF RATS EXPOSED TO HIGH PRESSURES OF OXYGEN.

Brain and cerebrospinal oxygen tensions have been measured in rats breathing air or in various high pressures of oxygen (OHP). Addition of 5% CO2 to the inspired oxygen raised cerebral oxygen tensions when rats were exposed to 2 atm abs or above. Inhibition of 75% hemoglobin saturation by para-aminopropriophenone lowered cerebral pO2 in rats breathing air, but not in rats exposed to OHP. The rate of rise of cerebral pO2 to a steady level after rapid compression was found to be faster than the rate of fall to a steady level following decompression. Addition of CO2 to the inspired gas mixture increased the rate of rise of cerebral pO2. The anesthetics urethane and pentobarbital sodium did not affect cerebral pO2 in rats breathing air or oxygen at 4 atm. The results are discussed in relation to factors contributing to oxygen poisoning at high pressures. Submitted on October 30, 1962

On the heat transfer crisis in steam-generating pipes

The present article provides the results obtained in investigating the heat transfer crisis in the boiling of water in a vertical pipe for the case of forced motion of the steam-water mixture. The investigations were performed at a pressure of 150 atm abs in the range of mass velocities from 850 to 7000 kg/m2sec and of thermal loads of (0.46–1.65) × 106 kcal/m2hr. The mechanism of the development of the heat transfer crisis for an annular flow is described. Empirical formulas for the determination of critical thermal loads are recommended.

Alveolar gas exchange during breath-hold diving

Use of a recompression chamber permitted simulation of breath-hold dives to 33 ft of sea water (2 atm abs). Four normal subjects made such dives during rest and mild exertion while delivering alveolar gas samples at frequent intervals by a partial-rebreathing procedure. The course of alveolar gas exchange differed greatly from that in ordinary breath holding. Oxygen uptake remained at near normal levels until ascent owing to the maintenance of alveolar Po2 by increased ambient pressure. Reversal of CO2 transfer occurred during descent, and little CO2 moved in the normal direction until ascent. Greater uptake of oxygen and retention of CO2 in the body led to lower final values of both alveolar Po2 and Pco2 than in comparable breath holding at the surface. Hyperventilation made possible longer dives with harder work, and in these the Po2 reached very low values on ascent. One subject showed a final Po2 of 24 mm Hg with evidence of reversed O2 transfer. Acute hypoxia on ascent is a likely cause of drowning in breath-hold diving.

Response to high pressure oxygen of conscious volunteers and patients

A trial is described in which 19 fit volunteers and 49 patients with malignant tumors have breathed oxygen at a pressure of 3–4 atm abs for periods of from 21 to 67 min in a pressure chamber filled with oxygen. Subjects at complete rest will not safely tolerate 4 atm abs for frac12 hr but are unlikely to show signs of oxygen toxicity in a similar period at 3 atm abs. One patient convulsed during decompression after 46frac14 min at 3 atm pressure. A slow, even rate of pressurization did not prevent the occurrence of otitic barotrauma in nine of the volunteers. The patients had myringotomies performed. Temperature and pulse rate changes are described.

Über die dynamik der Blasenbildung beim begasen von Flüssigkeiten unter druck

The author describes experiments for the treatment of water with helium, argon and nitrogen at pressures of 1 to 80 atm abs. The greater kinetic energy possessed by gases at elevated pressures causes considerable deformation of the bubbles and more rapid disintegration of the gas stream into bubbles than in gassing at normal pressure. Striking discontinuities are observed, viz., a sudden rise in bubble frequency occurs at increased gas rates. Photographs show the bubble shapes and bubble ascent in various ranges of pressure, varying between introduction of the gas as single bubbles and as a coherent stream at high rates of throughput.