Aortic PO2 Research Articles

Central vascular flow patterns in the alligator Alligator mississipiensis.

Many different flow patterns have been described through the central circulation of crocodilian reptiles. We tested the hypothesis that the vagus nerve stimulation promotes right-to-left (R-L) shunting in the alligator. Flow patterns were investigated before and during stimulation of the intact left vagus nerve using three methods. 1) Atrial and aortic PO2 were measured simultaneously and continuously by gas probes. 2) Atrial outflows were tracked with a blood tracer (helium). 3) Flows were assessed with echocardiography. Four different flow patterns were observed before vagal stimulation: left ventricular (LV) blood flowed into both the right (RAo) and left (LAo) aortas, whereas right ventricular (RV) blood flowed only into the LAo; both aortas received a mixture of LV and RV blood; only LV blood perfused both aortas; and RV blood flowed into both aortas, but LV blood flowed only into the RAo. During vagal stimulation, both aortas received a mixture of LV and RV blood in half of the animals, and in the other half, both aortas received RV blood, but LV blood flowed only into the RAo. Doppler and contrast echocardiography demonstrated swirling flow in the foramen of Panizza and the base of the LAo during systole. These data indicate that vagal stimulation either maintains or produces R-L shunting, flow patterns are variable, and blood can swirl in the foramen of Panizza and LAo base.

Protective effects of halothane but not isoflurane against global ischaemic injury in the isolated working rat heart

The effects of equi-anaesthetic concentrations of halothane (HAL) and isoflurane (ISO) on myocardial performance, perfusion, oxygenation and lactate release were studied before, during and after a low-flow, global ischaemic insult in isolated, paced rat left heart preparations. An antegrade perfusion technique was used, where left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other. Aortic flow, coronary flow (CF) and PO2 in venous coronary effluent were continuously recorded and stroke volume, myocardial oxygen consumption (MVO2) and myocardial oxygen extraction as well as lactate release were calculated. The hearts were exposed for at least ten minutes to the perfusate without (control, n = 10) or with HAL (n = 10) or ISO (n = 10) at a MAP of 80 mmHg (10.4 kPa) and a LAP of 7.5 mmHg (1.0 kPa). After baseline measurements, MAP was reduced to 25 mmHg (3,2 kPa) for a total of nine minutes. Thereafter MAP was increased to 80 mmHg (10.4 kPa) for another nine minute period. During the whole experimental procedure, LAP was maintained at 7.5 mmHg (1.0 kPa) and heart rate at 325 beats per minute. In the pre-ischaemic control period, MVO2 was lower with HAL compared to ISO (P < 0.05) and control (P < 0.05). Stroke volume was also lower with HAL compared to control (P < 0.05). During hypoperfusion, lactate release was twice as high in the control group (P < 0.01) and with ISO (P < 0.01) compared to HAL.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial Po2, acid‐base status, and red cell nucleoside triphosphates in rainbow trout transferred from fresh water to 20‰ sea water

Transfer of rainbow trout from fresh water to 20‰ sea water decreased dorsal aortic Po2 from 90 to 60 mmHg within 1 h. Arterial Po2 was depressed for 24 h before it returned to control values. The internal hypoxia rapidly reduced the red cell nucleoside triphosphate content, suggesting prompt regulation of blood O2 affinity. The extracellular acid‐base status changed towards a small mixed metabolic and respiratory acidosis.

Arterial PO2, acid-base status, and red cell nucleoside triphosphates in rainbow trout transferred from fresh water to 20% sea water

Transfer of rainbow trout from fresh water to 20‰ sea water decreased dorsal aortic Po2 from 90 to 60 mmHg within 1 h. Arterial Po2 was depressed for 24 h before it returned to control values. The internal hypoxia rapidly reduced the red cell nucleoside triphosphate content, suggesting prompt regulation of blood O2 affinity. The extracellular acid-base status changed towards a small mixed metabolic and respiratory acidosis.

Oxygen delivery and myocardial function in rabbit hearts perfused with cell-free hemoglobin

Isolated rabbit hearts were perfused with Krebs-Henseleit buffer that contained 1.5 g/dl hemoglobin Ao [HbAo; PO2 at which half-saturation of hemoglobin occurs = 12 Torr], human hemoglobin cross-linked between alpha-chains with bis(3,5-dibromosalicyl)fumarate (alpha alpha-Hb; PO2 at which half-saturation of hemoglobin occurs = 30 Torr), or fatty acid-free bovine serum albumin (BSA). Myocardial performance and oxygen uptake were determined at different aortic PO2's [arterial PO2 (PaO2)] by use of an isovolumic Langendorff preparation. Function and oxygen uptake were comparable among the three different groups of hearts at an average mean PaO2 of 557 Torr. As PaO2 decreased, myocardial function was preserved better in hearts perfused with hemoglobin than in hearts perfused with Krebs-Henseleit buffer alone or with BSA. Hearts perfused with either HbAo or alpha alpha-Hb exhibited similar 10% decreases in left ventricular developed pressure and rate of change in left ventricular developed pressure at PaO2 of 141 Torr compared with a 58% decrease with BSA. However, corresponding venous PO2's were lower with HbAo (20 Torr) than with alpha alpha-Hb (35 Torr), and oxygen uptake decreased by 36% with HbAo but remained constant with alpha alpha-Hb. These data suggest that although myocardial function can be sustained over a fairly broad range of hemoglobin oxygen affinities, tissue oxygen gradients and myocardial oxygen uptake are maintained better by cell-free hemoglobin with an oxygen affinity in the normal physiological range.

Improvement in oxygen tensions and pulmonary blood flow with intermittent distal aortic compression during normoxia, hypoxic hypoxia, and hyperoxia in neonatal piglets

We investigated the hypothesis that, in a newborn piglet during normoxia, hypoxia, and hyperoxia, increasing aortic pressure transiently by intermittent short-duration aortic compression would affect left-to-right shunting of blood and thus increase pulmonary artery blood flow, pulmonary arterial PO2, and aortic PO2 proximal to the point of compression. We also investigated whether a balloon atrial septostomy, by providing an open channel for communication between the right- and left-sided circulations, would further improve pulmonary blood flow and aortic PO2. Studies were performed in eight 7- to 10-day-old newborn piglets in three phases (FIO2 of 0.21, 0.12, and 1.0) before and after balloon arterial septostomy in each piglet. Blood gas measurements and hemodynamic variables were recorded before and at the end of a 30-sec period of aortic compression. During aortic compression, all the animals demonstrated a 50 to 70 mm Hg increase in aortic pressure proximal to the compression. Before balloon septostomy, there were 21%, 41%, and 8% increases in aortic PO2 in the room air, hypoxic, and hyperoxic phases of the experiment, respectively. There were also statistically significant increments in pulmonary blood flow and arterial pressures. After balloon septostomy, there were 35%, 25%, and 21% increments in aortic PO2 during the room air, hypoxic, and hyperoxic phases of the experiment, respectively. However, there was no statistically significant further improvement in the effects of aortic compression on PO2 with septostomy compared with those effects before septostomy. Our results suggest that increasing systemic arterial pressures in order to forcibly affect left-to-right shunting of blood may be potentially beneficial in the management of hypoxia in situations where low pulmonary artery blood flow may be contributing to hypoxia, e.g., in persistent pulmonary hypertension of the newborn.

Blood flow and oxygen delivery to fetal organs and tissues during sustained hypoxemia

To examine the fetal cardiovascular responses to a sustained reduction in O2 delivery (DO2), studies were conducted on 13 chronically instrumented fetal lambs (128-138 days gestation) made hypoxemic for 7.9 +/- 0.5 h by lowering maternal inspired O2 concentration to 9-10%. Fetal descending aortic PO2 fell initially from 18.0 +/- 1.0 to 10.7 +/- 0.6 mmHg, whereas pH decreased progressively from 7.326 +/- 0.006 to 6.843 +/- 0.023. Blood flow to the cerebral hemispheres, myocardium, and adrenal glands rose maximally by 110.2 +/- 22.5, 253.7 +/- 41.1, and 338.7 +/- 55.0%. Cerebral hemispheric DO2 fell progressively, whereas DO2 to the myocardium and adrenal was maintained until 7.9 h, when it fell significantly. There was also a rise in blood flow to brown adipose tissue. Blood flow to the gut and skeletal muscle was maintained, whereas flow to the spleen and kidney fell. DO2 to all these tissues fell markedly because of the progressive decline in blood O2 content. It is concluded that fetal cardiovascular function was well maintained in the face of severe hypoxemia and marked acidemia.

Responses to acute hypoxemia in fetal sheep at 0.6-0.7 gestation.

A majority of previous studies of fetal responses to acute hypoxemia has focused on the response of the sheep fetus greater than 120 days of gestation when many regulatory systems have been established. To assess the response of younger, less well-developed fetuses, we exposed two groups of fetal sheep (I, 84-91 days; II, 97-99 days gestational age) to acute hypoxemia by giving the ewe a gas mixture containing 9% O2 to breathe. We decreased descending aortic PO2 in both groups of fetuses [I, 24 +/- 6 to 14 +/- 3 (SD) Torr; II, 23 +/- 3 to 12 +/- 4 Torr] by a degree similar to that achieved in previous studies of fetuses greater than 120 days of gestation. Mean arterial blood pressure (I, 31 +/- 6; II, 40 +/- 3 Torr) did not change significantly from control values, and heart rate (I, 224 +/- 27; II, 203 +/- 16 beats/min) increased significantly in group II fetuses with hypoxemia. In group I and II fetuses, as in older fetuses, cerebral, myocardial, and adrenal blood flows, measured by the microsphere technique, increased, and pulmonary blood flow decreased. These responses mature early and are likely local vascular responses to decreases in oxygen content. Combined ventricular output and umbilical-placental blood flow decreased significantly in both groups. Unlike the response of the fetus greater than 120 days, acute hypoxemia did not decrease blood flow to the musculoskeletal and cutaneous circulations (group I only), gastrointestinal, or renal circulations.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Hemodilution on Peripheral Circulation

In 7 anesthetized dogs the authors produced anemia by exchanging isovo lemic blood with plasma substitute and thus reducing hemoglobin gradually from 17.9 ± 0.7 to 8.5 ± 0.7 gr/dL in three steps. Samples were taken from pe ripheral blood at the animals' normal hemoglobin and at different degrees of hemodilution for the determination of Hb, viscosity, fibrinogen, venous blood lactate and pyruvate, pH, pO2, and oxygen saturation, while cardiac output, heart rate, and aortic pressure were measured. Total peripheral resistance, oxy gen content, and oxygen transport were calculated. Progressive hemodilution resulted in a significant increase in cardiac output from 2.5±0.1 to 4.2±0.2 L/min (p &lt; 0.001), while peripheral resistance decreased clearly parallel with the whole blood viscosity (from 2.2±0.1 to 1.2±0.1 mm Hg/mL/sec, p &lt; 0.001). The value of arterial oxygen content was decreased from 22.6±1.1 to 10.1 ±0.7 mL/dL of blood (p &lt; 0.001), but the systemic oxygen transport was completely compensated at hemodilution step A, and moderately at steps B and C, because of the increased cardiac output. Oxygen consumption was slightly decreased, while aortic pressure, pH, pO2, and oxygen saturation did not change. These data support the concept that moderate normovolemic hemodilution improves the peripheral circulation and does not jeopardize tissue oxygenation.

Effects of halothane, enflurane, and isoflurane on coronary vascular tone, myocardial performance, and oxygen consumption during controlled changes in aortic and left atrial pressure. Studies on isolated working rat hearts in vitro.

The effects of equi-anesthetic concentrations of halothane (HAL, n = 11), enflurane (ENF, n = 11) and isoflurane (ISO, n = 10) on cardiac function were studied and compared with a control group (n = 12) in isolated paced rat hearts by means of an antegrade heart perfusion technique. Left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other, and aortic flow, coronary flow (CF), and po2 in venous coronary effluent were continuously recorded. Stroke volume (SV), myocardial oxygen consumption (MVO2), and myocardial oxygen extraction were calculated: 1) MAP was altered from 60 to 120 mmHg at a constant LAP (7.5 mmHg), and 2) LAP was varied from 4 to 12.5 mmHg at a constant MAP (80 mmHg). Left ventricular function curves (LVFC) were constructed and the maximal SV (SVmax) was obtained. The LAP needed to perform 75% of the maximal SV (LAP0.75) was estimated to assess the effect of the anesthetics on diastolic function. HAL ENF and ISO decreased SVmax significantly compared to control. This decrease was more pronounced for HAL (41%) compared to both ENF (26%) and ISO (26%). Accordingly, SV, at various levels of MAP, at a constant LAP, was significantly lower for HAL than for both ENF and ISO, while there was no significant difference between the latter two. None of the anesthetics shifted the LVFC to the right, i.e., did not affect diastolic properties. HAL induced the most pronounced decrease in MVO2, while there was no significant difference between ENF and ISO in this respect. Coronary flow (CF), at controlled perfusion pressures, decreased significantly with HAL but not with ENF or ISO compared to control. CF was significantly higher with ISO compared to both ENF and HAL. HAL and ISO, but not ENF, decreased myocardial oxygen extraction significantly compared to control and, thus, increased the myocardial oxygen supply-to-demand ratio.

Acute hemodynamic effects of increasing hemoglobin concentration in children with a right to left ventricular shunt and relative anemia

The short-term effects of increasing hemoglobin concentration were evaluated at cardiac catheterization in seven children (aged 0.3 to 7.5 years) with a right to left ventricular shunt and relative anemia. Diagnoses were tetralogy of Fallot in six and L-transposition of the great vessels with ventricular septal defect and pulmonary stenosis in one. Before and 20 minutes after isovolumic partial exchange transfusion with 20 ml/kg packed red cells, the following variables were measured: hemoglobin, partial pressure of oxygen (PO2), oxygen consumption, oxygen saturation and pressure in the aorta, superior vena cava and right and left atria. After partial exchange transfusion, hemoglobin increased from 13.7 +/- 0.5 to 16.4 +/- 0.4 g/100 ml (p less than 0.001, mean +/- SEM). Aortic PO2 increased from 55.0 +/- 3.5 to 62.0 +/- 4.1 mm Hg (p less than 0.01) and aortic oxygen saturation increased from 84.3 +/- 2.3 to 90.9 +/- 1.3% (p less than 0.002). Effective pulmonary blood flow increased by 17% from 2.72 +/- 0.10 to 3.17 +/- 0.10 liters/min per m2 (p less than 0.01), and right to left shunt decreased by 59% from 1.44 +/- 0.29 to 0.59 +/- 0.10 liters/min per m2 (p less than 0.01). Systemic oxygen transport increased from 658 +/- 48 to 738 +/- 46 ml/min per m2 (p less than 0.002). After partial exchange transfusion, systemic vascular resistance increased from 15.9 +/- 1.1 to 20.0 +/- 1.4 units (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Reliability of femoral artery sampling during cardiopulmonary resuscitation

A study was undertaken to determine whether femoral arterial blood gas (ABG) content adequately reflects central oxygenation and acid base status during cardiopulmonary resuscitation (CPR) from fibrillatory arrest in the canine model. Six dogs were fibrillated electrically. After 3 minutes, CPR was begun. ABG samples were taken simultaneously from femoral and thoracic aortic catheters at 0, 3, 8, 13, 23, and 28 minutes of ventricular fibrillation. Pair analysis revealed a statistically significant difference between aortic and femoral PO2 values throughout the duration of external chest compression and assisted ventilation (P less than .05). The aortic PO2 was 12% more than the femoral PO2. There was no difference in pH and PCO2 between the femoral and aortic blood gas samples. The lower femoral PO2 observed may be the result of poorer blood flow to the lower half of the body. It was concluded that femoral PO2 underestimates aortic PO2 during external chest compression and assisted ventilation in the canine model.

Effect of Oxygen Tension on NMR Spin-Lattice Relaxation Rate of Blood in vivo

Spin-lattice relaxation rate (1/T1) was measured in the left (LV) and right (RV) ventricular cavities in four conscious normal humans and four anesthetized greyhound dogs breathing spontaneously. Inspired oxygen concentration (FIO2) was varied in five steps from 21 to 100%. In dogs, blood was sampled from indwelling catheters in the pulmonary artery and aorta for measurement of PO2. Saturation-recovery and inversion-recovery tomographic images of the ventricular cavities were obtained supine during quiet breathing using a whole-body NMR scanner operating at a static magnetic field strength of 0.15 Tesla. From FIO2 21 to 100%, 1/T1 of LV increased by 11.6% in humans and 9.6% in dogs. In dogs, 1/T1 increased by 2.8% per 100 mm Hg increase in aortic PO2 (r greater than 0.87). There was no correlation in dogs between 1/T1 in RV and pulmonary artery PO2. The LV/RV 1/T1 ratio in dogs increased by 4% per 100 mm Hg increase in the LV-RV PO2 difference, and by 8% in humans as FIO2 increased from 21 to 100%. A rise in dissolved oxygen concentration increases NMR spin-lattice relaxation rates of blood in vivo to a small but significant extent.

ACUTE METABOLIC ACIDOSIS: EFFECTS ON ARGININE IN VASOPRESSIN(AVP) RELEASE IN FETAL SHEEP

Acute asphyxia results in AVP hypersecretion in fetal sheep. Since acidosis, hypoxia, and hypercapnea occur simultaneously with asphyxia, it is unclear which is primarily responsible for AVP release. We have shown that hypoxia has no effect until aortic PO2 (PaO2) is 8μU/ml, 30.2μU/ml. We conclude that: 1) acidosis, like hypoxemia alone, does not result in marked fetal AVP release; 2) whereas AVP release is related linearly to pHa, there appears to be a threshold value for PaO2; and 3) acidosis and hypoxia appear synergistic for AVP release, but the role of PaCO2 is unknown. *p<.05.

HEMODYNAMIC EFFECTS OF INCREASING HEMOGLOBIN(HGB) CONCENTRATION IN CHILDREN WITH A RIGHT-TO-LEFT(RL) VENTRICULAR SHUNT AND RELATIVE ANEMIA

The acute effects of increasing Hgb concentration were evaluated at cardiac catheterization in 7 children (age 0.3-7.5 yr) with a R→L ventricular shunt and relative anemia. Diagnoses were tetralogy of Fallot in 6 and L-transposition with VSD and PS in 1. Before and 20 minutes after isovolumic partial exchange transfusion(PET) with 20ml/kg packed red cells the following were measured: Hgb, pO2, O2 consumption, O2 saturation (sat) and pressure in aorta, superior vena cava, right and left atrium. After PET, Hgb increased from 13.7±0.5 to 16.4±0.4gm% (p<.001, mean±SEM). Aortic (Ao) pO2 increased from 55.0±3.5 to 62.0±4.1 torr (p<.01) and Ao sat from 84.3±2.3 to 90.9±1.3% (p<.002). Effective pulmonary blood flow (Qef) increased by 17% from 2.72±0.10 to 3.17±0.10 L/min/M2 (p<.01) while R→L shunt decreased by 59% from 1.44±0.29 to 0.59±0.10 L/min/M2 (p<.01). Systemic O2 transport increased from 658±48 to 738±46 ml/min/M2 (p<.002). After PET systemic resistance (Rs) increased from 15.9±1.1 to 20.0±1.4 units (p<.01). A significant relationship was found between % increase in Rs and both % decrease in R→L shunt (y=20.44×0.32, r=.90,p<.01) and % increase in pO2 (y=.36×+2.88,r=.83,p<.02). Thus, increasing Hgb concentration in 7 children with a R→L ventricular shunt and relative anemia decreased R→L shunt and increased Qef, Ao sat, pO2, and O2 transport. These effects appear related to the increase in Rs following PET. Correcting relative anemia in children with a R→L ventricular shunt may have significant hemodynamic benefits.

Palliative right ventricular outflow tract construction for patients with pulmonary atresia, ventricular septal defect, and hypoplastic pulmonary arteries

From December, 1977, through June, 1981, 15 patients with pulmonary atresia, ventricular septal defect, and hypoplastic pulmonary arteries underwent a palliative right ventricular outflow tract construction. In seven (Group A) this was the first surgical procedure, whereas in the remaining eight (Group B) previous systemic-pulmonary artery anastomoses had been performed. A high morbidity of the pulmonary arteries was present in Group B, resulting in part from the previous shunting procedures. The left pulmonary artery was severely hypoplastic in five patients; the right was hypoplastic in seven of the eight patients and was severely stenotic or atretic in three. All the patients in Group A survived the palliative right ventricular outflow tract reconstruction, and only one in Group B died. Almost all patients had an increase in the aortic PO2 and oxygen saturations after palliative right ventricular outflow tract construction, with a concomitant fall in hemoglobin concentration. Three of the five patients in Group A who underwent postoperative angiography were found to have proximal left pulmonary artery stenosis, and three had lesser involvement of the proximal right pulmonary artery as well. Three of the six patients in Group B who were studied postoperatively also had severe stenosis or proximal atresia of the right pulmonary artery, and three patients had stenosis and hypoplasia of the left pulmonary artery as well, two severe. Thus in no patient in this series were normal pulmonary arteries achieved by palliative right ventricular outflow tract construction will provide the potential for ultimate complete repair. The rather constant finding of severe proximal left pulmonary artery stenosis and hypoplasia in Group A is disappointing.

244 EFFECTS OF INCREASED UMBILICAL VENOUS (UV) OXYGENATION 0N FETAL SHUNTS

We used the microsphere method to assess the effect of increasing UV blood O2 on fetal cardiac output (CO) and vascular shunts by giving the ewe 100% inspired oxygen (MO2). Two groups of fetal lambs with normal pH were studied; 5 had normal aortic PO2 (20.4±2.4) and 5 were spontaneously hypoxemic (12.0±2.0). Although magnitude of shunts differed in the two groups, they changed in similar direction so the two groups were analyzed together. UV Hgb O2 saturation increased from 61.6±20.7 to 85.5±15.8% (p<0.005) during MO2. CO and umbilical blood flow (UBF) did not change from control values of 537±82 and 208±30 ml/min/kg. 59.7±6.6% of UV blood passed through the ductus venosus (DV); this did not change with MO2. The percent DV blood crossing the foramen ovale to enter the upper body decreased from 38.5±8.7 to 23.5±5.5% (p<0.001) and the percent DV blood returning to the placenta without perfusing the fetal body increased from 32.1±5.8 to 37.9±8.0% (p<0.05). Lung blood flow as percent of CO increased from 4.9±3.6 to 13.8±6.4 (p<0.005) during MO2. Thus, increasing UV O2 modifies shunting of DV blood through the foramen ovale and to the placenta; this probably results from the decrease of pulmonary vascular resistance. (Supported by NIH grants HL 06285 and HL 24056.)

Clinical implications of blood gas analysis of chest tube drainage.

Blood gas analysis of chest tube drainage following thoracostomy for experimental and clinical penetrating chest injuries was evaluated to determine its usefulness in predicting the etiology of the injury. Twenty dogs were divided into four groups and sustained right chest injury as follows: Group I--closed chest lung laceration; Group II--open chest lung laceration; Group IIII-gunshot wounds; Group IV--thoracotomy and injection of autologous, mixed venous blood. All animals and 14 patients who sustained penetrating chest injury were made simultaneously from chest tube draininage, systemic artery, and central vein in all dogs and patients. Eight patients (Group A) had pneumothorax; six patients (Group B) did not. Mean control canine aortic PO2 and pulmonary arterial PO2 values in Group I did not differ significantly from those in the other three canine groups, nor from the two human groups. Group II dogs exhibited chest tube PO2 which was significantly (p less than 0.01) above aortic PO2. In Group IV, chest tube PO2 was increased significantly above pulmonary arterial blood. Patients without pneumothorax had values for PO2 in chest tube drainage and aorta which were not significantly different, whereas when pneumothorax was present, PO2 of chest tube drainage was significantly higher than that of aortic PO2. Thus blood gas determinations on chest tube drainage may reflect the nature of the injury; however, the presence of air in the pleural space can result in oxygenation of contained blood well above systemic arterial levels.

Investigations of the toxic mechanisms of ammonia to fish–gas exchange in rainbow trout (Salmo gairdneri) exposed to acutely lethal concentrations

Exposure to acutely lethal un‐ionised ammonia concentrations resulted in a 3.3‐fold increase in oxygen consumption. This was associated with increases in ventilation volume, respiratory frequency and amplitude. ‘Cough’ frequency was not significantly affected. Heart rate and dorsal aortic blood pressure were increased and cardiac output was estimated to have more than doubled. Dorsal aortic blood Po2 decreased but no significant changes in erythrocyte number, haematocrit, haemoglobin concentration, blood pH or P50 were observed. Possible toxic actions of ammonia were discussed and it was speculated that, as in mammals, ammonia may act by impairing cerebral energy metabolism.

Sustained Hyperoxemia Without Cicatricial Retrolental Fibroplasia

Twenty infants weighing between 890 and 1,750 gm at birth who survived the respiratory distress syndrome had sustained aortic Po2 values &amp;gt;150 mm Hg for 10 to 43 hours; 16 of the 20 had sustained aortic Po2 values &amp;gt;200 mm Hg for 4 to 40 hours; 11 had sustained aortic Po2 values &amp;gt;300 mm Hg for 1 to 21 hours. At 5 months of age or beyond, 19 had no evidence of cicatricial retrolental fibroplasia, while one who died at 6 weeks of age had no eye abnormalities two weeks earlier. These findings suggest there may be one or more factors other than oxygen operative in the etiology of cicatricial retrolental fibroplasia.