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PubMed2005

Vasodilator tone in the llama fetus: the role of nitric oxide during normoxemia and hypoxemia.

The fetal llama responds to hypoxemia, with a marked peripheral vasoconstriction but, unlike the sheep, with little or no increase in cerebral blood flow. We tested the hypothesis that the role of nitric oxide (NO) may be increased during hypoxemia in this species, to counterbalance a strong vasoconstrictor effect. Ten fetal llamas were operated under general anesthesia. Mean arterial pressure (MAP), heart rate, cardiac output, total vascular resistance, blood flows, and vascular resistances in cerebral, carotid and femoral vascular beds were determined. Two groups were studied, one with nitric oxide synthase (NOS) blocker N(G)-nitro-L-arginine methyl ester (L-NAME), and the other with 0.9% NaCl (control group), during normoxemia, hypoxemia, and recovery. During normoxemia, L-NAME produced an increase in fetal MAP and a rapid bradycardia. Cerebral, carotid, and femoral vascular resistance increased and blood flow decreased to carotid and femoral beds, while cerebral blood flow did not change significantly. However, during hypoxemia cerebral and carotid vascular resistance fell by 44% from its value in normoxemia after L-NAME, although femoral vascular resistance progressively increased and remained high during recovery. We conclude that in the llama fetus: 1) NO has an important role in maintaining a vasodilator tone during both normoxemia and hypoxemia in cerebral and femoral vascular beds and 2) during hypoxemia, NOS blockade unmasked the action of other vasodilator agents that contribute, with nitric oxide, to preserving blood flow and oxygen delivery to the tissues.

Animals↗

PubMed1999

Renal responses to prolonged (48 h) hypoxemia without acidemia in the late-gestation ovine fetus.

The effect of sustained moderate hypoxia on renal blood flow and renal function was studied in the ovine fetus (123-129 days). The experiments consisted of 48 h of isocapnic hypoxia, not resulting in acidemia, but sufficient to produce redistribution of blood flow in favor of the brain at the expense of the carcass. Hypoxemia was induced by maternal nitrogen inhalation. Fetal arterial O(2) saturation and arterial O(2) pressure (Pa(O(2))) decreased from, respectively, 50.6 +/- 3.0% and 17.2 +/- 0.9 mmHg during control to 36.4 +/- 2.7% and 13.4 +/- 0.7 mmHg on the first and to 32.2 +/- 2. 2% and 12.4 +/- 0.7 mmHg on the second day of hypoxemia. Fetal renal blood flow and urine production rate were continuously measured using ultrasonic flow transducers. Fetal renal blood flow increased during hypoxemia from 11.8 +/- 1.6 to 15.6 +/- 1.8 ml/min and remained elevated throughout the 48-h hypoxemia period (P < 0.01). Renal blood flow was inversely correlated with fetal Pa(O(2)) (r is -0.69, P < 0.0001). Fetal urine production rate, glomerular filtration rate, filtration factor, osmotic clearance, and free water clearance did not significantly change from control values during hypoxemia or recovery. We conclude that hypoxemia without acidemia results in an immediate and considerable increase in fetal renal blood flow, which remains elevated for the entire hypoxemic period.

Acids↗

PubMed1985

Effect of hypoxemia on the renin-angiotensin-aldosterone system in humans.

Hypoxemia was induced in five subjects older than 40 (group 1) and five younger than 35 yr (group 2) on normal and low-salt diets by having the subjects breathe hypoxic gas. The fractional inspired O2 of the hypoxic gas was regulated so that group 1 hemoglobin saturations fell to 90% for 1 h. Group 2 subjects had desaturation to 90% for 1 h followed by desaturation to 80% for a 2nd h. Plasma renin activity (PRA), angiotensin-converting enzyme activity (ACE), and plasma cortisol levels did not change during hypoxemia. Plasma aldosterone levels fell in both groups during the 1st h of hypoxemia. Decreases were greatest during salt restriction and were significant (P less than 0.01) for the combined groups. Plasma aldosterone levels plateaued during the 2nd h of more severe hypoxemia in group 2. Hepatic blood flow, measured by indocyanine green clearance, and the adrenal response to exogenous adrenocorticotropic hormone, measured by changes in plasma cortisol and aldosterone, were not changed by hypoxemia in group 2 subjects. These results indicate that plasma aldosterone falls during hypoxemia despite unchanged PRA, ACE, hepatic blood flow, and adrenal function.

Adrenal Glands↗

PubMed1986

Diaphragmatic function during hypoxemia: neonatal and developmental aspects.

The effect of acute hypoxemia on diaphragmatic force output was studied in five young (age 4-8 days, wt 1.3-2.2 kg) and five older (age 16-19 days, wt 2.8-3.3 kg), anesthetized, spontaneously breathing piglets. Diaphragmatic force output was assessed by analysis of the transdiaphragmatic pressure (Pdi) generated during an occluded inspiratory effort, at end-expiratory lung volume, triggered by supramaximal transvenous stimulation of both phrenic nerves at frequencies of 20, 30, 50, and 100 Hz. During pressure measurements, the piglets were fitted with a rigid plaster cast covering the abdomen and lower third of the chest to ensure a consistency in diaphragmatic shortening during phrenic nerve stimulation. Pdi was measured under base-line conditions [inspired O2 fractional concentration (FIO2) = 0.50] and after 10 min of hypoxemia induced by breathing 12-14% FIO2. Pdi was significantly less than base line during acute hypoxemia at all frequencies of stimulation in both young and older piglets. The decline in the older piglets' Pdi during hypoxemia was significantly greater than that seen in younger piglets. We conclude that acute hypoxemia impairs the capacity of the developing piglet diaphragm to generate force. Furthermore, our data suggest that the young piglet is more resistant to the depressant effects of hypoxemia when compared to its older counterpart.

Age Factors↗

PubMed1988

Bioenergetics of rabbit skeletal muscle during hypoxemia and ischemia.

A blood-perfused rabbit hindlimb preparation was exposed to total ischemia (n = 4) or to severe hypoxemia (n = 4) where arterial PO2 was 5 +/- 2 (SE) Torr. O2 consumption (VO2), O2 transport (TO2), venous PO2 (PVO2), venous lactate concentration, and venous glucose concentration were measured. The relative concentration of ATP, phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH (pHi) were monitored with 31P magnetic resonance spectroscopy. PCr/Pi decreased with the onset of ischemia or hypoxemia. The preparation was reoxygenated and allowed to recover for 30 min once PCr/Pi was less than 1.0. The periods of hypoxemia and ischemia lasted 56.0 +/- 10.0 and 63.8 +/- 2.5 min, respectively (NS). During ischemia PCr decreased and Pi increased compared with control (P less than 0.05) but returned to control with reperfusion. With hypoxemia PCr also decreased and Pi increased with respect to control (P less than 0.01) but did not recover with reoxygenation. VO2 and PVO2 in both groups returned to control during recovery. ATP did not change with ischemia but decreased with hypoxemia (P less than 0.05). Venous lactate concentration did not change with ischemia but increased with hypoxemia (P less than 0.05) and continued to rise during recovery. During recovery pHi decreased in the hypoxemic group (P less than 0.05) but not in the ischemic group. These data show that, under the conditions tested, rabbit skeletal muscle does not resynthesize PCr after a severe hypoxemic episode. Furthermore it appears that VO2 and PVO2 fail to portray the true state of cellular bioenergetics after a severe hypotemic insult.

Adenosine Triphosphate↗

PubMed1992

Effect of inspiratory resistive loaded breathing and hypoxemia on diaphragmatic function in the piglet.

The combined effects of inspiratory resistive loaded breathing (IRL) and hypoxemia on transdiaphragmatic pressure (Pdi) in nine 1-mo-old Yorkshire piglets were studied. IRL was adjusted to increase spontaneously generated Pdi five to six times above baseline but maintain arterial PCO2 < 70 Torr to prevent hypercapnic depression of diaphragmatic contractility. Measurements of ventilation, blood gases and pH, Pdi, diaphragmatic electromyogram, Pdi during phrenic nerve stimulation, diaphragmatic blood flow, and end-expiratory lung volume were obtained at baseline, after 2 h of IRL, and then after 1 h of hypoxemia (arterial PO2 approximately 40 Torr) combined with IRL. Diaphragmatic muscle samples were obtained after study completion and immediately frozen in liquid nitrogen for determination of tissue ATP, phosphocreatine, lactate, and glycogen levels. Ten 1-mo-old piglets were subjected to IRL alone and served as controls. IRL alone resulted in significant impairment of Pdi generation. The addition of hypoxemia for 1 h did not further compromise Pdi in comparison to control animals who were subjected to IRL alone. Blood flow to both the costal and crural segments of the diaphragm increased significantly during IRL; the addition of the hypoxemic stress resulted in further significant augmentation of blood flow to both segments of the diaphragm. No differences were noted in diaphragmatic muscle tissue ATP, phosphocreatine, or glycogen between control and IRL animals or between control and IRL plus hypoxemia animals. Muscle lactate levels increased significantly in the IRL plus hypoxemia animals only. The data from this study suggest that moderate hypoxemia during resistive-loaded breathing in the piglet does not accentuate diaphragmatic fatigue.

Animals↗

PubMed1994

Hypoxemia regulates effect of lipopolysaccharide on polymorphonuclear leukocyte CD11b/CD18 expression.

Expression of the receptor CD11b/CD18 on the polymorphonuclear leukocyte (PMN) surface is important for several aspects of PMN function during endotoxemia. The mechanisms underlying regulation of CD11b/CD18 expression during hypoxemia and endotoxemia, however, are less clear. We investigated the effects of exposure of whole blood PMNs to lipopolysaccharide (LPS) during hypoxemia. During hypoxemia (10-30% O2 saturation), LPS reduced CD11b/CD18 expression. Both kinetic assays and experiments with microfilament stabilizers (phalloidin, cytochalasin B) demonstrated that this was most likely due to receptor shedding. Incubation of whole blood PMNs with an anti-CD14 monoclonal antibody (MEM18) largely prevented the LPS-induced reduction of CD11b/CD18 expression. Decreased CD11b/CD18 expression reduced PMN functional capability, as the binding of its ligand (erythrocytes opsonized with the 3rd component of complement Cbi) and intracellular H2O2 production were reduced. After exposure to LPS, N-formyl-methionyl-leucyl-phenylalanine could rapidly induce new CD11b/CD18 receptors to the cell surface, and this was not inhibited by actinomycin D or cycloheximide. After reoxygenation (> 90% O2 saturation), CD11b/CD18 expression was restored, and this was abrogated by exposure to cytochalasin B. Lipid A was able to reproduce the effects of LPS during hypoxemia and hypoxemia-reoxygenation but required a 10-fold greater concentration to do so. These results demonstrate that during hypoxemia an important pathophysiological property of LPS is to reduce CD11b/CD18 expression. This results in diminished PMN functional capability, which would contribute to the pathogenicity of LPS during acute infectious states.

Antibodies, Monoclonal↗

PubMedDate not supplied

Spirometric predictors for the exclusion of severe hypoxemia in chronic obstructive pulmonary disease.

BACKGROUND: Controversy has existed over the need for routine arterial blood gas (ABG) analysis in patients with chronic obstructive pulmonary disease (COPD). Some authors recommend it in all patients with COPD, but others find it unnecessary if the forced expiratory volume in 1 s (FEV(1)) is 50% of predicted or greater. OBJECTIVES: To clarify this controversy, and to investigate correlations between severe hypoxemia and multiple spirometric parameters in patients with COPD with FEV(1) 50% of predicted or greater. PATIENTS AND METHODS: In 103 consecutive patients with COPD with FEV(1) 50% of predicted or greater, and without any other cardiopulmonary disorder, the incidence of severe hypoxemia (partial pressure of arterial oxygen less than 60 mmHg) was established by ABG analysis. Positive and negative predictive values (PPVs and NPVs, respectively) for severe hypoxemia for multiple spirometric parameters (FEV(1), FEV(1)/forced vital capacity [FVC], peak expiratory flow [PEF], maximal midexpiratory flow rate [FEF(25-75)]) were evaluated in a stepwise manner. RESULTS: Twenty-two patients (21%) were found to be severely hypoxemic. In the severely hypoxemic group, the mean values for FEV(1), FEV(1)/FVC, PEF and FEF(25-75) were 59.0+/-8.19%, 53.6+/-11.3, 50.6+/-9.3 and 34.4+/-14.2% of predicted, respectively. The mean values for the same parameters in the other patients were 58.0+/-4.6%, 52.7+/-7.8, 51.5+/-7.5 and 39.1+/-7.7% of predicted, respectively. Comparing these parameters between the two groups, only the difference in FEF(25-75) was statistically significant (P<0.01). Valid PPVs and NPVs could not be established for any of the parameters at any level, except for the NPV for FEF(25-75) 50% of predicted or greater, which was 92%. This threshold value resulted in a false negative finding in less than 5% of the patients with hypoxemia. CONCLUSIONS: The results of the present study showed that one in five patients with COPD with FEV(1) 50% of predicted or greater was severely hypoxemic. In such patients, hypoxemia may be excluded, and ABG analysis may not be needed when the FEF(25-75) is also 50% of predicted or greater. The FEV(1), FEV(1)/FVC and PEF parameters failed to predict or exclude severe hypoxemia.

Aged↗

PubMed2002

Nitric oxide synthesis inhibition during cerebral hypoxemia and reoxygenation with 100% oxygen in newborn pigs.

The objective of our study was to evaluate the effects of N(sigma)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of the nitric oxide (NO) pathway, on cerebral microcirculation during hypoxemia and reoxygenation with 100% oxygen in newborn pigs. Twenty-two pigs were randomized to hypoxemia [inspired fraction of oxygen (FIO(2)) 0.08; 20 min] and reoxygenation (FIO(2) 1.0; 60 min) or normoxia. The hypoxemic animals were further randomized to receive either an intravenous bolus injection of 5 mg/kg L-NAME (n = 8) or a corresponding volume of isotonic saline (n = 8) 30 min before the onset of hypoxemia. The normoxemic group (n = 6) received the same pretreatment with L-NAME. Cerebral hemodynamics were assessed by laser Doppler flowmetry and intracranial pressure monitoring. The cerebral NO concentration was continuously measured using an electrochemical sensor. Pretreatment with L-NAME resulted in a more severe systemic hypotension and reduced cerebral microcirculation during the period of hypoxemia compared with the saline/hypoxemia group. NO synthesis inhibition during reoxygenation with 100% oxygen, however, blunted the increase in NO concentration (p < 0.05) without reduction of cerebral blood flow and cerebral perfusion pressure. In conclusion, in this newborn pig model, pretreatment with a bolus infusion of L-NAME induced severe hypotension and reduced cerebral microcirculation during hypoxemia. However, it appears to have no significant adverse effect on cerebral hemodynamics during the period of reoxygenation with 100% oxygen. This deleterious effect during hypoxemia limits the use of L-NAME as a preventive drug but suggests beneficial effects during reoxygenation with 100% oxygen.

Animals↗

PubMed1993

Effect of hypoxemia and hypovolemia on retinal and choroidal blood flow in the newborn piglet.

The effect of hypoxemia and/or hypovolemia on ocular blood flow was studied in paralyzed and mechanically ventilated newborn piglets with the isotope-labelled microsphere method. Twenty-six piglets were studied in four different groups. One group of piglets (n = 6) was made hypoxemic by breathing 10% O2, a second group (n = 7) and a third group (n = 7) were studied during hypoxemia (10% O2), followed by hypovolemia (bleeding 20 and 30% of estimated blood volume, respectively). A fourth group of piglets (n = 6) was made hypovolemic by bleeding 20% of estimated blood volume. Hypoxemia resulted in a 2- to 3-fold increase in retinal blood flow (RBF), while hypovolemia did not change RBF, not even when preceded by a period of hypoxemia. In the case of choroidal blood flow (ChBF), the increase caused by hypoxemia was only 10-40%. Although ChBF decreased significantly during hypovolemia, no significant correlation between mean arterial blood pressure and ChBF was found. The results indicate that autoregulation is normally seen in RBF, but probably not in ChBF. However, during hypoxemia autoregulation was found neither in RBF nor in ChBF.

Animals↗

PubMed1993

Detection and correction of hypoxemia associated with air travel.

Hypoxemia occurs during air travel because the pressure in aircraft cabins is not maintained equal to barometric pressure at sea level. Identification of patients who will develop significant arterial hypoxemia is most conveniently achieved by exposing these individuals to inspired oxygen tensions similar to those experienced during air travel. We utilized commercial Venturi devices with nitrogen as a source gas to lower inspired oxygen tensions (114 and 99 mm Hg) to simulate exposure to altitude (6,700 and 10,000 feet) that occurs with air travel. Oxygen was administered by nasal cannulas to correct the induced hypoxemia. Eleven normal subjects had baseline oxygen saturations of 97.3% as determined by ear oximetry. Exposure to reduced oxygen tensions for 20 min using 35 and 40% Venturi devices caused minimal O2 desaturation (94.8 and 93.8%, respectively). Mean baseline arterial oxygen saturation was 93.2% in 11 patients with chronic obstructive lung disease. Oxygen saturation fell to 89.5 and 87.5%, respectively, with exposure to the two levels of reduced oxygen tensions. Hypoxemia was corrected with administration of O2 by nasal cannulas at rates of 1.2 and 1.5 L/min, respectively. We conclude that individual patients can be evaluated conveniently for possible development of hypoxemia associated with air travel using available Venturi devices. This approach also permits determination of the oxygen therapy needed to correct hypoxemia.

Air Pressure↗

PubMed1984

Influence of hypercapnia and/or hypoxemia and metabolic acidosis on theophylline kinetics in the conscious rabbit.

This study investigated the effect of acute changes in blood gases and pH on theophylline kinetics. Groups of 6 conscious rabbits were exposed to air (control) or to a high CO2 and/or low O2 atmosphere for 570 minutes, or received 47 ml/kg of 0.3N HCl by gavage. Once blood gases or pH were stabilized, they received 2.5 mg/kg theophylline intravenously. Urine, blood samples, and cerebrospinal fluid were collected. Metabolic acidosis did not modify theophylline kinetics. Theophylline serum concentrations increased with hypercapnia (p less than 0.05), hypoxemia (p less than 0.01), and hypercapnia combined with hypoxemia (p less than 0.001), compared with those in control animals. These increases were related to a decrease in theophylline nonrenal clearance (Clnr). Thus, Clnr decreased from 1.52 +/- 0.05 ml/min/kg in control animals to 1.13 +/- 0.13 in hypercapnia (p less than 0.01), 1.09 +/- 0.09 in hypoxemia (p less than 0.001), and 1.02 +/- 0.02 in hypoxemia combined with hypercapnia (p less than 0.001). Theophylline protein binding was not affected by any of the experimental conditions. The ratio of central nervous system to serum theophylline concentration was increased by 16% (p less than 0.05) with hypercapnia combined with hypoxemia. It was concluded that both hypercapnia and/or hypoxemia decreased theophylline biotransformation. Such a decrease may be the cause of toxicity.

Acidosis, Respiratory↗

PubMed1985

The influence of hypoxemia on tritiated digoxin plasma kinetics and tissue distribution in the conscious dog.

The goals of this study were to document the effect of hypoxemia on the distribution of digoxin in conscious dogs. For this purpose, 6 beagles were exposed to air and 6 others to an atmosphere containing 10% O2, to generate a PaO2 equal to 46.3 +/- 0.3 mmHg (mean +/- SEM). The animals received 25 micrograms/kg of digoxin containing 2.17 micrograms/kg of 3H-digoxin, and then blood and urine samples were collected over the next 48 h, at which time they were killed to determine digoxin concentrations in several tissues. Five additional beagles were used to assess the influence of hypoxemia on the blood perfusion to these tissues using radioactive microspheres. The results, expressed as digoxin equivalents, indicated that hypoxemia increased the digoxin apparent volume of distribution (2.85 +/- 0.10 versus 2.01 +/- 0.11 L/kg; p less than 0.001) and the time required to achieve this distribution (9.7 +/- 1.4 versus 2.6 +/- 0.3 h; p less than 0.01). As digoxin clearance was not influenced by hypoxemia, the half-life was increased from 25.2 +/- 1.5 to 33.4 +/- 1.3 h (p less than 0.01). With hypoxemia, digoxin concentrations increased significantly in the brain and diaphragmatic muscle, but only marginally in other organs, including the heart, the latter despite a significant increase in blood flow. It is concluded that hypoxia does change digoxin disposition but does not increase digoxin heart concentrations. Therefore, factors other than changes in digoxin plasma kinetics and heart distribution may be responsible for the decrease in digitalis tolerance during hypoxemia.

Animals↗

PubMed1984

Role of arginine vasopressin and angiotensin II in cardiovascular responses to combined acute hypoxemia and hypercapnic acidosis in conscious dogs.

The physiological relationship of increased circulating angiotensin II and vasopressin to circulatory changes during combined hypoxemia and hypercapnic acidosis is unclear. To evaluate the role(s) of angiotensin II and vasopressin, seven unanesthetized female mongrel dogs with controlled sodium intake (80 meq/24 h X 4 d) were studied during 40 min of combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 mmHg; PaCO2, 55 +/- 2 mmHg; pH = 7.16 +/- 0.04) under the following conditions: (a) intact state with infusion of vehicles alone; (b) beta-adrenergic blockade with infusion of d,l-propranolol (1.0 mg/kg bolus, 0.5 mg/kg per h); of the vasopressin pressor antagonist d-(CH2)5Tyr(methyl)arginine-vasopressin (10 micrograms/kg); and (d) simultaneous vasopressin pressor and angiotensin II inhibition with the additional infusion of 1-sarcosine, 8-alanine angiotensin II (2.0 micrograms/kg per min). The rise in mean arterial pressure during the combined blood-gas derangement with vehicles appeared to be related to increased cardiac output, since total peripheral resistance fell. Beta-adrenergic blockade abolished the fall in total peripheral resistance and diminished the rise in cardiac output during combined hypoxemia and hypercapnic acidosis, but the systemic pressor response was unchanged. In addition, the rise in mean arterial pressure during the combined blood-gas derangement was unaltered with vasopressin pressor antagonism alone. In contrast, the simultaneous administration of the vasopressin pressor and angiotensin II inhibitors during combined hypoxemia and hypercapnic acidosis resulted in the abrogation of the overall systemic pressor response despite increased cardiac output, owing to a more pronounced fall in total peripheral resistance. Circulating catecholamines were increased during the combined blood-gas derangement with vasopressin pressor and angiotensin II blockade, suggesting that the abolition of the systemic pressor response in the last 30 min of combined hypoxemia and hypercapnic acidosis was not related to diminished activity of the sympathetic nervous system. These studies show that vasopressin and angiotensin II are major contributors to the systemic pressor response during combined acute hypoxemia and hypercapnic acidosis.

Angiotensin II↗

PubMed1986

Comparative effects of metabolic acidemia and hypoxemia on cardiac output and regional blood flows in unanesthetized newborn lambs.

We studied the comparative effects of HCl-induced metabolic acidemia (pH = 7.11 +/- 0.03, mean +/- SE) and hypoxemia (PO2 = 28 +/- 1 torr) on cardiac output and regional blood flows in newborn lambs 3 days after the surgical placement of catheters in the left atrium and aorta and pacing wires on the left atrium. Cardiac output decreased by 49 +/- 6% during metabolic acidemia in contrast to the 12 +/- 2% increase during hypoxemia. The adrenal glands and the diaphragm were the only organs that received increased blood flows during acidemia and hypoxemia. Cerebral and myocardial blood flows decreased during acidemia but increased during hypoxemia. Blood flows decreased to the carcass and gastrointestinal tract during acidemia but did not change significantly during hypoxemia. Renal and splenic blood flows decreased during both stresses, but the reductions were more severe during acidemia. The changes in regional blood flows were not a passive result of the respective changes in cardiac output. HCl-induced metabolic acidemia and hypoxemia each result in significant redistributions of available blood flows which are quantitatively and qualitatively different from each other.

Acidosis↗

PubMed1988

Repeated exposure to rapidly developing hypoxemia influences the interaction between oxygen and carbon dioxide in initiating arousal from sleep in lambs.

Experiments were done on 12 lambs to determine if repeated exposure to hypoxemia influences the interaction between oxygen and carbon dioxide in causing arousal response from sleep. Each lamb was anesthetized and instrumented for sleep staging and measurements of arterial Hb oxygen saturation. No sooner than 3 days after surgery, measurements were made in quiet and active sleep during control periods when the lambs were breathing 21% oxygen and during experimental periods when the lambs were breathing either 5% O2-0% CO2, 5% O2-5% CO2 or 5% O2-10% CO2. Each experimental period was terminated during each epoch by changing the inspired gas mixture back to 21% oxygen once the animal aroused from sleep. The lambs were divided into two groups. One group (n = 7) was studied without prior exposure to hypoxemia and the other group (n = 5) was studied after exposure to 5% oxygen during approximately 100 epochs of sleep until they aroused. In lambs not previously exposed to hypoxemia, there was evidence for a slight interaction between oxygen and carbon dioxide in initiating arousal but only from quiet sleep. Repeated exposure to hypoxemia resulted in an arousal response decrement to hypoxemia. In lambs previously exposed to hypoxemia, there was evidence for an interaction between oxygen and carbon dioxide in initiating arousal from both quiet and active sleep (i.e. the time to arousal decreased and the saturation at arousal increased as increasing amounts of carbon dioxide were added to the hypoxic gas mixture).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Regional cerebral glucose utilization in immature fetal guinea pigs during maternal isocapnic hypoxemia.

Recent studies in immature fetal animals demonstrated only a slight or variable increase in the cerebral glycolytic rate during moderate isocapnic hypoxemia. However, the methods used in those studies did not allow for detection of small differences or of regional redistributions of the cerebral glycolytic rate. Hence, a global increase or a regional redistribution of the cerebral glycolytic rate during hypoxemia accompanied by a severe increase in tissue lactate concentration in a few brain areas may have been overlooked in these studies. Because these pathophysiologic mechanisms seem to considerably exacerbate neuronal cell damage due to hypoxic/ischemic insults, we were keen to clarify this point. We, therefore, applied the 2-deoxyglucose method to fetal guinea pigs in utero and measured total and regional cerebral glucose utilization in fetuses of this species at 0.75 of gestation during maternal isocapnic hypoxemia. At 0.75 of gestation guinea pig dams were chronically catheterized. Control groups were exposed to room air, whereas study groups were exposed to a hypoxic atmosphere (10% oxygen, 2% carbon dioxide, and 88% nitrogen). To measure total and regional cerebral glucose utilization during normoxemia and isocapnic hypoxemia, we injected i.v. 100 microCi of 2-[3H]deoxyglucose into the dams. Total and regional cerebral glucose utilization were determined from the steady-state clearance of 2-deoxyglucose between the maternal arterial plasma and the fetal brain, the glucose concentration in the maternal arterial plasma, and the "lumped constant." During isocapnic hypoxemia, total fetal cerebral glucose utilization was not significantly higher than that previously measured during normoxemia (8 +/- 0.8 versus 8 +/- 1.0 micromol/100 g/min). Furthermore, no redistribution of cerebral glucose utilization could be detected. We conclude that moderate isocapnic hypoxemia in the immature fetal brain does not lead to any significant increase or redistribution of glucose utilization or to any major lactate accumulation. This may be related to the low cerebral metabolic demands of brain tissue at this stage of development. Whether this is the main reason for the known resistance of the immature fetal brain toward ischemic neuronal cell damage remains to be established.

Animals↗

PubMed2001

Plasma adrenocorticotropin and cortisol concentrations during acute hypoxemia after a reversible period of adverse intrauterine conditions in the ovine fetus during late gestation.

The present study determined the pituitary-adrenal responses to acute hypoxemia after a period of reversible adverse intrauterine conditions produced by partial compression of the umbilical cord for 3 days in the sheep fetus during late gestation. At 118 +/- 2 days gestation (term is approximately 145 days), 12 sheep fetuses were instrumented under halothane anesthesia with an occluder cuff around the umbilical cord, amniotic and vascular catheters, and a transit-time flow probe around an umbilical artery. In 6 of the fetuses at 125 days, umbilical blood flow was reduced by about 30% from baseline for 3 days (UCC), after which the occluder was deflated. The remaining 6 fetuses acted as sham-operated controls in which the occluder was not inflated. All fetuses were then subsequently subjected to 2 periods of acute hypoxemia, elicited by reducing the maternal inspired fraction of oxygen (FiO(2)) at 2 +/- 1 and 5 +/- 2 days after the end of cord compression or sham compression. In addition, 4 fetuses from each group were subjected to an ACTH challenge 1-2 days after the final episode of acute hypoxemia. Maternal and fetal arterial blood samples were taken at appropriate intervals during cord compression, acute hypoxemia, and ACTH challenge for analyses of blood gases, pH, and plasma ACTH and cortisol concentrations. Partial compression of the umbilical cord produced reversible mild fetal asphyxia, a transient increase in fetal plasma ACTH, and a progressive increase in fetal plasma cortisol. At 5 +/- 2 days after the end of compression, despite similar blood gas status between the groups, basal plasma cortisol, but not ACTH, concentrations were significantly greater in compressed fetuses relative to sham controls. However, this dissociation did not affect a similar increment in fetal plasma ACTH and cortisol concentrations during acute hypoxemia or in the fetal plasma cortisol response to the ACTH challenge in either group. An increase in adrenocortical mass occurred in fetuses preexposed to partial compression of the umbilical cord relative to sham controls. The data suggest that fetal exposure to a reversible period of adverse intrauterine conditions produced by partial compression of the umbilical cord does not affect the magnitude of the fetal hypothalamic-pituitary-adrenal axis response to subsequent acute hypoxemia, but it leads to resetting of basal hypothalamic-pituitary-adrenal axis function in the fetus. The mechanism for this resetting may include an increase in adrenocortical steroidogenic synthetic capacity, but it is not due to a change in adrenocortical sensitivity to ACTH. Inappropriate fetal glucocorticoid exposure after reversible periods of adverse intrauterine conditions has important implications for fetal and postnatal development.

Acute Disease↗