SEARCH · PubMed Health

Results for “hypoxemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed1999

Pulmonary hemodynamics in newborn piglets during hypoxemia and reoxygenation: blocking of the endothelin-1 receptors.

The effects of blocking endothelin (ET) receptors in pulmonary circulation during hypoxemia and reoxygenation were studied in five groups of piglets. Ten minutes before hypoxemia, the Hyp group (n = 10) was given saline and the 1-mg (n = 9) and 5-mg group (n = 9), respectively, were given 1 and 5 mg/kg i.v. SB 217242 (an ET receptor antagonist). Two groups served as normoxic controls. The piglets were ventilated with 8% O2 until base excess was <-20 mmol/L or mean arterial blood pressure was <20 mm Hg. Reoxygenation was performed with air. The increase of mean pulmonary artery pressure was significantly attenuated during hypoxemia and reoxygenation in the 1-mg group (p = 0.006). The pulmonary vascular resistance index increased significantly at the end of hypoxemia in the Hyp and 5-mg groups but was comparable to baseline in the 1-mg group. During the study period, the changes in pulmonary vascular resistance index were significantly attenuated in the 1-mg group compared with the 5-mg group. Stroke volume index was significantly attenuated compared with baseline in the 5-mg group during both hypoxemia and reoxygenation, whereas, in the Hyp and 1-mg group, stroke volume index was attenuated only at the end of hypoxemia. During hypoxemia, plasma ET-1 decreased from 1.9+/-0.2 to 1.3+/-0.3 ng/L (p = 0.008) in the Hyp group, remained unchanged in the 1-mg group, and increased from 1.6+/-0.2 to 6.6+/-1.6 ng/L (p = 0.008) in the 5-mg group. We conclude that blocking ET receptors attenuates pulmonary vasoconstriction during hypoxemia and reoxygenation in piglets.

Acid-Base Equilibrium↗

PubMed2000

Neuropeptide Y in the sheep fetus: effects of acute hypoxemia and dexamethasone during late gestation.

Plasma concentrations of neuropeptide Y (NPY) were measured in pregnant ewes and their fetuses under basal conditions and in response to acute hypoxemia during late gestation. The effects of fetal treatment with dexamethasone on these NPY responses were also examined. Under general anesthesia, 10 Welsh Mountain ewes and their fetuses were chronically instrumented between 117-120 days gestation (dGA; term is approximately 145 dGA) with vascular and amniotic catheters, and an ultrasonic probe around a femoral artery of each fetus. At 124 dGA, five fetuses were continuously infused i.v. with dexamethasone for 48 h at a rate of 1.73 +/- 0.16 microg x kg(-1) x h(-1) while the remaining five fetuses received vehicle at the same rate. At 126 dGA, 45 h from the onset of either infusion, 1 h of materno-fetal hypoxemia was induced by reducing maternal FiO2. During normoxia, maternal plasma NPY concentrations were three times those measured in fetal plasma in both groups. During hypoxemia, PaO2 fell to similar levels in the control and dexamethasone-treated groups in both mothers and fetuses. In control animals, there was a significant increase in the NPY concentration in fetal, but not maternal, plasma during hypoxemia. Fetal treatment with dexamethasone significantly enhanced the fetal NPY response to acute hypoxemia but had no effects on basal NPY levels in the fetal or maternal plasma or on the maternal response to acute hypoxemia. These data show: 1) differences between the maternal and fetal plasma NPY response to maternal inhalation hypoxia; 2) that NPY may play a role in mediating fetal defense responses to acute hypoxemia; and 3) that fetal exposure to glucocorticoids modifies the fetal plasma NPY response to acute hypoxemia.

Animals↗

PubMed1999

Hypoxemia and hypercapnia during exercise and sleep in patients with cystic fibrosis.

BACKGROUND: In patients with cystic fibrosis (CF), it has been proposed that hypoxemia and hypercapnia occur during episodes of stress, such as exercise and sleep, and that respiratory muscle weakness because of malnutrition may be responsible. METHODS: Pulmonary function, respiratory muscle strength, and nutrition were assessed and correlated with the degree of hypoxemia and hypercapnia during exercise and sleep in 14 patients with CF and 8 control subjects. RESULTS: Despite no differences in maximum static inspiratory pressure (PImax) between the two groups, the CF group developed more severe hypoxemia (minimum oxyhemoglobin saturation [SpO2], 89 +/- 5% vs 96 +/- 2%; p < 0.001) and hypercapnia (maximum transcutaneous CO2 tension [PtcCO2], 43 +/- 6 vs 33 +/- 7 mm Hg; p < 0.01) during exercise. Similarly, during sleep, the CF group developed greater hypoxemia (minimum SpO2, 82 +/- 8% vs 91 +/- 2%; p < 0.005), although CO2 levels were not significantly different (maximum PtcCO2, 48 +/- 7 vs 50 +/- 2 mm Hg). Within the CF group, exercise-related hypoxemia and hypercapnia did not correlate with FEV1, residual volume/total lung capacity ratio (RV/TLC), PImax, or body mass index (BMI). Hypoxemia and hypercapnia during sleep correlated with markers of gas trapping (RV vs minimum arterial oxygen saturation [r = -0.654; p < 0.05]), RV vs maximum PtcCO2 (r = 0.878; p < 0.001), and RV/TLC vs maximum PtcCO2 (r = 0.790; p < 0.01) but not with PImax or BMI. CONCLUSION: Patients with moderately severe CF develop hypoxemia and hypercapnia during exercise and sleep to a greater extent than healthy subjects with similar respiratory muscle strength and nutritional status. Neither respiratory muscle weakness nor malnutrition are necessary to develop hypoxemia or hypercapnia during exercise or sleep.

Adult↗

PubMed1986

Cognitive impairment in patients with obstructive sleep apnea and associated hypoxemia.

Twenty-six patients with sleep apnea had neuropsychologic testing prior to nocturnal sleep study in a sleep disorders clinic. The cognitive functioning of patients who had sleep apnea with associated hypoxemia was compared to nonhypoxemic patients with sleep apnea. The patients who had sleep apnea with hypoxemia had more severe cognitive impairment than those with sleep apnea without hypoxemia. The hypoxemic patients with sleep apnea had significantly poorer cognitive functioning on four of eight tests (p less than 0.05). In addition, the patients who had sleep apnea with hypoxemia had mean performance scores in the impaired range on measures of attention, concentration, complex problem-solving, and short-term recall of verbal and spatial information. In contrast, the patients who had sleep apnea without hypoxemia had no mean performance score in the impaired range. The degree of hypoxemia during sleep and wakefulness significantly correlated with the degree of overall cognitive impairment as rated by a neuropsychologist; however, measures of sleep fragmentation did not significantly correlate with overall cognitive impairment in patients with sleep apnea. We conclude that patients who have sleep apnea with associated hypoxemia have cognitive impairment which is more severe than those with sleep apnea without hypoxemia.

Cognition Disorders↗

PubMed1988

Theophylline effect on the cerebral blood flow response to hypoxemia.

Cerebral oxygen delivery (CO2D) remains nearly constant over a wide range of cerebral perfusion pressure and arterial oxygen content. In response to a decrease in arterial oxygen content secondary to hypoxemia, cerebral blood flow (CBF) increases, a response likely mediated by the release of adenosine. We studied the effect of theophylline, a potent adenosine antagonist, on CBF and cerebral oxygen delivery (CO2D) during hypoxemia in five healthy adult male volunteers. The CBF was measured using 133Xe clearance under conditions of (1) normoxemia (O2 saturation greater than 95 percent); (2) hypoxemia (O2 saturation = 80 percent); (3) normoxemia following aminophylline (the ethylene diamine salt of theophylline) 6 mg/kg intravenously; and (4) hypoxemia following aminophylline. Aminophylline decreased CBF and CO2D during both normoxemia and hypoxemia, but did not prevent the increase in CBF accompanying hypoxemia, suggesting that the increase in CBF in response to hypoxemia may not be mediated by adenosine or that customary doses of aminophylline are insufficient to inhibit adenosine-mediated cerebral vasodilation in response to hypoxemia. The significant decrease in CBF and CO2D observed following aminophylline is potentially clinically important and should be considered in the selection of bronchodilator therapy.

Adult↗

PubMed2004

Can clinical symptoms or signs accurately predict hypoxemia in children with acute lower respiratory tract infections?

OBJECTIVES: To determine clinical predictors of hypoxemia in children with acute lower respiratory tract infection (ALRI). DESIGN: Cross-sectional study. SETTING: Emergency department of All India Institute of Medical Sciences, a tertiary care hospital. SUBJECTS: 109 under five children, with ALRI. METHODS: Clinical symptoms and signs were recorded. Oxygen saturation was determined by a pulse oximeter. Hypoxemia was defined as oxygen saturation less than 90%. The ability of various clinical symptoms and signs to predict the presence of hypoxemia was evaluated. RESULTS: Twenty-eight (25.7%) children were hypoxemic. No symptoms were statistically associated with hypoxemia. Tachypnea, suprasternal indrawing, intercostal indrawing, lower chest indrawing, cyanosis, crepitations, and rhonchi were statistically significantly associated with hypoxemia. A simple model using the presence of rapid breathing (> or =80/min in children < or =3 m, > or =70/min in >3-12 m and > or =60/min in >12 m) or lower chest indrawing had a sensitivity of 78.5% and specificity of 66.7% for detecting hypoxemia. No individual clinical symptom/sign or a combination had both sufficient sensitivity and specificity to identify hypoxemia. CONCLUSION: None of the clinical features either alone or in combination have desirable sensitivity and specificity to predict hypoxemia in children with acute lower respiratory tract infection.

Acute Disease↗

PubMed1996

Decreased body-core temperature during acute hypoxemia in guinea pigs during postnatal maturation: a regulated thermoregulatory response.

In newborn mammals, hypoxemia produces a decrease in body-core temperature (Tbc), the mechanism of which is unknown. Experiments were therefore carried out to determine whether this decrease results from a regulated or a forced thermoregulatory response. Seven Hartley strain guinea pigs were studied on postnatal days 2, 5, 10, 15, and 26 following implantation of a biotelemetry transmitter into the peritoneal cavity on day 1 to measure Tbc. During each experiment, Tbc and selected ambient temperature were determined in a thermocline (15-40 degrees C gradient) during a control period of normoxemia, an experimental period of hypoxemia (produced by decreasing the fraction of inspired oxygen from 0.21 to 0.10), and a recovery period of normoxemia. We reasoned that no change or a decrease in selected ambient temperature while Tbc decreased during hypoxemia would indicate a regulated thermoregulatory response, whereas an increase in selected ambient temperature while Tbc decreased during hypoxemia would indicate a forced thermoregulatory response. Tbc decreased during hypoxemia at all ages; the response was accentuated on days 15 and 26 compared with day 2. Selected ambient temperature decreased during hypoxemia in the youngest animals but remained the same in the older animals. Our data provide evidence that postnatal maturation influences the thermoregulatory response to hypoxemia in guinea pigs and support the hypothesis that the decrease in Tbc during hypoxemia results from a regulated thermoregulatory response.

Acute Disease↗

PubMed1998

[Short-duration nocturnal hypoxemia and persistent pulmonary hypertension].

Can daily short-duration hypoxemia (4-8 hours) induce pulmonary hypertension and right ventricular hypertrophy? A clinical model of this type of hypoxemia does exist: isolated nocturnal hypoxemia in patients with obstructive sleep apnea syndrome (OSAS) or chronic obstructive pulmonary disease (COPD). By investigating the pulmonary hemodynamics of these patients, it should be possible to determine whether nocturnal hypoxemia alone can induce pulmonary hypertension. Although nocturnal hypoxemia (in OSAS as well as in COPD) can induce acute episodes of pulmonary hypertension, it would not appear that nocturnal hypoxemia alone would be sufficient to provoke permanent diurnal pulmonary hypertension. This is the conclusion of recent studies concerning diurnal pulmonary hemodynamics in OSAS and COPD patients exhibiting minimal hypoxemia during the day but significant nocturnal desaturation. The therapeutic consequences of these data, particularly in COPD are important: current evidence is insufficient to treat with nocturnal oxygen therapy COPD patients who have minimal diurnal hypoxemia but significant nocturnal desaturation.

Hemodynamics↗

PubMed2002

Interactions between endogenous nitric oxide and hypoxemia in activation of group IV muscle afferents.

It has previously been shown that both hypoxemia and nitric oxide (NO) synthase blockade depress the activation of group IV muscle afferents after muscle stimulation (MS). In the present study, we questioned whether hypoxemia exerts a specific inhibitory influence, independently from its effects on endogenous NO formation. This hypothesis was tested in two groups of anesthetized rabbits in which we examined the effects of hypoxemia, and then of subsequent NO synthase blockade by N(G)-nitro-L-arginine methyl ester (L-NAME), and vice versa. In each protocol, group IV afferent activity was recorded from the resting tibialis anterior muscle and after 3-min periods of MS that elicited a significant decrease in muscle force. NO synthase blockade in normoxemia suppressed the group IV afferent response to MS, and hypoxemia alone significantly reduced the post-MS activation of these nerve afferents (+18% vs. +28% in normoxemia). In hypoxemic rabbits, further NO synthase blockade abolished the post-MS activation of group IV afferents. Moreover, when hypoxemia followed the NO synthase blockade, MS significantly reduced the discharge of group IV afferents (-28%). Thus, while these muscle afferents are activated after fatiguing muscle contractions when the endogenous NO production is present, they are deactivated by hypoxemia when NO production is blocked. We conclude that endogenous NO production and hypoxemia exert opposite effects on the activation of the group IV afferents. Our data anticipate the neuromuscular side effects of treatments using exogenous NO or drugs acting on endogenous NO production.

Animals↗

PubMed2002

Effects of acute moderate hypoxemia on kinetics of metoclopramide and its metabolites in chronically instrumented sheep.

Hypoxemia is known to induce various physiological changes which can result in alteration in drug pharmacokinetics. To examine the effect of acute moderate hypoxemia on metoclopramide (MCP) pharmacokinetics, a continuous 14-hour infusion of MCP during a normoxemic, hypoxemic and subsequent normoxemic period was conducted in eight adult sheep. Arterial blood and urine samples were collected to examine the effects on the pharmacokinetics of MCP and its deethylated metabolites. MCP and its mono- and di-deethylated metabolites were quantitated using a GC/MS method. Steady-state concentrations of MCP were achieved in each of the three periods. During hypoxemia, MCP plasma steady-state concentration increased significantly from 50.72 +/- 1.06 to 63.62 +/- 1.79 ng/mL, and later decreased to 55.83 +/- 1.15 ng/mL during the post-hypoxemic recovery period. Total body clearance (CL(TB)) of MCP was significantly decreased from 274.2 +/- 48.0 L/h to 205.40 +/- 28.2 L/h during hypoxemia, and later restored to 245.8 +/- 44.2 L/h during the post-hypoxemic period. Plasma mono-deethylated MCP concentration (32.78 +/- 1.73 ng/mL) also increased, compared to the control group (21.20 +/- 1.39 ng/mL), during hypoxemia and subsequent normoxemic period. Renal excretion of MCP and its metabolites was also decreased during hypoxemia, while urine flow was increased with a concomitant decrease in urine osmolality. Thus, the results indicate that acute moderate hypoxemia affects MCP pharmacokinetics.

Acute Disease↗

PubMed2002

Comparison between the effects of chronic and acute hypoxemia on muscle afferent activities from the tibialis anterior muscle.

The reflex loops initiated by the activation of muscle afferents are altered by a reduction of the oxygen supply. This has been shown in different mammalian species under experimental conditions of acute or chronic hypoxemia. In the present study in rats, we compared the effects of acute and chronic hypoxemia on the activity of afferents from the tibialis anterior muscle to investigate the existence of possible adaptive mechanisms to hypoxaemia. The activity in groups I and II (mechanosensitive) and groups III and IV (mechano- and mostly chemosensitive) muscle afferents was recorded under conditions of normoxaemia and acute and chronic hypoxemia. Chronic hypoxaemia was achieved by exposing the rats for 45 consecutive days to a gas mixture containing 10% oxygen in nitrogen, whereas acute hypoxaemia was limited to a 1-h exposure to a 10% oxygen mixture. Different test agents: muscle stimulation (MS), arterial injection of KCl or lactic acid and tendon vibrations, were used to activate muscle afferents. Both acute and chronic hypoxaemia suppressed the post-MS activation of groups III and IV muscle afferents and significantly depressed the response of these afferents to KCl and lactic acid. The pattern of response of mechanosensitive afferents to mechanical tendon vibration was similar under the three conditions but chronic hypoxemia significantly reduced the response to 10-50 Hz vibrations. We conclude that inhibitory effects on muscle metabosensitive afferents occurred in the first minutes following acute hypoxemia and was prolonged with chronic hypoxemia. Our data also suggest that chronic hypoxemia depresses mechanosensitive muscle afferents. This may explain the observation that sensorimotor control of skeletal muscles is often markedly impaired in hypoxemic humans.

Action Potentials↗

PubMed1977

Brain amino acids in conscious rats in chronic normocapnic and hypocapnic hypoxemia.

The influence of hypoxemia on the brain content of several organic acids and NH+4, AND ITS RELATIONship to the accompanying hypocapnia was studied in unanesthetized rats subjected to hypoxemia for periods ranging between 2 hours and 7 days. Under acute conditions, 'mild' hypoxemia (FO2 = 6--7%), these increases were greater and accompanied by increased gamma-aminobutyric acid (GABA) and decreased glutamic and aspartic acid levels; glutamine and NH+4 remained normal. When hypocapnia was prevented, 'severe' hypoxemia induced only a rise in GABA and slight elevations in lactic and alpha-ketoglutaric acid. During prolonged severe hypoxemia, the effects on the brain amino acids were maintained throughout, indicating that they are independent from the intracerebral pH which should progressively normalize. The effect on lactic acid gradually disappeared. The results show that during hypocapnic hypoxemia the rise in brain GABA is hypoxemia dependent, the decrease in glutamic and aspartic acid is hypocapnia dependent and the increase in lactic acid is in a large way alkalosis dependent.

Amino Acids↗

PubMed1980

The effect of fetal heart rate on cardiovascular function during hypoxemia.

The effect of heart rate changes on cardiovascular function during hypoxemia was studied in lamb fetuses. In chronic preparations, we determined fetal heart rate, descending aortic blood flow (by electromagnetic flowmeter), PO2, PCO2, and pH and calculated fetal cardiac output (CO) and organ blood flows (with the use of 15 mu nuclide-labeled microspheres). Observations were made during control and hypoxemic states either alone or in the presence of parasympathetic blockade by atropine. Fetuses exposed to moderate hypoxemia (ewe breathing 10% oxygen) developed a significant bradycardia which was prevented by atropine pretreatment; no significant change in CO occurred in either case. Fetuses exposed to severe hypoxemia (8% oxygen) developed bradycardia and a significant decrease in CO; atropine pretreatment prevented the bradycardia but failed to prevent the decrease in CO. Atropine administered to the already severely hypoxemic fetus increased the heart rate but did not restore the depressed CO. The redistribution of blood flow from low-priority (e.g., viscera) to high-priority (e.g., myocardium) tissues correlated with the degree of hypoxemia. Myocardial blood flow was greater during hypoxemia when bradycardia was prevented by atropine than during hypoxemia alone; otherwise, blood flow distribution in response to hypoxemia was unaffected by atropine blockade.

Acetylcholine↗

PubMed1997

Effects of prolonged hypoxemia on fetal renal function and amniotic fluid volume in sheep.

OBJECTIVE: Our purpose was to determine the effects of prolonged hypoxemia on fetal renal function and amniotic fluid volume and composition. STUDY DESIGN: Twelve pregnant ewes underwent surgery at 115 +/- 2 days after mating (term approximately 147 days) for the implantation of fetal vascular, bladder, and amniotic sac catheters. At 125 +/- 1 days seven fetuses were studied during 6 days of hypoxemia and five control fetuses were studied over six days of normoxemia. Index values of fetal renal function and amniotic fluid volume were measured. RESULTS: During hypoxemia fetal SaO2 and PaO2 were reduced from 60.9% +/- 1.6% and 21.9 +/- 0.6 mm Hg to 29.6% +/- 3.8% and 14.9 +/- 0.8 mm Hg, respectively. Fetal hypoxemia was associated with a transient acidemia (arterial pH 7.29 +/- 0.02) at 4 hours. There were no sustained alterations in fetal urine production (9.5 +/- 0.8 ml/hr/kg) or glomerular filtration rate (1.3 +/- 0.1 ml/min/kg) during hypoxemia. In control fetuses the amniotic fluid volume increased over 7 days, from 717 +/- 169 ml to 1031 +/- 147 ml, whereas in the hypoxemic fetuses it did not change (741 +/- 68 ml) over the same period. CONCLUSION: During prolonged fetal hypoxemia in the absence of acidemia, fetal urine production is maintained, whereas the normal gestational increase in amniotic fluid volume is prevented, raising the possibility that intramembranous reabsorption of amniotic fluid is increased by hypoxemia.

Amniotic Fluid↗

PubMed2001

Nitric oxide synthase activity in brain tissues from llama fetuses submitted to hypoxemia.

The fetal llama (Lama glama; a species adapted to live in chronic hypoxia in the highlands of the Andes) did not increase cerebral blood flow and reduce the brain oxygen uptake during hypoxemia. Although nitric oxide (NO) is a normal mediator in the regulation of vascular tone and synaptic transmission, NO overproduction by hypoxemia could produce neuronal damage. We hypothesized that nitric oxide synthase (NOS) activity is either maintained or reduced in the central nervous system of the llama fetuses submitted to chronic hypoxemia. Approximately 85% of the Ca(2+)-dependent NOS activity was soluble, at least 12% was associated with the mitochondrial fraction, and less than 5% remains associated with microsomes. To understand the role of NO in chronic hypoxemia, we determined the effect of 24-h hypoxemia on NOS activity in the central nervous system. No changes in activity or the subcellular distribution of NOS activity in brain tissues after hypoxemia were found. We proposed that the lack of changes in NOS activity in the llama under hypoxemia could be a cytoprotective mechanism inherent to the llama, against possible toxic effects of NO.

Animals↗

PubMed2000

Amniotic gas values and acid-base status during acute maternal hyperoxemia and hypoxemia in the early fetal sheep.

OBJECTIVE: This study was undertaken to determine amniotic fluid gas values and acid-base balance during maternal hyperoxemia and hypoxemia in early pregnancy. STUDY DESIGN: Anesthetized sheep (n = 12) in early and mid pregnancy (0.3 to 0.5 gestation) were subjected to hyperoxemia followed by hypoxemia. Amniotic fluid PO (2), pH, PCO (2), bicarbonate concentration, and base excess were monitored continuously with a multiparameter Paratrend (Diametrics Medical Inc, St Paul, Minn) sensor and compared between 0.3 and 0.5 gestation. RESULTS: During maternal normoxemia all parameters were constant. At all gestational ages maternal hyperoxemia caused no changes apart from a rapid increase in amniotic fluid PO (2) (P <.001). Maternal hypoxemia led to a reduced amniotic fluid PO (2) (P <.001), whereas the PCO (2) and the bicarbonate concentration increased (P <.001). Changes in amniotic fluid gas values and acid-base balance were more pronounced at 0.3 gestation than at 0.5 gestation. Amniotic fluid Po(2) responded earlier to maternal hyperoxemia than to hypoxemia (9. 5 vs 14.3 minutes; P <.001). During hypoxemia maternal PaCO (2) changed faster than did amniotic fluid PCO (2) (P <.001). CONCLUSIONS: Acute maternal hypoxemia during early pregnancy was quickly reflected in amniotic fluid gas values and acid-base balance, whereas hyperoxygenation induced the quickest changes in amniotic fluid PO (2). The metabolic effects of maternal hyperoxemia and hypoxemia were also more pronounced during early pregnancy than at mid pregnancy.

Amniotic Fluid↗

PubMed2004

Effects of maternally administered dexamethasone and acute hypoxemia at 0.7 gestation on blood pressure and placental perfusion in sheep.

Glucocorticoid administration to women in premature labor significantly decreases preterm infant morbidity and mortality. Fetal exposure to maternally administered glucocorticoids in late gestation causes fetal hypertension. We determined the effects of a single course (4 injections at 12-hr intervals) of dexamethasone (DM; 2 mg, a weight-adjusted dose equivalent to one-third the dose administered to pregnant women) or saline (S) in sheep at 103-104 days of gestation (dGA; term 149 dGA) on maternal and fetal blood pressure (BP). We also determined the BP and placental perfusion effects of acute maternal hypoxemia. Venous and arterial catheters were placed in 10 ewes and fetuses (DM = 6, S = 4) at 96 +/- 1 dGA. Maternal and fetal placental perfusion was determined with fluorescent microspheres. Dexamethasone increased fetal but not maternal BP; maternal and fetal placental blood flow and vascular resistance (VR) were unchanged. At 105 dGA, hypoxemia was induced for 1 hr by maternal nitrogen gas inhalation to decrease fetal PaO2 by 40%. Hypoxemia increased BP in DM but not S fetuses or mothers in either group. Hypoxemia decreased maternal placental blood flow by 39 +/- 7% and 51 +/- 9% and increased maternal placental VR by 65 +/- 7% and 69 +/- 6% in S and DM mothers, respectively. Hypoxemia did not alter fetal placental blood flow or VR in either treatment group. In summary, at 0.7 gestation, DM induces a hypertensive response to fetal hypoxemia that is characteristic of older fetuses but does not alter hypoxemia-induced reductions in maternal placental blood flow.

Acute Disease↗

PubMed1992

Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

Oxygen tension (PO2) was measured with microelectrodes within the retina of anesthetized cats during normoxia and hypoxemia (i.e., systemic hypoxia), and photoreceptor oxygen consumption was determined by fitting PO2 measurements to a model of steady-state oxygen diffusion and consumption. Choroidal PO2 fell linearly during hypoxemia, about 0.64 mmHg/mmHg decrease in arterial PO2 (PaO2). The choroidal circulation provided approximately 91% of the photoreceptors' oxygen supply under dark-adapted conditions during both normoxia and hypoxemia. In light adaptation the choroid supplied all of the oxygen during normoxia, but at PaO2's less than 60 mmHg the retinal circulation supplied approximately 10% of the oxygen. In the dark-adapted retina the decrease in choroidal PO2 caused a large decrease in photoreceptor oxygen consumption, from approximately 5.1 ml O2/100 g.min during normoxia to 2.6 ml O2/100 g.min at a PaO2 of 50 mmHg. When the retina was adapted to a rod saturating background, normoxic oxygen consumption was approximately 33% of the dark-adapted value, and hypoxemia caused almost no change in oxygen consumption. This difference in metabolic effects of hypoxemia in light and dark explains why the standing potential of the eye and retinal extracellular potassium concentration were previously found to be more affected by hypoxemia in darkness. Frequency histograms of intraretinal PO2 were used to characterize the oxygenation of the vascularized inner half of the retina, where the oxygen distribution is heterogeneous and simple diffusion models cannot be used. Inner retinal PO2 during normoxia was relatively low: 18 +/- 12 mmHg (mean and SD; n = 8,328 values from 36 profiles) in dark adaptation, and significantly lower, 13 +/- 6 mmHg (n = 4,349 values from 19 profiles) in light adaptation. Even in the dark-adapted retina, 30% of the values were less than 10 mmHg. The mean PO2 in the inner (i.e., proximal) half of the retina was well regulated during hypoxemia. In dark adaptation it was significantly reduced only at PaO2's less than 45 mmHg, and it was reduced less at these PaO2's in light adaptation.

Adaptation, Biological↗