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 145 records · Page 8Linked to original sources

PubMed1997

Hypoxemia and hypoxic pulmonary vasoconstriction: autonomic nervous system versus mixed venous PO2.

Hypoxemia interferes with hypoxic pulmonary vasoconstriction (HPV). We investigated the respective roles of the autonomic nervous system and the mixed venous PO2 (PVO2) in the attenuation of HPV by hypoxemia. Pentobarbital-anesthetized dogs had their lungs separately ventilated with a dual-lumen endotracheal tube. Left (Ql) and total (Qt) pulmonary blood flows were determined using electromagnetic flow probes. HPV was initiated by ventilating the left lung with nitrogen for 5-10 min while the right lung received 100% oxygen. The animals were subsequently made hypoxemic by switching the right lung to room air ventilation (5-10 min). Two different protocol groups received either intravenous atropine during hypoxemia (group I) or intravenous propranolol prior to protocol initiation (group II). A third group of dogs (group III) had their mixed venous PO2S maintained above 30 torr during hypoxemia. In response to left lung hypoxia, Ql/Qt decreased from 44 +/- 5, 48 +/- 3 and 46 +/- 2% to 25 +/- 4, 28 +/- 2 and 26 +/- 3% in the three groups, respectively. During hypoxemia Ql/Qt increased to 50 +/- 7 and 47 +/- 3% in groups I and II. In group III dogs, Ql/Qt remained significantly decreased at 31 +/- 3%. Subsequent administration of atropine in group I had no effect on Ql/Qt. We conclude that the loss of flow diversion from a hypoxic lung during hypoxemia may be mediated primarily by a decreased in mixed venous PO2 when PVO2 is allowed to decrease to 15-20 torr.

Animals↗

PubMed1998

Effect of chronic hypoxemia on the regulation of nitric-oxide synthase in the fetal sheep brain.

We tested the hypothesis that chronic hypoxemia modulates NO production of the fetal brain by altering its gene and protein expression. Chronically instrumented preterm fetal sheep were made hypoxemic by placental embolization for 21 days. Fetal oxygen content was measured to determine the level of hypoxemia. The expression of both eNOS and nNOS proteins and mRNA and enzyme activities of fetal sheep cerebrum were measured and compared between normoxic and hypoxemic animals. Our results show that in utero hypoxemia downregulates both Ca2+ dependent NOS activity and expression of eNOS protein and mRNA in the fetal sheep brain. In contrast, hypoxemia increased nNOS protein and mRNA levels in the cerebrum. This suggests that chronic hypoxemia has an opposing effect on eNOS and nNOS gene regulation. We propose that increased nNOS activity during chronic hypoxemia may excessively stimulate the neurons and contribute to fetal brain injury. On the other hand, downregulation of eNOS activity and expression may compromise the neuroprotective effect of eNOS and, therefore, further exacerbate brain injury.

Animals↗

PubMed1985

Dialysis-induced hypoxemia: membrane dependent and membrane independent causes.

Hypoxemia during hemodialysis may result from several differing processes. We initially studied patients undergoing standard acetate hemodialysis. At 15 minutes of dialysis, leukopenia (primarily neutropenia), a decline of platelet count, and hypoxemia occurred, but without a significant change in mean minute ventilation. Complement activation (V/A ratios of C5a greater than 1.0) persisted throughout dialysis. Leukocyte count returned to baseline by one hour. To separate the effects of solute and/or gas fluxes from those of blood-membrane interaction we studied changes in Po2, WBC, C5a, TxB2, and PGI2 during a period of blood membrane interaction without dialysis, and during subsequent acetate dialysis. Patients were studied with both polyacrylonitrile (PAN) and cuprophan membranes containing different priming solutions during membrane contact alone. Despite leukopenia and complement activation, hypoxemia failed to occur during membrane contact alone. At 15 minutes of subsequent acetate dialysis, significant hypoxemia occurred with both membranes. However, the degree of hypoxemia was twice as great with a cuprophan membrane primed with acetate (18.6 +/- 3.3 mm Hg) compared with air or bicarbonate (9.1 +/- 1.4 and 7.0 +/- 2.0 mm Hg, respectively), or compared with PAN (8 +/- 2.8 mm Hg). Changes in thromboxane B2, PGI2, and C5a did not correlate with changes in Po2. We conclude that there are two major components to dialysis related hypoxemia. One is membrane independent, and may relate to the metabolic effects of acetate or to dialyzer CO2 loss. The remaining portion is membrane dependent, occurring with cuprophan, but not with PAN, and is conditioned by an acetate dependent interaction between blood and membrane.

Adolescent↗

PubMed2001

Renal and cerebral responses to hypoxemia in the ovine fetus.

Mild to moderate hypoxemia without major changes in pH and pCO(2) does not reduce fetal renal blood flow and fetal urine production rate. Other factors such as acidemia, hypercapnia or changes in lung liquid production or fetal swallowing are candidates for the reduced amniotic fluid in the growth retarded fetus. Mild hypoxemia influences the fetal brain development in that the migration of PKC immunoreactive cells is delayed after a period of 48 h of hypoxemia. This could be due to the fact that under these circumstances the expected compensatory increase in fetal cerebral blood flow was only significant 1 h after the onset of hypoxemia. Further research on the final position of the hippocampal neurons in term lambs, subjected to fetal mild hypoxemia, can give more information on the effects of hypoxemia on the fetal brain.

Animals↗

PubMed1996

Can prehospital personnel detect hypoxemia without the aid of pulse oximeters?

Although pulse oximeters have been proven accurate in the prehospital environment, they have not been proven to be necessary. This study was undertaken to determine if emergency medical services (EMS) providers can identify hypoxemia without pulse oximetry. An oximeter was placed at the ambulance entrance to the emergency department (ED), and EMS personnel obtained saturation levels on all patients on arrival. Hypoxemia was defined as a saturation level of 95% or less. The hypoxemia was classified as "recognized" if the patient received aggressive intervention and "unrecognized" if the patient did not. One hundred eighty patients were enrolled in the study; 30 had a saturation level of 95% or less. Twenty-seven (90%) of those patients had "unrecognized" hypoxemia. Twenty-three (85.2%) of the 27 patients with "unrecognized" hypoxemia did not complain of respiratory distress. Thus, there are patients whose hypoxemia is unrecognized by EMS providers, and this occurs most frequently in patients who do not complain of respiratory distress.

Chi-Square Distribution↗

PubMed2003

Significance of pulmonary artery pressure in emphysema patients with mild-to-moderate hypoxemia.

The guidelines of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) do not recommend the measurement of pulmonary artery pressure in patients with chronic obstructive pulmonary disease (COPD). This is on the basis that the mean pulmonary artery pressure (mPAP) does not provide more clinical information than measurement of the oxygen tension in arterial blood (PaO2). The mPAP correlates well with PaO2 in emphysema patients with severe hypoxemia (PaO2 < or = 7.3 kPa (55 mmHg)). However, the occurrence and significance of mPAP is unclear in patients without severe hypoxemia (PaO2 > 7.3 kPa (55 mmHg)). In order to evaluate the usefulness of measurement of mPAP in emphysema patients without severe hypoxemia, we performed right heart catheterization and investigated the pulmonary hemodynamics of 53 patients without severe hypoxemia. In addition, we identified long-term prognostic factors with a mean follow-up term of 77 months after right heart catheterization. Seventeen of 27 patients with mild-to-moderate hypoxemia exhibited pulmonary hypertension (mPAP > or = 2.7 kPa (20 mmHg)) and the classification according to severity in GOLD exhibited a greater correlation to mPAP than PaO2. Moreover, only mPAP was found to be a significant prognostic factor according to multivariate proportional hazards analysis (P = 0.01). We conclude that mPAP is more informative about the severity of emphysema than PaO2 in patients with mild-to-moderate hypoxemia.

Aged↗

PubMedDate not supplied

Effects of magnesium sulfate on the fetal heart rate response during acute hypoxemia in goats.

OBJECTIVE: The effects of magnesium sulfate on fetal heart rate (FHR) response during acute hypoxemia in goats were investigated. METHODS: The FHR responses due to hypoxemia during magnesium sulfate infusion (Mg study) were compared with those during vehicle infusion (controls) in six chronically instrumented goat fetuses at 125-130 days' gestation. RESULTS: Four-hour infusions of magnesium sulfate significantly increased fetal plasma concentrations of magnesium from 2.3 to 6.5 mg/dL. During the hypoxemic period, the fetal arterial oxygen pressure was significantly decreased from 29.0 +/- 2.5 to 14.6 +/- 2.6 torr in the controls, and from 28.9 +/- 3.9 to 13.7 +/- 4.7 torr during the Mg study. Neither arterial carbon dioxide pressure nor pH was significantly altered. In the controls, FHR was significantly decreased by hypoxemia, accompanied by increases in variability. In the Mg study, FHR was not significantly decreased by hypoxemia. Acute hypoxemia also increased the FHR variability during magnesium infusion, which was significantly reduced compared with those in the control population. CONCLUSION: Magnesium sulfate masks FHR-slowing responses during acute hypoxemia in fetal goats.

Animals↗

PubMed2002

Computerize anesthesia record keeping in thoracic surgery--suitability of electronic anesthesia records in evaluating predictors for hypoxemia during one-lung ventilation.

OBJECTIVE: The aim of this retrospective study was to assess the suitability of routine data gathered with a computerized anesthesia record keeping system in investigating predictors for intraoperative hypoxemia (SpO2 < 90%) during one-lung ventilation (OLV) in pulmonary surgery. METHODS: Over a four-year period data of 705 patients undergoing thoracic surgery (pneumonectomy: 78; lobectomy: 292; minor pulmonary resections: 335) were recorded online using an automated anesthesia record-keeping system. Twenty-six patient-related, surgery-related and anesthesia-related variables were studied for a possible association with the occurrence of intraoperative hypoxemia during OLV. Data were analyzed using univariate and multivariate (logistic regression) analysis (p < 0.05). The model's discriminative power on hypoxemia was checked with a receiver operating characteristic (ROC) curve. Calibration was tested using the Hosmer-Lemeshow goodness-of-fit test. RESULTS: An intraoperative incidence of hypoxemia during OLV was found in 67 patients (9.5%). Using logistic regression with a forward stepwise algorithm, body-mass-index (BMI, p = 0.018) and preoperative existing pneumonia (p = 0.043) could be detected as independent predictors having an influence on the incidence of hypoxemia during OLV. An acceptable goodness-of-fit could be observed using cross validation for the model (C = 8.21, p = 0.370, degrees of freedom, df 8; H = 3.21, p = 0.350, df 3), the discriminative power was poor with an area under the ROC curve of 0.58 [0.51-0.66]. CONCLUSIONS: In contrast to conventional performed retrospective studies, data were directly available for analyses without any manual intervention. Due to incomplete information and imprecise definitions of parameters, data of computerized anesthesia records collected in routine are helpful but not satisfactory in evaluating risk factors for hypoxemia during OLV.

Adult↗

PubMed1988

Theophylline prevents the hypoxemia-induced renal hemodynamic changes in rabbits.

The acute renal effects of hypoxemia and the ability of theophylline to prevent these effects were assessed in anesthetized and mechanically-ventilated newborn and adult rabbits. Renal blood flow (RBF) and glomerular filtration rate (GFR) were determined by the clearance of para-aminohippuric acid and inulin, respectively. Each animal acted as his own control. In 14 newborn rabbits (group 1), hypoxemia was significantly associated with a fall in GFR (-22 +/- 6%) and filtration fraction (-17 +/- 3%) and with an increase in renal vascular resistance (+13 +/- 6%). Hypoxemia also induced a significant decline in GFR (-27 +/- 6%) and RBF (-29 +/- 6%) in 7 adult rabbits (group 3). Intravenous theophylline (0.5 mg/kg) completely prevented the hypoxemia-induced changes in GFR, filtration fraction (FF) and renal vascular resistance (RVR) in 8 newborn rabbits (group 2). An intravenous dose of 2.4 mg theophylline given after the induction of hypoxemia partially reversed the drop in GFR in adult rabbits (group 3). Separate renal functions were studied in 8 additional adult rabbits (group 4). Low-dose theophylline (27 micrograms/min) infused intra-arterially in the left kidney partially prevented the hypoxemia-induced decline in urine flow rate, GFR, RBF, FF as well as the increase in renal vascular resistance. The beneficial effects of theophylline could be mediated by its adenosine antagonistic properties.

Adenosine↗

PubMed2002

Utility of pulse oximetry in the detection of arterial hypoxemia in liver transplant candidates.

Hepatopulmonary syndrome, arterial hypoxemia caused by intrapulmonary vasodilatation, occurs in approximately 10% of patients with cirrhosis. The severity of hypoxemia affects liver transplant candidacy and is associated with increased morbidity and mortality posttransplantation. Screening guidelines for detecting the presence of arterial hypoxemia do not exist. The aim of this study is to investigate the accuracy and utility of pulse oximetry in the detection of hypoxemia (PaO(2) < 70 mm Hg) in patients with cirrhosis. Two hundred prospective liver transplant candidates were compared with 94 controls. Arterial oxyhemoglobin saturation was obtained by pulse oximetry (SpO(2)) and compared with simultaneous arterial blood gas (ABG) oxyhemoglobin values (SaO(2); bias = the difference). PaO(2), carboxyhemoglobin, methemoglobin, and routine clinical and biochemical parameters were investigated to account for the bias. SpO(2) overestimated SaO(2) in 98% of patients with cirrhosis (mean bias, 3.37%; range, -1% to 10%). Forty-four percent of patients with cirrhosis and controls had a bias of 4% or greater. No clinical or biochemical parameters of cirrhosis accounted for the overestimation of pulse oximetry. Twenty-five subjects with cirrhosis were hypoxemic, and an SpO(2) of 97% or less showed a sensitivity of 96% and a positive likelihood ratio of 3.9 for detecting hypoxemia. An SpO(2) of 94% or less detected all subjects with an arterial PaO(2) less than 60 mm Hg. Pulse oximetry significantly overestimates arterial oxygenation, and the inaccuracy is not influenced by liver disease. Nevertheless, pulse oximetry can be a useful screening tool to detect arterial hypoxemia in patients with cirrhosis, but a higher threshold for obtaining an ABG must be used.

Adult↗

PubMed1998

Does interpleural bupivacaine blockade reduce arterial hypoxemia and pain in endoscopic retrograde cholangiopancreatography? A prospective randomized trial.

BACKGROUND AND STUDY AIMS: Interpleural blockade with bupivacaine has been used in operations and for the treatment of pain with promising results. Endoscopy may be followed by serious complications associated with the use of intravenous drugs. Drug-induced hypoxemia has an important role in the pathophysiology. PATIENTS AND METHODS: A randomized study to assess whether interpleural bupivacaine blockade compared with a standard procedure reduced the risk of hypoxemia and the need of medication in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP). Other variables studied were its acceptability to patients and morbidity. RESULTS: Ninety patients were included. Interpleural blockade (n = 43) was followed by minor complications. The blockade itself induced mild hypoxemia in four patients (9%). Overall, eight patients (27%) developed hypoxemia. There were correlations between age, drugs given and hypoxemia in the total series and in the two study groups individually. During ERCP eight (19%) in the blockade group and 16 (34%) in the standard procedure group developed hypoxemia. During the recovery period the opposite pattern was observed: (26%) compared with four (9%) (p = 0.05). Drug requirements did not differ. Procedure-related discomfort did not differ. More patients in the blockade group would prefer another sedative procedure. CONCLUSIONS: Interpleural bupivacaine blockade did not contribute to patients' comfort or safety during ERCP.

Adult↗

PubMed2000

Cardiovascular responses to arginine vasopressin blockade during acute hypoxemia in the llama fetus.

The fetal llama has a marked increase in the peripheral vascular resistance and no augmentation of brain blood flow during hypoxemia. In spite of the substantial plasma arginine-vasopressin (AVP) increase during hypoxemia, up to 8 times greater than in fetal sheep, there are no changes of carotid and femoral blood flows during hypoxemia with a V1 receptor blockade, as is seen in the fetal sheep. The aim of this study was to assess the role of AVP function in mediating the combined ventricular output and organ blood flow in the hypoxemic llama fetus. Six fetal llamas at 0.65 of gestation were instrumented under general anesthesia, and cardiorespiratory responses and blood flows determined under normoxemic and hypoxemic conditions. The AVP effect was determined using a V1 antagonist during normoxemic and hypoxemic conditions. Organ blood flows were measured with the radioactive microsphere technique. No significant differences in organ blood flow or in their vascular resistances were seen between the control and treated fetuses during hypoxemia. We conclude that V1 blockade did not have any important role in the cardiovascular response to acute hypoxemia in the llama fetus, in contrast with lowland fetuses. AVP may be playing a role in other regions, possibly in kidney or lung, during hypoxemia.

Acute Disease↗

PubMed1994

Orthotopic liver transplantation in children with chronic liver disease and severe hypoxemia.

Liver transplantation has been considered until recently as an absolute contraindication in hypoxemic patients. We report our experience in nine patients who had orthotopic liver transplantation between June 1986 and June 1992. These patients had cirrhosis-related hypoxemia with intrapulmonary shunting (IPS). The arterial oxygen pressure (PaO2) on room air ranged from 47 to 78 mmHg. OLT resulted in resolution of hypoxemia and closure of IPS in five patients whose hypoxemia was higher than 60 mmHg, and in death for the remaining four patients who had severe hypoxemia (PaO2 < 60 mmHg). We conclude that hypoxemia is no longer a contraindication to liver transplantation. Patients having PaO2 levels higher than 60 mmHg should have OLT as soon as possible before reaching lower levels of PaO2, and combined lung-liver transplantation or heart-lung-liver transplantation should be discussed in patients with severe hypoxemia (PaO2 < 60 mmHg).

Adolescent↗

PubMed1994

Regulation of whole blood polymorphonuclear leukocyte phagocytosis following hypoxemia and hypoxemia/reoxygenation.

Phagocytosis of whole blood polymorphonuclear leukocytes (PMN) was evaluated following periods of hypoxemia or hypoxemia/reoxygenation. Hypoxemia (O2 saturation 5-20%) significantly increased the percentage of PMN positive for phagocytosis. This effect required mobilization of intracellular Ca2+ stores and was accompanied by a significant increase in CD16, CD32w, and CD35 expression assayed using FITC-labeled Mabs. PMA (10 ng/ml) increased CD32w expression while protein kinase C inhibitors H-7 and staurosporine but not the protein kinase A inhibitor H-9 reversed the effect of hypoxemia on phagocytosis and receptor expression. Further, genistein (tyronsine kinase inhibition) reversed hypoxemia-induced increases in phagocytosis (ID50-50 microM). Reoxygenation (O2 saturation 97-99%) reduced the percentage of PMN positive for phagocytosis back to baseline values without affecting mean channel fluorescence. Reoxygenation reduced CD32w and CD16 expression with kinetics assays demonstrating concordance between reduced phagocytosis and CD32w and CD16 expression. Reoxygenation-induced decreases in CD32w and CD16 expression were prevented if whole blood PMN were incubated with either NaN3 (10 mM), dimethyl sulfoxide (DMSO) (10 mM), or taurine (15 mM) prior to reoxygenation. These results demonstrated that hypoxemia and hypoxemia/reoxygenation recruit and suppress distinct populations of whole blood PMN for phagocytosis. Intracellular kinase activation and Ca2+ mobilization are required for hypoxemia-induced increases in phagocytosis. Reoxygenation reduces whole blood PMN phagocytosis via an oxident-derived reduction of surface CD16 and CD32w expression.

Calcium↗

PubMedDate not supplied

Respiratory, cardiovascular, and metabolic adjustments to hypoxemia during sleep in piglets.

The influence of sleep on ventilation, metabolic rate, cardiovascular function, and regional distribution of blood flow during hypoxemia (PaO2 of 45-50 mm Hg (1 mm Hg = 133.3 Pa)) was studied in piglets at 6+/-1 and 34+/-5 days (mean+/-SD). Measurement of ventilation and metabolic rate was done in a metabolic chamber, and blood flow was measured using the microsphere technique. A subgroup of animals was instrumented for cardiac output measurement (dye-dilution technique) and continuous monitoring of the hemoglobin saturation in oxygen (SaO2). We found that although sleep did not influence the metabolic and cardiac output response to hypoxemia, it affected the ventilatory response as well as the brain and the respiratory muscle blood flows. During active sleep in the older animals, the ventilatory response to hypoxemia was smaller than in the other two states; marked drops in SaO2 occurred with changes in the breathing pattern; and that state was associated with the highest rate of brain blood flow. As well, age affected the ventilatory and metabolic response, but not the cardiovascular response to hypoxemia. The age-dependent ventilatory changes with hypoxemia (smaller ventilatory response in the young than in the older animals) were related to the different levels of oxygen consumption. In summary, active sleep was responsible for all the sleep-dependent changes in the response to a moderate degree of hypoxemia.

Adaptation, Physiological↗

PubMed1990

Threshold of hormonal and biophysical responses to acute hypoxemia in fetal sheep at different gestational ages.

We examined whether there was a threshold for change in fetal arterial PO2 to elicit alterations in plasma adrenocorticotropic hormone, arginine vasopressin, or cortisol, or to affect the incidence of fetal breathing movements or eye movements and we determined whether such a threshold changed with gestational age. Fetal sheep were exposed to two levels of hypoxemia, mild (4.6-5.3 mmHg PO2 drop) and moderate (8.3-8.8 mmHg PO2 drop) (1 mmHg = 133.322 Pa) for 1 h without pH change at 125-129 or 134-147 days of gestation within 7 days of spontaneous labor. Hypoxemia was induced by altering the inspired percent oxygen of the mother. No significant hormonal and biophysical changes were observed in mild hypoxemia at either age. In moderate hypoxemia at 125-129 days of gestation, there were significant increases of fetal adrenocorticotropic hormone, arginine vasopressin, and cortisol concentrations, and a decreased incidence of fetal breathing movements and eye movements. At 134-147 days of pregnancy, moderate hypoxemia induced a significant increase in adrenocorticotropic hormone, but the response was less than at 125-129 days of gestation. The arginine vasopressin response was similar to that at 125-129 days and there was no significant change in cortisol. There was a significant decrease in fetal breathing movements but not in eye movements. We conclude that a threshold of fetal arterial PO2 drop exists between 5 and 8 mmHg to elicit endocrine or biophysical responses to hypoxemia in fetal sheep at 125-129 days of gestation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1990

Hormonal and biophysical responses to acute hypoxemia in fetal sheep at 0.7-0.8 gestation.

We examined whether there was a minimal change in fetal arterial Po2 necessary to elicit alterations in plasma adrenocorticotropic hormone, arginine vasopressin, or cortisol or to affect the incidence of breathing movements or eye movements in fetal sheep at 106-117 days of gestation. Fetal sheep were exposed to two levels of hypoxemia, mild (4.1 mmHg Po2 drop) (1 mmHg = 133.32 Pa) and moderate (8.4 mmHg Po2 drop), for 1 h without acidemia. Hypoxemia was induced by altering the inspired percent oxygen of the mother. No significant hormonal and biophysical changes were observed in mild hypoxemia. In moderate hypoxemia, there were significant increases of fetal adrenocorticotropic hormone and arginine vasopressin and decreased incidence of fetal breathing movements. However, there were no significant changes in cortisol or eye movements. We conclude that a fetal arterial Po2 drop of between 4.1 and 8.4 mmHg is necessary to elicit responses to hypoxemia in fetal sheep at 106-117 days of gestation in adrenocorticotropic hormone, arginine vasopressin, and fetal breathing movements, but this degree of hypoxemia does not cause changes in cortisol or fetal eye movements.

Adrenocorticotropic Hormone↗

PubMed1996

Dynamics of myocardial adaptation to low-flow ischemia and hypoxemia.

We investigated whether one or more factors control performance in O2-limited hearts. For this purpose, we measured the dynamics of myocardial adaptation to reduced O2 supply with a specially designed setup, analyzing early changes after reduction in either flow of the perfusion medium or its PO2. For 10 min, 38 isolated rat hearts underwent low-flow ischemia or hypoxemia, matched for O2 supply. Early during ischemia, developed pressure declined at a rate of 311 +/- 25 mmHg/s; lactate release increased and then leveled off to 3.4 +/- 0.7 mumol/min within 2 min. During hypoxemia, pressure dropped initially, as observed during ischemia. However, it then increased before slowly decreasing. Lactate release during hypoxemia peaked at 13.0 +/- 2.3 mumol/min after 2 min, leveling off to 3.5 +/- 1.3 mumol/min. Glycogen decreased by 52 and 81% in ischemic and hypoxemic hearts, respectively (P < 0.05). Reexposure to ischemia or hypoxemia induced comparable changes in both groups. We conclude that, at the beginning of ischemia, a single factor does limit myocardial performance. This variable, which remains undisturbed for 10 min, is presumably O2 availability. In contrast, approximately 20 s after induction of hypoxemia, glycolytic ATP production can partially override low O2 availability by providing most of the energy needed. During repeated restriction of O2 supply, O2 availability alone limits performance during both ischemia and hypoxemia.

Adaptation, Physiological↗