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Results for “hypoxemia”

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At least 19 recordsLinked to original sources

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↗

PubMed1979

Prostaglandin control of the renal circulation in response to hypoxemia in the fetal lamb in utero.

We studied the effects of 10-minute periods of hypoxemia in unanesthetized fetal lambs in utero instrumented for measurements of arterial pressure and renal and iliac blood flows. Fetal hypoxemia, induced by delivering a hypoxic gas mixture to the ewe, was characterized by a reduction in fetal PaO2 from 20.1 +/- 1.4 to 8.8 +/- 1.0 mm Hg (mean +/- SE). The fetus responded with bradycardia and persistent vasoconstriction in the iliac bed throughout the 10-minute period. In contrast, renal resistance rose significantly only at the end of the hypoxemic period. After 5-7 minutes of hypoxemia, when iliac flow had fallen by 40 +/- 4% and iliac resistance had risen by 86 +/- 13%, renal flow and resistance were not changed significantly from control; in fact, we found that renal flow rose substantially at this time in several fetal lambs. After blockade of prostaglandin synthesis with either indomethacin or meclofenamate, renal flow fell after 5-7 minutes of hypoxemia by 36 +/- 5%. The reduction in renal flow and increases in renal resistance were significantly greater than was observed prior to blockade of prostaglandin synthesis. Thus, fetal hypoxemia elicits bradycardia and intense peripheral vasoconstriction reflected by the changes in the iliac bed, with relative sparing of the reanl bed. The relative protection of the renal bed during fetal hypoxemia appears to be related to a mechanism involving prostaglandins, since after blockade of prostaglandin synthesis, hypoxemia results in intense renal vasoconstriction.

Animals↗

PubMed1992

[The effects due to reduced coronary inflow and hypoxemia during myocardial ischemia].

The events associated to myocardial ischemia result from 2 overlapping phenomena due to reduced blood flow (ischemia) and reduced O2 supply (hypoxemia). To distinguish these effects, 2 groups of isolated rat hearts were perfused through the aorta (Langendorff's method) with Krebs-Henseleit buffer, and were exposed for 20 min to hypoxemia or ischemia, matched in terms of the O2 supply (10% of baseline), with continuous monitoring of cardiac contractility, O2 uptake and lactate production. The developed pressure and the O2 uptake were similar in hypoxemic and ischemic hearts; heart rate, end-diastolic pressure and lactate production rate were higher in hypoxemia than in ischemia; the recovery from hypoxemia was less than that from ischemia, despite the same O2 supplies; treatment with superoxide dismutase and catalase, scavengers of the O2 derived free radicals, during hypoxemia, allowed hypoxemic hearts to recover as ischemic hearts. Therefore, the main determinant of the reperfusion injury is to be attributed to the low O2 supply rather than to the low coronary flow; part of the injury is due to free radicals; a substantial portion is mediated by the energy demand during the stress which was higher in hypoxemia than in ischemia.

Animals↗

PubMed1975

Effect of hypoxemia on responses to norepinephrine and angiotensin in coronary and muscular vessels.

The purpose of this study was to determine the relative effects of acute hypoxemia on constrictor responses to norepinephrine and angiotensin in two vascular beds, the coronary and skeletal muscle. The left circumflex coronary and gracilis muscle arteries of anesthetized dogs were perfused at constant flow. Practolol or propranolol was administered to block indirect myocardial effects of norepinephrine on coronary resistance. When Po2 of arterial blood perfusing the coronary and muscle beds was reduced from 101 to 44 mm while systemic Pco2 remained normal, constrictor responses to both norepinephrine and angiotensin were inhibited in coronary vessels but not in muscle vessels. When local Po2 was reduced to 27 mm Hg, inhibition of responses was again observed in the coronary circulation with both drugs; in the muscle, responses to angiotensin but not to norepinephrine were depressed significantly. Since intracoronary infusion of adenosine increased, rather than inhibited, vasoconstrictor responses to angiotensin, it is unlikely that release of adenosine during hypoxemia accounts for inhibition of vasoconstriction in the coronary circulation. Indomethacin did not alter the inhibition of coronary vasoconstrictor responses to angiotensin during hypoxemia, which suggests that releease of prostglandins during htpoxemia is not the primary mechanism for inhibition of coronary vascular responses. When contractions in the gracilis muscle were produced by electrical stimulation, vasconstrictor responses to norepinnephrine were inhibited during hypoxemia. We conclude that depression of constrictor responses by hypoxemia is more pronounced in the coronay circulation than in resting muscle, but when muscle is contracting, vasoconstrictor responses are impaired during hypoxemia.

Adenosine↗

PubMed1979

Leukopenia and hypoxemia. Unrelated effects of hemodialysis.

Hemodialysis-induced hypoxemia has been attributed to membrane-related complement activation leading to pulmonary leukostasis and to hypoventilation secondary to carbon dioxide losses via the dialyzer. We have separately assessed the role of membrane- and dialysis-related factors by using different dialyzers and sequential ultrafiltration and hemodialysis with first-use cellulose dialyzers produced both leukopenia and hypoxemia. With reused cellulose and polyacrylonitrile dialyzers, hypoxemia still occurred, but without leukopenia. Ultrafiltration produced leukopenia and no changes in Pao2; during the subsequent hemodialysis, hypoxemia developed as the leukocyte count increased by 50%. Our data indicate that leukopenia and hypoxemia are unrelated effects of hemodialysis, and favor hypoventilation as the major determinant of hypoxemia during hemodialysis.

Adult↗

PubMed1976

Differences in the altered energy metabolism of hemorrhagic shock and hypoxemia.

The effect of hemorrhagic shock, hypoxemia, and anoxia on the levels of adenine and pyridine nucleotides of liver and kidney was assessed. ATP levels in liver and kidney of animals in shock or animals subjected to 7 min of anoxia decreased by 85 and 73%, respectively. Under hypoxic conditions (arterial PO2 AT 18 MMHg), the decrease was only 62 and 48% in liver and kidney, respectively. Tissue NAD levels decreased and NADH levels increased during shock but were found to be essentially unaltered during experimental hypoxemia. Thus, shock produced greater alterations in adenine and pyridine nucleotides than did hypoxemia alone, indicating that stagnant hypoxemia due to shock is more deleterious to energy metabolism than is severe hypoxemia with an otherwise normal circulation. The results also suggest that if an anterial PO2 OF 18 MMHg represents the initial stages of tissue hypoxia, then tissue ATP levels are a more sensitive indicator of this than NAD levels.

Adenine Nucleotides↗

PubMed1992

Fetal iron and cytochrome c status after intrauterine hypoxemia and erythropoietin administration.

Chronic fetal hypoxemia stimulates erythropoiesis and may result in a redistribution of fetal iron from plasma into erythrocytes. We studied the response of fetal plasma erythropoietin (Ep) to hypoxemia, the role of Ep in stimulating erythropoiesis in utero, and the effect of augmented erythropoiesis on fetal plasma Ep and iron and tissue cytochrome c concentrations in 19 chronically instrumented late-gestation fetal sheep. The fetuses were stimulated to produce 28 erythropoietic responses after exposure to 1) acute hypoxemia (1-5 days), 2) chronic hypoxemia (greater than 7 days), and/or 3) administration of 1,500 U recombinant human Ep concurrently during normoxemia. Plasma Ep peaked less than 12 h after the onset of hypoxemia or Ep bolus. Plasma iron decreased 24-48 h later and returned to baseline 48-96 h after normalization of Ep levels to baseline. The plasma iron response was directly related to the erythropoietin stimulus (r = 0.79, P less than 0.001) and inversely related to liver iron concentration at death (r = -0.84, P less than 0.001). Nine fetuses with depleted liver iron concentrations at autopsy had significantly lower heart and skeletal muscle iron concentrations compared with animals with 10% of control liver iron remaining. Skeletal muscle and heart iron and cytochrome c concentrations were significantly correlated. Ep has a potent biological effect on fetal erythropoiesis and iron metabolism. Augmented fetal erythropoiesis, mediated by Ep, results in decreased plasma iron, hepatic storage iron, and skeletal and cardiac muscle iron and cytochrome c. The model potentially explains the iron abnormalities found in newborn infants after fetal hypoxia.

Animals↗

PubMed1977

The effect of chronic hypoxemia on regional myocardial blood flow in the conscious dog after acute coronary artery occlusion.

Chronic hypoxemia was produced in 16 dogs by surgical transposition of the caudal vena cava to the left atrium to determine if chronic hypoxemia would alter the response of the myocardium to acute ischemia. An electromagnetic aortic flow probe, left atrial tube, and occlusive cuff on the left circumflex coronary artery were permanently implanted in 11 hypoxemic and 26 normal control dogs. The animals were studied in the conscious state after recovery from the surgery. Dogs with hypoxemia had a blood hematocrit value of 54.3 +/- 1.0% (SE), arterial PO(2) of 43.2 +/- 1.4 mm Hg, and 80.2 +/- 1.6% oxygen saturation. There was no difference from control animals in the ratio of left ventricular weight to body weight, but the right ventricular weight was significantly decreased in the hypoxemic dogs. Cardiac output from the left ventricle was twice that of the right ventricle. Aortic blood flow was 3.68 +/- 0.22 liters/min in hypoxemic animals and 2.64 +/- 0.19 liters/min in normal dogs. Myocardial blood flow measured with 15-mu diameter tracer microspheres was increased from 79 +/- 10 and 59 +/- 8 ml/100 g/min in left ventricular endocardial and epicardial halves, respectively, in normal dogs to 212 +/- 48 and 172 +/- 39 in dogs with chronic hypoxemia. There were no deaths in 10 hypoxemic dogs within 24 hours after complete circumflex coronary artery occlusion; 7 of 26 (27%) normal dogs died after circumflex coronary artery occlusion during the conscious state. Gross infarct size was extremely variable in both groups. Median infarct size was smaller in dogs with hypoxemia and was directly correlated with arterial PO(2) in hypoxemic dogs. There was a mild, but statistically not significant, increase in the anastomotic index of hypoxemic dogs compared with that of normal animals, suggesting that a metabolic adaptive change rather than increased collateral circulation may have been responsible for the decreased mortality and smaller infarct size in hypoxemic dogs.

Animals↗

PubMed1975

Effects of hypoxemia on the extent of myocardial necrosis after experimental coronary occlusion.

Arterial oxygen tension is variable in patients with acute myocardial infarction, and the effect of hypoxemia on the extent of myocardial necrosis after coronary occlusion has not been defined. In 11 anesthetized open chest dogs the left anterior descending coronary artery or one of its major branches was occluded for 20 minutes, and 10 to 15 epicardial electrocardiographic leads were recorded in the distribution and vicinity of the site of occlusion. Average S-T segment elevation and the number of sites showing S-T segment elevation greater than 2 mv, 15 minutes after occlusion were used as indexes of the severity and extent of ischemic injury. After occlusion with an inspired oxygen concentration of 20 percent these indexes were, respectively, 2.0 plus or minus 0.5 mv (mean plus or minus standard error) and 3.6 plus or minus 0.8 sites; the respective values increased to 3.3 plus or minus 0.5 mv (P smaller than 0.01) and 6.7 plus or minus 0.7 sites (P smaller than 0.01) after occlusion with an inspired oxygen concentration of 10 percent, and arterial partial pressure of oxygen decreased from 92 plus or minus 5 to 45 plus or minus 3 mm Hg. In 23 dogs the occlusion was maintained for 24 hours and the S-T segment elevation 15 minutes after occlusion was compared with myocardial creatine phosphokinase (CPK) activity and histologic appearance 24 hours later. In control dogs (inspired oxygen concentration of 20 percent) sites with no S-T segment elevation 15 minutes after occlusion showed normal myocardial CPK activity 24 hours later, whereas in sites with S-T segment elevation exceeding 2 mv there was an inverse relation between S-T segment elevation in each site and its myocardial CPK activity 24 hours later. Histologic examination revealed early myocardial necrosis in 98 percent (82 of 84) of sites with S-T segment elevation greater than 2 mv. In experimental dogs (inhaling a 10 percent oxygen concentration for the first 8 of the 24 hours of occlusion) many sites that showed no S-T segment elevation before hypoxemia was induced exhibited S-T segment elevation before hypoxemia was induced exhibited S-T segment elevations 30 minutes later and showed abnormally low CPK activity and histologic evidence of early necrosis. We conclude that after experimental coronary occlusion, hypoxemia is deleterious because it substantially increases myocardial damage.

Animals↗

PubMed1992

Protection from hypoxemia-induced renal dysfunction by the thiophosphate WR-2721.

The acute renal effects of hypoxemia-reoxygenation and the putative protective action of WR-2721 [S-, 2-(3-aminopropyl-amino)-, etylphosphosphorothioic acid], a drug with specific properties such as PTH-secretion inhibiting, calcium lowering and free radical scavenging activities, were investigated in anesthetized-ventilated rabbits. Glomerular filtration rate (GFR) and renal blood flow (RBF) were assessed by the clearance of inulin and para-aminohippuric acid, respectively. Each animal acted as its own control. Normoxemic control rabbits showed no changes in renal hemodynamics and function during 150 minutes. The administration of WR-2721 (75 mg/kg body wt i.v.) to normoxemic animals induced a significant decrease in MBP, RBF and diuresis, without affecting GFR. It significantly reduced plasma levels of PTH, decreased calcemia and increased urinary calcium excretion. In untreated hypoxemic-reoxygenated rabbits, 45 minutes of severe hypoxemia (PO2 around 35 mm Hg) induced a significant fall in MBP, GFR, RBF and diuresis, which persisted during the 60-minute reoxygenation period. The administration of WR-2721 before hypoxemia or reoxygenation prevented the hypoxemia-induced decrease in GFR and diuresis. Filtration fraction increased significantly. The renal functional improvement observed in hypoxemic rabbits administered WR-2721 could be mediated by its effect on calcium metabolism and/or its oxygen free radical scavenging properties.

Amifostine↗

PubMed1976

Liver hemodynamics and liver function in cats during graded hypoxic hypoxemia.

In 15 cats, anesthetized with chloralose and curarized, liver hemodynamics and liver function were followed during graded hypoxic hypoxemia. Hepatic arterial and intrahepatic portal venous conductance were not influenced by hypoxia, whereas severe hypoxemia increased gastrointestinal conductance. Total liver blood flow remained constant and hypoxemia was compensated for by an increase in hepatic extraction of oxygen approaching 100%. Only when the hepatic venous pO2 fell below 5-10 mmHg did hypoxemia decrease liver function. The results indicate that the sinusoidal perfusion is homogeneous.

Animals↗

PubMed1979

Arterial hypoxemia in patients with anterior and posterior nasal packings.

Previous clinical reports indicate that nasal packing is frequently associated with arterial hypoxemia. Anesthesia and surgery in hypoxemic patients can be hazardous, especially when it is associated with acute blood loss. Nine patients with severe epistaxis, who failed to respond to anterior and posterior nasal packing, were anesthetized for emergency internal maxillary artery ligation. Arterial blood-gas and pH changes during the procedure were evaluated. The results indicate some degree of arterial hypoxemia and high alveolar/arterial PO2 difference without significant change in PaCO2 and pH in most of the patients observed. Arterial PO2 was within normal range 24 hours after operation. The anesthetic management is described and the various causes of such arterial hypoxemia are reviewed. It is important to recognize the presence of arterial hypoxemia and treat accordingly during surgery for such patients.

Adult↗

PubMed1979

Hypoxemia after thoracentesis. A predictable and treatable condition.

Hypoxemia was observed at 20 minutes and two hours postprocedure in 15 patients who had a thoracentesis. The hypoxemia resolved after 24 hours. No effect on pH, PaCO2, or bicarbonate ion was observed. The degree of hypoxemia was correlated directly with the volume of fluid removed. Oxygen therapy was found to reverse this effect. Hypoxemia that follows thoracentesis may be caused by several factors, the most important being frank pulmonary edema.

Adult↗

PubMed1977

Sequential cerebral biochemical and physiological events in controlled hypoxemia.

Effects of controlled hypoxemia on cerebral functional activity were studied in rats using cyclic adenosine monophosphate (cAMP) and aminergic neurotransmitters in the brain tissue as special references. Evidence is presented that: (1) mild hypoxemic stress (PaO2 60 to 40 torr) may activate cerebral glycolysis with no evidence of anaerobic metabolism but that further reduction of PaO2 impairs cellular respiration, as evidenced by accumulation of glycolytic products; (2) glycogenolysis in the brain tissue, leakage of potassium ions from the brain cell, increase in brain water, and suppression of neural functional activity occur concomitant with accumulation of cAMP and prior to the fall of adenosine triphosphate; (3) the diminution of cerebral high-energy phosphates during hypoxia is associated with and may be caused by hypoxemia-induced neuroglycopenia and occurs at PaO2 15 torr; (4) induced hypoxemia per se does not affect the level or aminergic neurotransmitter substances in brain tissue.

Adenosine Diphosphate↗

PubMed1978

The relationship between transfusion and hypoxemia in combat casualties.

The relationship between transfusion and subsequent hypoxemia was examined retrospectively in the records of combat casualties studied by the first three U.S. Army Surgical Research Teams in Vietnam. There was no evident relationship in 425 casualties studied before anesthesia and operation. In 199 casualties studied preoperatively and on at least two of the first three postoperative days, there was no evident relationship in those with injuries not involving the chest or abdomen. Eighteen such casualties received over ten units of blood each (average 24.5) and exhibited subsequent changes in arterial oxygen tension (PaO2) which were indistinguishable from those transfused lesser amounts or not all. Similar observations were made in casualties with injuries to the abdomen, although there was a tendency to lower PaO2 two days after injury in those heavily transfused. In those with thoracic injury, there was statistically significantly lower PaO2 on the first two postoperative days in those heavily transfused. Two possible interpretations are considered, one that blood transfusion contributed to hypoxemia, and alternatively, that a greater magnitude of the injuries accounted for both the worsened hypoxemia and the need for more transfusions. The latter was thought more likely. The differences in PaO2 related to the type of injury exceeded the differences associated with transfusion.

Adult↗

PubMed1979

Hypoxemia during hemodialysis.

Five mechanically ventilated patients were studied during hemodialysis. The aim was to determine if hypoxemia would develop, and to identify the causes. Respiratory variables (dynamic compliance, peak airway pressure, CO2production); oxygen uptake, and transport variables (alveolar and arterial PO2, pulmonary venous admixture, oxygen consumption); respiratory quotient; pulmonary vascular resistances and white blood cells (WBC) were measured. PaO2 decreased during dialysis, as did PaO2. However, the fall in alveolar oxygen tension failed to explain the hypoxemia. Lung volume did not change significantly, because dynamic compliance, peak airway pressure, and pulmonary vascular resistance were not modified. CO2 losses through the dialysis coil were of little clinical significance. WBC count fell significantly. The authors conclude that ventilation/perfusion and diffusion abnormalities related to leuko-agglutination are responsible for hypoxemia during dialysis.

Carbon Dioxide↗

PubMed1976

Ventilatory control in peripheral chemoreceptor-denervated ponies during chronic hypoxemia.

The present study was designed to provide further insight into the role of the carotid and aortic chemoreceptors in ventilatory (VE) acclimatization during sojourn at altitude. Measurements were made: 1) on 10 ponies near sea level (SL, 740 Torr) under normal conditions, 2) on 6 of these at SL following chemoreceptor denervation (CD), and 3) subsequently on all 10 during 4 days of hypobaric hypoxia (PaO2 = 40-47 Torr). CD resulteo in hypoventilation at SL (deltaPaCO2 = d8 Torr, P less than 0.05), and it prevented hyperventilation normally observed with injection of NaCN and acute exposure to hypoxia (less than 1 h). In contrast, hyperventilation was evident in normal ponies during acute hypoxia (deltaPaCO2 = -6.7 Torr). Ventilation increased in both groups between the 2nd and 8th h of hypoxia (deltaPaCO2 from 1 h = -4 Torr, P less than 0.05). This change, a common characteristic of acclimatization, persisted throughout 4 days of hypoxia in the normal ponies. However, in the CD ponies this change was evident consistently only through the 12th h and after the 44 h hyperventilation was no longer evident. We conclude that the peripheral chemoreceptors are essential in ponies for normal VE acclimatization to this degree of hypoxemia. Two additional findings in CD ponies suggest the presence of a CNS inhibitory influence on the VE control center during chronic hypoxemia. First, acute hyperoxygenation on the 4th day of hypoxemia induced hyperventilation (deltaPaCO2 = -5 Torr, P less than 0.05). Second, again on the 4th day and during hyperoxygenation, VE responsiveness to CO2 and doxapram HCl was greater than at sea level.

Acclimatization↗

PubMed1979

Accentuated hypoxemia at high altitude in subjects susceptible to high-altitude pulmonary edema.

To investigate the hypotheses that activated coagulation, catecholamine release, or arginine vasopressin release are involved in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured these variables in seven subjects susceptible to HAPE and in nine control subjects at an altitude of 1,600 m, and after 6 and 12 h at a simulated altitude of 4,150 m. Each subject was studied twice, once after 3 days of placebo medication and once after 3 days of premedication with aspirin and dipyridamole. At high altitude, HAPE-susceptible subjects showed significantly exaggerated hypoxemia and a slightly higher end-tidal carbon dioxide partial pressure that did not account fully for the hypoxemia. Fibrinolytic activity was significantly accelerated in both groups at high altitude, whereas other coagulation measurements, catecholamines and arginine vasopressin levels, and pulmonary function tests were not significantly changed. Similar findings were obtained after both placebo and platelet-inhibitor premedication. The results indicate that none of the three hypothesized mechanisms, i.e., activated coagulation, excessive catecholamine release, or antidiuresis, would account for HAPE susceptibility. Instead, HAPE-susceptible subjects exhibited exaggerated hypoxemia associated with relative hypoventilation and a widened alveolar-arterial gas pressure difference.

Adolescent↗