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 199 records · Page 11Linked to original sources

PubMed1989

Effect of prolonged hypoxemia on fetal heart rate accelerations and decelerations in sheep.

Experiments were conducted in 10 chronically catheterized fetal sheep to determine the effect of 24 hours of hypoxemia in the absence of progressive acidemia on fetal heart rate accelerations and decelerations. Fetal hypoxemia was produced by mechanically restricting uterine blood flow with a vascular clamp placed around the maternal common internal iliac artery. Fetal arterial oxygen tension decreased from 22.3 +/- 1.8 to 17.8 +/- 1.5 mm Hg at 2 hours and remained low for the 24-hour experimental period. Fetal pH decreased from 7.34 +/- 0.01 to 7.20 +/- 0.05 at 2 hours and returned to normal values by 12 hours. No significant change was observed in the number or characteristics of fetal heart rate accelerations or decelerations during the 24-hour control period. There was a significant increase in the number of accelerations from 48 +/- 4 to 63 +/- 4 per hour at 8 hours of hypoxemia followed by a return to control values by 12 hours. There was no significant change in the mean amplitude or duration of accelerations. There was a significant increase in the number of decelerations per hour with an associated increase in the mean amplitude but a decrease in the mean duration of decelerations during the first 16 hours of hypoxemia. We conclude that prolonged hypoxemia in fetal sheep leads to an initial increase in the number of both accelerations and decelerations in fetal heart rate followed by a return to normal patterns indistinguishable from those of the normoexemic fetus.

Animals↗

PubMed1990

Nuchal muscle activity at different levels of hypoxemia in fetal sheep.

The effects of hypoxemia on nuchal muscle activity, a parameter of gross body movements, were studied during 12 experiments in five chronically instrumented fetal lambs. Hypoxemia was accomplished by tracheal infusion of nitrogen and did not result in significant changes in fetal arterial pH and PCO2. Fetal arterial blood gases and pH were continuously measured with an extracorporeal flow-through cuvette. Nuchal muscle activity was measured by electromyography and was expressed as the percentage of time spent moving. A decrease in fetal arterial oxygen saturation to three fourths of the initial value for 2 hours was not associated with significant changes in nuchal muscle activity. When fetal arterial oxygen saturation was further reduced for 2 hours to one half, fetal nuchal muscle activity fell significantly from 34.6% +/- 10.5% during normoxemia to 20.9% +/- 13.9% during hypoxemia. However, the most pronounced changes in fetal nuchal muscle activity occurred in the first 15 minutes after the changes in arterial oxygen saturation. A considerable transient increase in nuchal muscle activity was observed during the first 15 minutes after recovery from hypoxemia. During hypoxemia there was a relative predominance of short-lasting (less than 3 minute) movements.

Animals↗

PubMed1992

Evidence for the role of dialysis hypoxemia in the pathogenesis of hemodialysis-induced rise in tissue-type plasminogen activator.

It is well known that hemodialysis (HD) causes a rise in plasma tissue-type plasminogen activator (t-PA). Although there have been several suggested mechanisms responsible for this effect of HD, the precise cause has not been well understood yet. Another complication of HD, when performed with acetate-containing dialysate, is hypoxemia, which is commonly observed during the first hour of the session. The purpose of this study was to investigate the relationship between dialysis hypoxemia and HD-induced t-PA changes during the first two hours of HD. HD caused significant increase in plasma t-PA antigen levels. When individual t-PA profiles versus time were examined, two patterns were observed. Whilst ten subjects (%56) experienced minimal or no increase, t-PA antigen level of the remaining eight subjects began to rise at 30 minutes and continued at that level up to 90 minutes, when the last samples were drawn. The courses of pO2 were also different; whilst the former group had "early-onset and short-term" hypoxemia, the latter had "late-onset and prolonged" hypoxemia. The amount of increase in t-PA antigen and the amount of decrease in pO2 were correlated at 60 and 90 minutes of the HD session. Thus, it is concluded that dialysis hypoxemia may contribute to HD-induced rise in plasma t-PA levels. Further studies comparing different dialysates and dialyser membranes are required to confirm this hypothesis.

Adult↗

PubMed2006

Predictors of acute lung injury and severe hypoxemia in patients undergoing operative talc pleurodesis.

BACKGROUND: Acute lung injury (ALI) is a life-threatening complication of talc pleurodesis. This study defines characteristics that predispose patients to ALI and severe hypoxemia in patients after video-assisted thoracoscopic surgery (VATS) talc pleurodesis. METHODS: Charts of patients who underwent talc pleurodesis at Northwestern Memorial Hospital between January 1, 1997 and December 31, 2003 were retrospectively reviewed. We sought variables associated with the development of postoperative ALI or severe hypoxemia, defined as an increase in fraction of the inspired oxygen by more than 0.15 within 24 hours after the surgery. The analysis included 84 patients (58 women, 26 men) who underwent VATS talc pleurodesis for malignant (n = 74) or benign (n = 10) indications. RESULTS: ALI developed in 5 patients (5.9%), severe hypoxemia developed in 25 (29.8%), and 54 (64.3%) did not have postoperative complications. In multivariate analysis, the presence of peripheral edema before pleurodesis (p = 0.005), any preoperative requirement for supplemental oxygen (p = 0.032), and chemotherapy within 14 days before pleurodesis (p = 0.04) were identified as predictors of ALI or severe postoperative hypoxemia. CONCLUSIONS: Oxygen supplementation, recent chemotherapy, and presence of peripheral edema were independent predictors of a combined outcome of ALI or severe hypoxemia after VATS talc pleurodesis. Patients with these characteristics might be at risk for adverse outcomes of talc pleurodesis and should be considered for alternative therapy for their effusions.

Aged↗

PubMed2006

Excitatory amino acid release and electrocortical brain activity after hypoxemia in near-term lambs.

BACKGROUND: Energy failure due to insufficient cerebral O(2)-supply leads to excess accumulation of calcium ions in presynaptic neurons, followed by excess release of excitatory amino acids (EAAs), which are potent neurotoxins, into the synaptic cleft. AIM: The aim of the present study was to determine whether extracellular EAAs release after prolonged hypoxemia affects electrocortical brain activity (ECBA), as a measure of brain cell function, in near-term born lambs. METHODS: Ten near-term lambs (term: 147 days) were delivered at 131 days of gestation. After a stabilization period, prolonged hypoxemia (FiO(2): 0.10; duration 2.5h) was induced. Mean values of physiologic variables, including ECBA, were calculated over the last 3 min of normoxemia as well as of hypoxemia. Cerebral arterial and venous blood gases were determined at the end of the normoxemic and hypoxemic periods. Cerebrospinal fluid (CSF) was obtained at the end of the hypoxemic period. CSF from six normoxemic sibs was used for comparison. HPLC was used to measure EAAs in the CSF. RESULTS: During hypoxemia, aspartate and glutamate concentration increased significantly (4.8 and 6.0 times, respectively), while asparagine and glutamine did not. ECBA decreased to 30% of the normoxemic value. Glutamate was significantly higher in lambs with a flat cerebral function monitor (CFM) tracing than in lambs with a burst-suppression pattern. CONCLUSIONS: After prolonged hypoxemia aspartate and glutamate accumulated excessively in the CSF of near-term born lambs. Especially glutamate concentrations in CSF were related to the decline in brain cell function.

Animals↗

PubMed2005

Anemia, tumor hypoxemia, and the cancer patient.

PURPOSE: To review the impact of anemia/tumor hypoxemia on the quality of life and survival in cancer patients, and to assess the problems associated with the correction of this difficulty. METHODS: MEDLINE searches were performed to find relevant literature regarding anemia and/or tumor hypoxia in cancer patients. Articles were evaluated in order to assess the epidemiology, adverse patient effects, anemia correction guidelines, and mechanisms of hypoxia-induced cancer cell growth and/or therapeutic resistance. Past and current clinical studies of radiosensitization via tumor oxygenation/hypoxic cell sensitization were reviewed. All clinical studies using multi-variate analysis were analyzed to show whether or not anemia and/or tumor hypoxemia affected tumor control and patient survival. Articles dealing with the correction of anemia via transfusion and/or erythropoietin were reviewed in order to show the impact of the rectification on the quality of life and survival of cancer patients. RESULTS: Approximately 40-64% of patients presenting for cancer therapy are anemic. The rate of anemia rises with the use of chemotherapy, radiotherapy, and hormonal therapy for prostate cancer. Anemia is associated with reductions both in quality of life and survival. Tumor hypoxemia has been hypothesized to lead to tumor growth and resistance to therapy because it leads to angiogenesis, genetic mutations, resistance to apoptosis, and a resistance to free radicals from chemotherapy and radiotherapy. Nineteen clinical studies of anemia and eight clinical studies of tumor hypoxemia were found that used multi-variate analysis to determine the effect of these conditions on the local control and/or survival of cancer patients. Despite differing definitions of anemia and hypoxemia, all studies have shown a correlation between low hemoglobin levels and/or higher amounts of tumor hypoxia with poorer prognosis. Radiosensitization through improvements in tumor oxygenation/hypoxic cell sensitization has met with limited success via the use of hyperbaric oxygen, electron-affinic radiosensitizers, and mitomycin. Improvements in tumor oxygenation via the use of carbogen and nicotinamide, RSR13, and tirapazamine have shown promising clinical results and are all currently being tested in Phase III trials. The National Comprehensive Cancer Network (NCCN) guidelines recommend transfusion or erythropoietin for symptomatic patients with a hemoglobin of 10-11 g/dl and state that erythropoietin should strongly be considered if hemoglobin falls to less than 10 g/dl. These recommendations were based on studies that revealed an improvement in the quality of life of cancer patients, but not patient survival with anemia correction. Phase III studies evaluating the correction of anemia via erythropoietin have shown mixed results with some studies reporting a decrease in patient survival despite an improvement in hemoglobin levels. Diverse functions of erythropoietin are reviewed, including its potential to inhibit apoptosis via the JAK2/STAT5/BCL-X pathway. Correction of anemia by the use of blood transfusions has also shown a decrement in patient survival, possibly through inflammatory and/or immunosuppressive pathways. CONCLUSIONS: Anemia is a prevalent condition associated with cancer and its therapies. Proper Phase III trials are necessary to find the best way to correct anemia for specific patients. Future studies of erythropoietin must evaluate the possible anti-apoptotic effects by directly assessing the tumor for erythropoietin receptors or the presence of the JAK2/STAT5/BCL-X pathway. Due to the ability of transfusions to cause immunosuppression, most probably through inflammatory pathways, it may be best to study the effects of transfusion with the prolonged use of anti-inflammatory medications.

Anemia↗

PubMed2004

Role of melatonin in carbon monoxide-induced hypoxemia.

Melatonin (MEL) works in tandem with serotonin (5HT), where an equilibrium exists in perfect health. Under stress or in crisis, it may be that the production of MEL predominates in conjunction with ever increasing production of reactive oxygen species (ROS), may lead to hypoxemia and consequently, to metabolic disruption. The Melatonin Hypothesis could offer an explanation towards certain clinical observation and may support the Catacholamine Hypothesis in the development of depression but it is the role played by carbon monoxide (CO) in inducing hypoxemia which may result in the Cascade Effect that could in turn explain the development of neurodegenerative, neurodevelopmental as well as immune dysfunctional type disorders, prevalent today. CO-induced hypoxemia is an important aspect in any discussion of cell integrity as CO is formed endogenously from the degradation of erythrocytic heme, any hemolytic disturbance or lipid peroxidation, may increase the level in blood. CO, in inducing hypoxemia, causes the generation of large quantities of hydroxyl (-OH) which could damage specific amino acid and disorder protein metabolism that may result in the creation of toxic metabolites. Hydroxyl damage is emerging as the precursor to low-grade inflammation in the presence of C Reactive Protein (CRP) that is currently speculated in the etiology of many known disorders. As disordered protein metabolism may play a crucial role in the formation of the cascade, the hypothesis aims to address the issues of cell viability and the process of cell replication in the event where cell integrity is severely compromised in the face of apoptotic and/or necrotic damage, as the intra-cellular and extra-cellular environments are becoming increasingly hostile. Where -OH damage to specific amino acid in protein may contribute to the Cascade Effect, the hypothesis goes further to explain the importance of the Circardian Cycle and the role of paradoxical sleep, by taking into consideration the need for repair and for regeneration in order to maintain morphology as any cellular event that depends on a redox state is likely to be compromised in an event of hypoxemia. As MEL enters a cell readily because of its high lipid solubility, the role of MEL becomes clear as in its diversity, MEL is a potent oxygen radical scavenger that operates throughout the cell.

Carbon Monoxide↗

PubMed1987

The effect of mild hypoxemia maintained for twenty-four hours on maternal and fetal glucose, lactate, cortisol, and arginine vasopressin in pregnant sheep at 122 to 139 days' gestation.

The effects of prolonged mild hypoxemia on the fetus have received little attention. We investigated the response to a decrease in fetal arterial Po2 of 5 mm Hg or less sustained for a period of 24 hours in the chronically instrumented fetal lamb. Hypoxemia was induced by an infusion of nitrogen via the maternal trachea for 24 hours in 13 pregnant sheep at 122 to 139 days' gestation. Two control periods of air infusion via the maternal trachea for 24 hours were alternated with hypoxemia. Fetal hypoxemia was not associated with any change in fetal pH. During the first and second exposures to hypoxemia, there was an increase in fetal plasma lactate of 22.8 +/- 22.3 and 15.3 +/- 14.6 mg.dl-1 (mean +/- SD) above preliminary values (p less than 0.05) compared with the control period. Fetal plasma cortisol also increased by 5.7 +/- 6.1 and 9.5 +/- 5.4 ng.ml-1 (mean +/- SD) (p less than 0.05) compared with the control period. These results suggest that the fetal lamb at 122 to 139 days' gestation is highly sensitive to small decrements in Po2 of 5 mm Hg or less.

Animals↗

PubMed1988

Vasoactive intestinal polypeptide potentiates the hypoxemia-induced decrease in splanchnic circulation in the rat.

The effects of acute infusion of vasoactive intestinal polypeptide (VIP) and hypoxemia on splanchnic circulation were examined in 35 awake Sprague-Dawley rats. Indwelling catheters were placed in the superior vena cava and the proximal aorta via the internal jugular vein and internal carotid artery, respectively, while the rats were under ether anesthesia. Four hours later, when the rats were awake and active, VIP (molecular lot 3226) was infused intraarterially for 30 minutes. The distribution of cardiac output was measured at the end of VIP infusion using 125I-labeled microspheres. VIP was administered at a low (1.5 ng/min) and a high infusion rate (44.1 ng/min) for 30 minutes. The effect of hypoxemia on circulatory response to VIP was examined only in the high VIP infusion group, by placing the rat in a 10% oxygen environment. Appropriate control experiments were performed with each group. The high-dose VIP resulted in a marked reduction in distribution of cardiac output to the splanchnic circulation. This effect was potentiated by hypoxemia, particularly in the distal ileum and colon. The metabolic clearance rate of VIP increased with the rate of VIP infusion and was decreased by hypoxemia. It was concluded that only in high concentration does VIP have any effect on splanchnic circulation. However, in the presence of hypoxemia, VIP may have an important role in cardiovascular compensatory response and may contribute to the development of ischemic bowel injury.

Animals↗

PubMed1995

Mechanisms for episodes of hypoxemia in preterm infants undergoing mechanical ventilation.

OBJECTIVE: To ascertain possible mechanisms implicated in the development of transient episodes of hypoxemia (oxygen saturation < 85%) frequently observed in preterm infants undergoing mechanical ventilation, even after the acute phase of respiratory failure has passed. STUDY DESIGN: Tidal flow, airway and esophageal pressure, and oxygen saturation were continuously recorded in 10 infants (mean +/- SD, birth weight 733 +/- 149 gm, gestational age 25.5 +/- 2.2 weeks, age 26.3 +/- 11.9 days) who had repeated episodes of hypoxemia without any evident cause. Measurements of minute ventilation (VE) inspiratory compliance (Ci), and inspiratory resistance (Ri) were compared before and during episodes of hypoxemia. RESULTS: All episodes of hypoxemia were preceded by an active exhalation that produced a mean decrease in end-expiratory lung volume of 6.4 +/- 2.8 ml/kg. The reduction in lung volume was immediately followed by a sudden decrease in tidal flow and volume, despite continuation of mechanical ventilation at the same rate and peak pressure. The resulting hypoventilation was associated with a drop in Ci to approximately one half and an increase in Ri to more than double the baseline values. Approximately 30 seconds after the beginning of hypoventilation, the arterial oxygen saturation reached a hypoxemic level (oxygen saturation < 85%)> CONCLUSION: Most hypoxemic episodes were triggered by an expiratory effort that produced a large decrease in lung volume. This reduction in lung volume probably leads to closure of small airways and the development of intrapulmonary shunts, which would explain the rapid development of hypoxemia.

Analysis of Variance↗

PubMed2002

Complementary effects of adenosine and angiotensin II in hypoxemia-induced renal dysfunction in the rabbit.

The acute renal effects of hypoxemia and the ability of the co-administration of an angiotensin converting enzyme inhibitor (perindoprilat) and an adenosine receptor antagonist (theophylline) to prevent these effects were assessed in anesthetized and mechanically-ventilated rabbits. Renal blood flow (RBF) and glomerular filtration rate (GFR) were determined by the clearances of para-aminohippuric acid and inulin, respectively. Each animal acted as its own control. In 8 untreated rabbits, hypoxemia induced a significant drop in mean blood pressure (-12 +/- 2%), GFR (-16 +/- 3%) and RBF (-12 +/- 3%) with a concomitant increase in renal vascular resistance (RVR) (+ 18 +/- 5%), without changes in filtration fraction (FF) (-4 +/- 2%). These results suggest the occurrence of both pre- and postglomerular vasoconstriction during the hypoxemic stress. In 7 rabbits pretreated with intravenous perindoprilat (20 microg/kg), the hypoxemia-induced changes in RBF and RVR were prevented. FF decreased significantly (-18 +/- 2%), while the drop in GFR was partially blunted. These results could be explained by the inhibition of the angiotensin-mediated efferent vasoconstriction by perindoprilat. In 7 additional rabbits, co-administration of perindoprilat and theophylline (1 mg/kg) completely prevented the hypoxemia-induced changes in RBF (+ 11 +/- 3%) and GFR (+ 2 +/- 3%), while RVR decreased significantly (-14 +/- 3%). Since adenosine and angiotensin II were both shown to participate, at least in part, in the renal changes induced by hypoxemia, the beneficial effects of perindoprilat and theophylline in this model could be mediated by complementary actions of angiotensin II and adenosine on the renal vasculature.

Adenosine↗

PubMed1997

Prevention of hypoxemia-induced renal dysfunction by perindoprilat in the rabbit.

The role of angiotensin II, a potent postglomerular vasoconstrictor, in the hypoxemia-induced renal changes is still controversial. The ability of perindoprilat, an angiotensin converting-enzyme inhibitor, to prevent the acute renal effects of hypoxemia was assessed in 22 anesthetized-ventilated rabbits. In 8 untreated rabbits, hypoxemia induced a significant drop in mean blood pressure (MBP) (-12 +/- 2%), glomerular filtration rate (GFR) (-16 +/- 3%) and renal blood flow (RBF) (-12 +/- 3%) with a concomittant increase in renal vascular resistance (RVR) (+18 +/- 5%) and urine flow rate (+33 +/- 14%), and without any changes in filtration fraction (FF) (-4 +/- 2%). This suggests the occurrence of glomerular vasoconstriction during the hypoxemic stress. In 7 normoxemic rabbits, intravenous perindoprilat (20 microg/kg) induced an increase in urine flow rate (+17 +/- 4%) and RBF (+17 +/- 4%), and a decrease in MBP (-6 +/- 1%), RVR (-14 +/- 3%) and FF (-11 +/- 2%) without a significant change in GFR. The drop in FF and the increase in RBF suggests preferential postglomerular vasodilatation. In 7 rabbits, perindoprilat prevented the occurence of the hypoxemia-induced changes in RBF and RVR without improving MBP. FF decreased significantly (-18 +/- 2%), while the drop in GFR (-7 +/- 2%) was partially blunted and the increase in urine flow rate (+25 +/- 9%) was confirmed. These results could be explained by the inhibition of the angiotensin-mediated efferent vasoconstriction and by the inhibition of bradykinin degradation by perindoprilat. These data confirm the ability of converting-enzyme inhibitors to prevent the renal hypoperfusion induced by acute hypoxemia.

Angiotensin II↗

PubMed1987

Severe hypoxemia associated with liver disease: Mayo Clinic experience and the experimental use of almitrine bismesylate.

Severe hypoxemia associated with chronic liver disease is an uncommon disorder most likely due to an intrapulmonary vascular abnormality that has characteristics of both ventilation-perfusion mismatching and diffusion limitation. Anatomically, the intrapulmonary vascular abnormalities can occasionally be detected by angiography. Physiologically, the gas exchange abnormalities can be substantiated by contrast-enhanced two-dimensional echocardiography. Although orthodeoxia and platypnea have frequently been found in these patients, echocardiographic data suggest that vascular abnormalities can exist in the absence of orthodeoxia. We describe 11 patients who had severe hypoxemia and chronic liver disease and review their pulmonary angiographic, contrast echocardiographic, and arterial blood gas findings. Among five of these patients who were given almitrine bismesylate, an experimental medication thought to alter ventilation-perfusion relationships in patients with chronic obstructive pulmonary disease, one had improved oxygenation. We recommend that patients with hypoxemia associated with chronic liver disease have detailed studies to rule out reversible forms of hypoxemia and that those with severe hypoxemia undergo testing to determine the existence of intrapulmonary vascular abnormalities, especially if liver transplantation is considered.

Adult↗

PubMed1995

Hypoxemia up-regulates interleukin-8 stimulated phagocytosis of polymorphonuclear leukocytes by differential regulation of CD32w and CD35 messenger RNA expression.

BACKGROUND: The purpose of these studies was to investigate the effect of hypoxemia on interleukin-8 (IL-8) regulation of phagocytosis and surface opsonic receptor expression of whole blood polymorphonuclear leukocytes (PMNs). METHODS: Whole blood PMNs were rendered hypoxemic (PvO2 less than 15 mm Hg) or normoxic (PvO2 equals 60 to 80 mm Hg) and incubated with IL-8 (50 ng/ml) before the sequential addition of serum-opsonized fluorescent microspheres (emission wavelength, 560 nm) and fluorescein isothiocyanate-conjugated mouse anti-human CD32w or CD35 antibodies (emission wavelength, 513 nm). Concomitant two color flow cytometric analysis was then performed to measure the mean channel fluorescence (MCF) and the percentage of positive PMNs. Steady-state messenger RNA levels for CD32w and CD35 were quantitated by means of Northern blot analysis by using total RNA extracted from purified PMNs from each study group. RESULTS: Hypoxemia increased IL-8 stimulated PMN phagocytosis (percentage of positive PMNs, 38 +/- 1.5 versus 27 +/- 2.0, MCF, 5491 +/- 182 versus 4060 +/- 121 for hypoxemia plus IL-8 versus normoxia plus IL-8, respectively; p < 0.05). Hypoxemia increased IL-8 stimulated PMN expression of CD32w and CD35 (MCF CD32w, 791 +/- 105 versus 336 +/- 81; MCF CD35, 542 +/- 87 versus 254 +/- 41; p < 0.05). Under normoxic conditions IL-8 decreased messenger RNA levels for both CD32w and CD35, but under hypoxemic conditions IL-8 increased messenger RNA levels only for CD32w. CONCLUSIONS: Hypoxemia directly regulates IL-8 control of PMNs by increasing phagocytosis, receptor expression, and messenger RNA for these receptors. Studies investigating cytokine regulation of PMN function need to take into account oxygen tension when establishing the fundamental effects of cytokines on PMN physiology.

Cytokines↗

PubMed1999

Delayed neuronal migration of protein kinase Cgamma immunoreactive cells in hippocampal CA1 area after 48 h of moderate hypoxemia in the near term ovine fetus.

The brain is uniquely sensitive to disturbances in energy and oxygen supply, particularly during the early stage of life. Since hypoxemia can indirectly activate the intracellular messenger protein kinase C (PKC), we studied the PKCgamma-immunoreaction in the fetal hippocampal CA1 region of naive (n=4), instrumented control (n=7), and instrumented hypoxemic fetuses (n=14), at a mean gestational age of 127 days. Forty-eight hours of mild to moderate hypoxemia, were followed by a 48-h recovery period. Hypoxemia resulted in an increase in carotid blood flow (137% of control), and a shift towards a higher percentage of high-voltage electrocortical activity. After recovery, the fetal brain was fixated by perfusion of both carotid arteries, sectioned and immunostained for PKCgamma. The distribution of PKCgamma-immunoreactive cells was significantly changed after 48 h of hypoxemia in that the migration of cells (from the ventricular region towards the stratum pyramidale) was delayed (p<0.01) compared to naive and instrumented control animals. In contrast to the distribution, the relative total optical density of PKCgamma-ir cells and fibres in the CA1 hippocampal area was not significant different between the animal groups. We conclude that hypoxemia delayed migration of PKCgamma-ir cells, without neuronal degeneration.

Animals↗

PubMed1997

Hypoxemia in patients with cirrhosis: relationship with liver failure and hemodynamic alterations.

BACKGROUND/AIMS: The relationship between hypoxemia, liver failure and the hemodynamic alterations in cirrhosis are unknown. This study examined the relationship between arterial hypoxemia, the severity of liver disease and hyperkinetic circulation in patients with cirrhosis. METHODS: Arterial blood gases, the severity of cirrhosis (Child-Pugh score), and splanchnic and systemic hemodynamics were measured in 120 patients with cirrhosis and without cardiopulmonary disease. Hypoxemia was considered to be present when PaO2 was < or = 70 mmHg. RESULTS: Seventeen patients had hypoxemia (14%). Hypoxemic patients had significantly lower pulmonary vascular resistance and a significantly higher alveolar-arterial oxygen gradient, Child-Pugh score and hepatic venous pressure gradient than non-hypoxemic patients. Cardiac index and right atrial and pulmonary pressures did not significantly differ between the two groups. CONCLUSIONS: Hypoxemia occurs mainly in patients with severe liver disease and is associated with pulmonary vasodilation.

Adult↗

PubMedDate not supplied

Patent foramen ovale presenting as refractory hypoxemia after heart transplantation.

Hypoxemia can be an early life-threatening complication of orthotopic heart transplantation. Commonly, hypoxemia after orthotopic heart transplantation is due to pulmonary hypertension or pulmonary complications. Rarely, structural defects either in the donor or recipient heart can lead to life-threatening hypoxemia. This case illustrates hypoxemia after orthotopic heart transplantation caused by the development of a right-to-left shunt through a patent foramen ovale in the recipient which had preoperatively been hemodynamically insignificant. The refractory hypoxemia required emergency surgical correction of the patent foramen ovale within the first postoperative week. In addition, this case illustrates the unique application of different methods of echocardiograms providing noninvasive diagnosis of structural defects in orthotopic heart transplantation.

Adult↗

PubMed1999

Delays in the detection of hypoxemia due to site of pulse oximetry probe placement.

STUDY OBJECTIVES: To determine if there were any differences in the time to detect hypoxemia related to the site of peripheral pulse oximetry (ear, hand, and foot) during the rapid induction of hypoxemia in healthy volunteers. DESIGN: Repeated-measures, longitudinal, observational study. SETTING: Anesthesia clinical research area of the Department of Anesthesiology. PATIENTS: 13 healthy volunteers, aged 18 to 44 years. INTERVENTIONS: Nellcor N-200 (Nellcor, Inc., Pleasanton, CA) oximeter probes were placed at the ear, hand, and foot. All units were turned on simultaneously with averaging times set for 5 seconds and signals sampled at 2 Hz. A computer-controlled anesthesia circuit was employed to induce mild hypercapnia and hyperoxia (end-tidal gas partial pressures: PETCO2 = 42 +/- 2 mmHg and PETO2 = 130 mmHg) for 5 minutes. PETO2 was then decreased to 45 +/- 2 mmHg over 60 seconds and held at that value for 5 minutes. MEASUREMENTS AND MAIN RESULTS: The mean differences in time (sec) for pulse oximeters to detect hypoxemia (read less than 90%) between probe sites were determined and compared. The following mean differences in time (sec) for pulse oximeters to detect hypoxemia (read less than 90%) between probe sites were found: ear-hand = 6; hand-foot = 57; ear-foot = 63. Paired t-tests revealed statistically significant mean time delay differences of 51 seconds (p < 0.005) and 57 seconds (p < 0.005) for ear-hand versus hand-foot and for ear-hand versus ear-foot, respectively. CONCLUSIONS: In healthy volunteers, significant delays in the detection of acute hypoxemia by pulse oximetry occur when pulse oximeters are placed at the toe as compared with probes at either the ear or hand.

Adolescent↗