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PubMed1997

Hepatopulmonary syndrome with progressive hypoxemia as an indication for liver transplantation: case reports and literature review.

In the hepatopulmonary syndrome (HPS), a pulmonary vascular complication of liver disease, severe hypoxemia due to pulmonary vascular dilatation can be extremely debilitating. Determining whether patients with advanced liver disease and HPS should be considered for liver transplantation is difficult. We describe three patients with progressive and severe hypoxemia who underwent successful liver transplantation and had resolution of their arterial hypoxemia. In these patients, the progressive pulmonary deterioration accelerated the need and was considered an indication for liver transplantation rather than being considered an absolute or relative contraindication. In addition, we review the literature on 81 pediatric and adult patients with HPS who underwent liver transplantation and specifically highlight mortality, morbidity, syndrome resolution, and prognostic factors. Posttransplantation mortality (16%) was associated with the severity of hypoxemia (mean arterial oxygen tension [PaO2] in 68 survivors was 54.2 +/- 13.2 mm Hg and in 13 nonsurvivors was 44.7 +/- 7.7 mm Hg; P<0.03). Patients with a pretransplantation PaO2 of 50 mm Hg or lower had significantly more frequent mortality (30%) in comparison with those with a PaO2 greater than 50 mm Hg (4%; P<0.02). Pulmonary recommendations that address the severity of hypoxemia and candidacy for liver transplantation are discussed.

Adult↗

PubMed1991

Acute reversible hypoxemia in systemic lupus erythematosus.

OBJECTIVE: To determine the frequency of unexplained reversible hypoxemia in patients with systemic lupus erythematosus and to assess the relation between hypoxemia and elevated plasma levels of complement split products. DESIGN: Cohort study. SETTING: Inpatient and outpatient facilities of the New York University Medical Center/Bellevue Hospital and the Hospital for Joint Diseases. PATIENTS: Case patients were 22 patients hospitalized with disease exacerbation and no evidence of parenchymal lung disease on chest roentgenogram. Four patients with stable disease were followed in the outpatient clinic, and five healthy normal volunteers served as controls. MEASUREMENTS: Plasma levels of complement split products (C3a, factor Bb fragment), alveolar-arterial (A-a) Po2 gradients, and pulmonary function were measured. MAIN RESULTS: Nine episodes of hypoxemia or hypocapnia (mean A-a gradient, 30.4 +/- 4.8 mm Hg) or both (despite normal chest roentgenogram results) were noted in six hospitalized patients (group 1). Gas exchange improved within 72 hours of steroid therapy (mean A-a gradient, 11.6 +/- 4.3 mm Hg; P less than 0.01). These patients had an elevated initial mean C3a level (938.4 +/- 246.8 ng/mL) that decreased within 72 hours (407.8 +/- 80.9 ng/mL; P less than 0.01), concomitant with improved oxygenation. Ventilation-perfusion scans, obtained for four of six group 1 patients, excluded pulmonary emboli. Four hospitalized patients (group 2) had a normal A-a gradient (mean, 7.5 +/- 2.7 mm Hg). The mean C3a level of this group (358.3 +/- 39.2 ng/mL) was lower than that of group 1 (P less than 0.05). Four patients with stable disease (group 3) had a mean A-a gradient and a mean C3a level of 3.3 +/- 2.7 mm Hg and 237.8 +/- 105.7 ng/mL, respectively, similar to values found in five normal volunteers, in whom the mean A-a gradient was 3.7 +/- 1.7 mm Hg and the mean C3a level was 124.8 +/- 9.2 ng/mL. CONCLUSION: A syndrome of reversible hypoxemia, unassociated with parenchymal lung disease, is unexpectedly common in acutely ill, hospitalized patients with systemic lupus erythematosus. The pathogenesis of this syndrome is unclear, although the data are compatible with the hypothesis that hypoxemia may be related to pulmonary leukoaggregation.

Acute Disease↗

PubMed2001

Treatment of hypoxemia during xylazine-tiletamine-zolazepam immobilization of wapiti.

Hypoxemia is a commonly observed complication during the chemical immobilization of wild ruminants. If severe and left untreated, it can predispose animals to arrhythmias, organ failure, and capture myopathy. The following prospective study was designed to measure the degree of hypoxemia in wapiti that were immobilized with a combination of xylazine and tiletamine-zolazepam and to assess the response to nasal oxygen therapy. Pulse oximetry and arterial blood gas analysis were used to assess the degree of hypoxemia prior to nasal insufflation of oxygen and to demonstrate any beneficial effects of this intervention. All wapiti exhibited mild to marked hypoxemia (PaO2 = 43 +/- 11.8 mmHg) prior to treatment and showed marked improvement after 5 minutes of nasal insufflation of oxygen at 10 L/min (PaO2 = 207 +/- 60 mmHg). This inexpensive, noninvasive technique has great benefit in treating clinical hypoxemia under field conditions, and we recommend that nasal insufflation of oxygen be implemented during xylazine-tiletamine-zolazepam-induced immobilization of wapiti and other wild ruminants.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Hypoglycemia increases the sensitivity of the cat electroretinogram to hypoxemia.

Kang Derwent and Linsenmeier (2000) reported that the a- and b-waves of the cat electroretinogram (ERG) are resistant to hypoxemia, at least for PaO2 above 40 mm Hg. The a-wave may be resistant because the photoreceptor can increase glycolysis during hypoxemia. This hypothesis was tested by making the animal hypoglycemic, which should minimize the ability of the photoreceptor to switch to glycolysis. The ERG of dark-adapted anesthetized cats was recorded between an Ag/AgCl electrode in the vitreous humor and a reference electrode near the eye. Responses to bright flashes of diffuse white light were recorded at 3-min intervals during hypoxic episodes at three levels of blood glucose. The moderate hypoglycemia (50 to 70 mg/dl) had a relatively small effect on the a-wave amplitude. Furthermore, the a-wave amplitude increased transiently by 16 +/- 7% within 30-40 min of the start of severe hypoglycemia (20 to 40 mg/dl), before recovering to near normal. Severe hypoglycemia alone decreased the b-wave amplitude by 15 +/- 13%. Combined hypoxemia and hypoglycemia decreased the b-wave amplitude more than the a-wave amplitude. At all levels of blood glucose, b-wave decreases began at a higher PaO2 than the a-wave changes. For both the a- and b-waves, hypoxemic effects began at higher PaO2 when the animal was hypoglycemic. The increased sensitivity to hypoxemia during severe hypoglycemia suggests that a switch from oxidative to glycolytic metabolism ordinarily protects the retina from moderate hypoxemia. Because the a- and b-waves were affected to different degrees and at different PaO2s, it is unlikely that inner retinal changes are caused completely by changes in the photoreceptor.

Animals↗

PubMedDate not supplied

Prevention of hemodialysis associated hypoxemia by use of low-concentration bicarbonate dialysate.

Hypoxemia during acetate dialysis is caused by hypoventilation due to bicarbonate loss across the dialyzer and its regeneration from acetate by a CO2 consuming process. Loss of bicarbonate is prevented by using a bicarbonate containing dialysate, but hypoxemia is still found by many authors. In the current study, ten patients were dialyzed twice against acetate dialysate, high concentration bicarbonate (36 mmol/L), and low concentration bicarbonate (29 mmol/L) dialysates. A significant decrease in PO2 was found during both acetate and high concentration bicarbonate dialysis. Hypoxemia was prevented by low concentration bicarbonate dialysate. A possible explanation for the hypoxemia in high concentration bicarbonate dialysis may be hypoventilation induced by alkalosis. It was concluded that low concentration bicarbonate dialysate prevents hypoxemia during hemodialysis.

Bicarbonates↗

PubMed1992

Hypotension and hypoxemia in the preterm newborn during the four days following delivery identify infants at risk of echosonographically demonstrable cerebral lesions.

This prospective study of 130 preterm newborns at less than 34 weeks gestational age has examined the predictive value of abnormalities in continuously recorded newborn blood pressure, heart rate, and oxygen tension during the 4 d following delivery for echosonographically demonstrable cerebral lesions (EDCL) identified in the infant by six months corrected age. EDCL consisting of intraventricular hemorrhage, ventriculomegaly, or hyperechoic parenchymal lesions in the brain were identified in 44 preterm newborns (34%). The incidence of EDCL in preterm newborns with no hypotension or hypoxemia was 13%. The incidence of EDCL was significantly increased in preterm newborns with either hypotension or hypoxemia. The probability of EDCL exceeded 50% when the total exposure to either hypotension or hypoxemia during the 4 d exceeded 50 mmHg-hours, or when newborn hypotension and hypoxemia occurred concurrently. No relationship to hypertension, bradycardia, or tachycardia was detected. These findings indicate that hypotension and hypoxemia in the preterm newborn during the 4 d following delivery are useful risk markers of EDCL.

Brain Diseases↗

PubMed1991

Computer analysis of hypoxemia during hemodialysis.

Arterial oxygen partial pressure decreases during hemodialysis if acetate as buffer is used or if certain types of bioincompatible dialyzer membranes are used. Several hypotheses considering the main cause of this hypoxemia have been proposed. To gain more insight into the mechanisms leading to this hypoxemia, a mathematical model for the computerized simulation of exchange processes during hemodialysis has been used. To simulate the ventilation-perfusion ratio (VA/Q), a simplified two-compartment model of the lung has been applied. The simulation results reveal that hypoxemia during hemodialysis has two reasons. In acetate hemodialysis, the main cause is a shift of the CO2-bicarbonate equilibrium caused by "consumption" of hydrogen ions during acetate metabolization resulting in hypoventilation due to a decrease in CO2 partial pressure. During hemodialysis with bioincompatible dialyzer membranes, the hypoxemia may be explained by an increase in inhomogeneity of the VA/Q ratio in the lung. The loss of CO2 and bicarbonate into the dialysate during acetate hemodialysis has only a minor effect on arterial PO2 and cannot explain the observed hypoxemia. The decrease of O2 diffusing capacity during hemodialysis with bioincompatible membranes has only a negligible effect on the arterial PO2. The simulation results show also that the venous PO2 in the brain may fall below a critical level of less than 25 mm Hg, thereby possibly causing oxygen deficiency in the cortex.

Acetates↗

PubMed1991

[Oxyhemoglobin dissociation curve and 2,3-diphosphoglycerate in chronic hypoxemia].

The measurement of the oxyhemoglobin dissociation curve (ODC) and 2,3-diphosphoglycerate (2,3-DPG) in patients with chronic hypoxemia is important from the view point of tissue oxygenation. However, there have been no consistent results that explain the relation among chronic hypoxemia, 2,3-DPG and P50, which is oxygen pressure at an oxygen saturation of 50 percent. The aim of this study is to clarify what factors affect P50 and 2,3-DPG. 1) Patients with chronic hypoxemia, who showed PaO2 less than 60 Torr, had significantly higher P50 than normal subjects. 2) The concentration of Hb showed significant negative correlation with both P50 and 2,3-DPG. 3) Arterial blood pH showed significant positive correlation with both P50 and 2,3-DPG. 4) In a group with normal levels of Hb and pH, there was significant negative relationship between PaO2 and P50. 5) In a group with normal levels of Hb and pH, there was significant positive relationship between PaCO2 and P50. 6) In a group with normal levels of Hb, pH and PaCO2, there was significant negative relationship between PaO2 and 2,3-DPG. In conclusion, P50 and 2,3-DPG are affected largely by Hb concentration or blood pH, with or without hypoxemia. However there is a mechanism by which P50 and 2,3-DPG are increased by hypoxemia itself in a group with normal levels of Hb, pH and PaCO2.

2,3-Diphosphoglycerate↗

PubMed1991

[Pulmonary artery hypertension and nocturnal hypoxemia in chronic obstructive bronchopneumopathy].

Permanent and marked hypoxemia (PaO2 less than or equal to 60 mmHg) is a major cause of pulmonary hypertension (PH) in patients with chronic obstructive lung disease (COLD). In these patients PH, although mild to moderate (with a mean pulmonary artery pressure generally comprised between 20 and 35 mmHg), is by itself an indicator of poor prognosis. During sleep, hypoventilation and exaggerated ventilation/perfusion ratio inequalities can induce severe desaturation dips responsible for sudden peaks of PH. However, in hypoxemic COLD patients, the prognostic value of sleep-related desaturation (and resulting PH) has not been demonstrated. In COLD patients without marked daytime hypoxemia (PaO2 greater than or equal to 60 mmHg) permanent PH in rather rare. Ventilatory changes during sleep may account for nocturnal desaturation and transient PH. Do these repeated transient pulmonary hypertensive peaks finally lead to permanent PH? This attractive hypothesis supposes that significant sleep desaturation can develop in patients without pronounced daytime hypoxemia, which has not been demonstrated yet. In fact very few studies have been devoted to the occurrence of nocturnal desaturation (and PH) in such patients and the above mentioned hypothesis could not be confirmed. Long-term oxygen therapy (greater than or equal to 16-18 h/day) is generally prescribed in COLD patients with marked and persistent daytime hypoxemia. Oxygen therapy including sleep time and several studies have shown that usual O2 flows (1, 5-3 l/mn) are efficient and increase O2 saturation during sleep over 90%, with a resulting improvement of nocturnal PH. It has been demonstrated that daytime PH is stabilized (or improved) in patients receiving long-term O2 therapy. In COLD patients with less severe daytime (and nighttime) hypoxemia, almitrine could be of interest. The benefit of isolated nocturnal oxygen therapy has not been yet clearly established.

Darkness↗

PubMed1989

[Response of the cervical sympathetic activity to acute hypoxemia in dogs and its modification by volatile anesthetics].

Response of the cervical sympathetic activity (CSA) to acute hypoxemia was studied in dogs in the absence and in the presence of either halothane (H), enflurane (E), isoflurane (I) or sevoflurane (S). Multifiber potentials of CSA, EEG, heart rate (HR), arterial blood pressure (ABP) and arterial oxygen saturation (SaO2) were continuously monitored. CSA increased responding to acutely induced hypoxemia at a speed of -6 - 9% (SaO2).min-1. The response of CSA was estimated in two ways as a function of SaO2: The threshold was determined at the SaO2 level where CSA increased by 3% over the basal level and the gain was determined by the slope of CSA increase divided by the SaO2 span. They were 92% and -1.88 in the absence of volatile anesthetics, respectively. The threshold and the gain decreased markedly in the presence of various concentrations of volatile anesthetics. They were 89.2% and -1.16; 81% and -0.74; 84.2% and -1.16 and 86.2% and -0.94 with 1 MAC of H, E, I and S, respectively. The depressant effects of volatile anesthetics on the CSA responses to acutely induced hypoxemia can cause depressed control of the autonomic nervous system against hypoxemia and conceal the manifestation of clinical signs of hypoxemia.

Anesthetics↗

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↗

PubMed1995

Influence of acidosis, hypoxemia, and hypotension on neurodevelopmental outcome in very low birth weight infants.

OBJECTIVE: We previously demonstrated that acidosis (pH < 7.15) predicts poor motor outcome in very low birth weight (VLBW) infants. The present study was undertaken to examine the association between acidosis and developmental outcome in more detail and to better understand the interrelationship of acidosis with related factors such as hypoxemia and hypotension. METHODS: The nursery records of 191 infants enrolled in our VLBW follow-up study were reviewed to identify the type of acidosis (metabolic or respiratory) present, measure the duration of single and cumulative episodes, and examine the interaction of acidosis with hypoxemia and hypotension. The Bayley Scales of Infant Development and a detailed neurologic examination were performed at 6 (n = 158) and 24 (n = 106) months corrected age. RESULTS: At 6 months, both respiratory and metabolic acidosis as well as the total duration and longest single episode of acidosis were significantly correlated with cognitive, motor, and neurologic outcome (P < .0001). By 24 months, only the association of the metabolic component of acidosis with all three outcome measures remained significant. Duration of hypotension independently correlated with outcome at both testing periods (P < .002) but isolated hypoxemia did not. The metabolic component of acidosis and isolated hypotension contributed significantly to the variance in all three outcome measures (P < .05). Duration of hypoxemia, but not hypotension, contributed significantly (53%) to the variance in the metabolic component of acidosis. CONCLUSION: We conclude that it is the metabolic component of acidosis that is important in predicting poor developmental outcome in VLBW infants. The detrimental effect of hypoxemia appears to be closely related to the occurrence of metabolic acidosis while hypotension has an independent effect on outcome.

Acidosis↗

PubMed1993

Cerebral energy metabolism in fetal guinea pigs during moderate maternal hypoxemia at 0.75 of gestation.

There is evidence from fetal sheep near term that cerebral oxygen delivery decreases during a moderate maternal hypoxemia, whereas cerebral oxygen consumption is maintained. However, since in immature fetuses circulatory centralization may be in part ineffective, cerebral concentrations of high-energy phosphates may fall during a moderate maternal hypoxemia due to an insufficient cerebral oxygen supply. On the other hand anaerobic glycolysis may accelerate to prevent the depletion of high-energy phosphates. To determine, whether or not there is an energy failure in the immature fetal brain in this situation, we studied the effects of 60 min moderate maternal hypoxemia on cerebral concentrations of high-energy phosphates and glycolytic intermediates in fetal guinea pigs at 0.75 gestation. Maternal hypoxemia resulted in no change in fetal mixed arterio-venous pH (7.41 +/- 0.05 vs. 7.38 +/- 0.05; n.s.) or PCO2 (39.0 +/- 4.2 vs. 36.4 +/- 5.6 mmHg; n.s.), but in a fall in fetal PO2 (17.3 +/- 2.2 vs. 11.2 +/- 1.9 mmHg; P < 0.01). There was an increase in fetal cerebral concentrations of lactate (1.50 +/- 0.24 vs. 2.82 +/- 0.91 mumol/g; P < 0.01), whereas those of high-energy phosphates remained unchanged. From these results we conclude that during moderate isocapnic hypoxemia cerebral energy metabolism of immature fetal guinea pigs is maintained by an acceleration of the anaerobic glycolytic rate.

Animals↗

PubMed1993

[Severe hypoxemia in cirrhosis].

Various respiratory signs (other than infectious pathology), either very frequent and mild or very rare but with a poor prognosis, can be observed in cirrhotic subjects. Hypoxemia raises the greatest diagnostic problems in these subjects. The poor homogeneity of ventilation-perfusion ratios is the most commonly proposed cause of hypoxemia in cirrhosis. In such cases, hypoxemia is typically moderate (60-80 mmHg). Conversely, anatomical shunts, especially intrapulmonary ones, account for severe hypoxemia (< 60 mmHg). We are reporting about the case of a severe form of hypoxemia without anatomical shunt, caused by an anomalous ventilation-perfusion ratio in a female patient with ethylic cirrhosis.

Blood Gas Analysis↗

PubMed1996

Effects of inhalation anesthetic agents on response of horses to three hours of hypoxemia.

OBJECTIVE: To study the effects of inhalation anesthetic agents on the response of horses to 3 hours of hypoxemia. DESIGN: Controlled crossover study. ANIMALS: Five healthy adult horses. PROCEDURE: Horses were anesthetized twice: once with halothane, and once with isoflurane in O2. Anesthetized horses were positioned in left lateral recumbency. Constant conditions for the study began at 2 hours of anesthesia. A constant agent dose of 1.2 minimum alveolar concentration, PaO2 of 50 +/- 5 mm of Hg, and PaCO2 of 45 +/- 5 mm of Hg were maintained for 3 hours. Circulatory measurements were made at 0.5, 1, 2, and 3 hours of hypoxemia (anesthesia hours 2.5, 3, 4, and 5). Blood was collected from horses for biochemical analyses before anesthesia, within a few minutes after standing, and at 1, 2, 4, and 7 days after anesthesia. RESULTS: Cardiac index was greater (P = 0.018) during isoflurane than halothane anesthesia. Cardiac index remained constant during the 3 hours of hypoxemia during halothane anesthesia, whereas it decreased from the baseline during isoflurane anesthesia. Marginally nonsignificant P values for an agent difference were detected for arterial O2 content (P = 0.051), and oxygen delivery (P = 0.057). Serum activities of aspartate transaminase (P = 0.050) and sorbitol dehydrogenase (P = 0.017) were higher in halothane-anesthetized horses than in isoflurane-anesthetized horses. Circulatory function was better in hypoxemic horses anesthetized with isoflurane than with halothane. Isoflurane resulted in less muscular injury in hypoxemia horses than did halothane anesthesia. Halothane anesthesia and hypoxemia were associated with hepatic insult. CONCLUSION: Isoflurane is better than halothane for hypoxemic horses.

Analysis of Variance↗

PubMed1997

Oxygen protocols for the prevention of hypoxemia. A review for case managers.

Case managers are challenged by the need to ensure quality care for patients in the face of increasing demands on the health care system to provide more economic care. These economic pressures often cause hospitalized patients to be transferred from critical care areas earlier than in years past. As a result, hypoxemia-inadequate oxygenation of the blood-is emerging as a serious patient safety problem in noncritical care areas of the hospital. The medical literature recently has begun to document hypoxemia in some patient groups on the general care floor, where continuous monitoring of patients' respiratory status usually is no longer employed. The serious health consequences of hypoxemia, the fact that it can affect nearly any hospitalized patient, and the potentially high cost of treating hypoxemia-related morbidity are drawing the attention of the medical community. Case managers are in a position to address this emerging problem by working with hospitals and health care institutions to identify at-risk patients and develop strategies to improve both clinical and financial outcomes. Patient care protocols are one effective strategy to standardize monitoring of patients deemed to be at risk. Early detection and treatment of hypoxemia have the potential to improve patient care while significantly reducing medical costs.

Case Management↗

PubMed1996

[A study on the mechanism of severe hypoxemia associated with acute unilateral atelectasis in dogs].

OBJECTIVE: To study the mechanism of severe hypoxemia associated with acute unilateral atelectasis (AUA). METHODS: Six dogs with acute left side atelectasis were studied during the period of rest and exercise. The pulmonary shunt and PaO2 were measured at different levels of ventilation of right lung. RESULTS: After the left side ateloctasis during resting condition, the right lung could compensate to produce only mild hypoxemia (PaO2 9 kPa). But with further increased ventilation by exercise the shunt increased (from 19% to 29%) and led to severe hypoxemia (PaO2 8 kPa). When an artificial pneumothorax was instituted on the left lung, the shunt decreased (from 29% to 18%) and PaO2 increased (from 8 kPa to 9 kPa). CONCLUSIONS: After AUA, whether severe hypoxemia would occur is determined by the volume of ventilation of the normal side lung. The excess increase of ventilation of the normal side lung by any reason may result in severe hypoxemia.

Animals↗

PubMed2005

Effect of hypoxemia and hyperglycemia on pH in the intact cat retina.

OBJECTIVE: To examine the effects of acute hypoxemia and hyperglycemia on retinal pH to understand hyperglycemia-induced changes in the normal intact cat retina. METHODS: Spatial profiles of extracellular hydrogen ion (H+) concentration were obtained from the cat retina, in vivo, using pH-sensitive microelectrodes during normoxia (arterial partial pressure of oxygen [PaO2] = 114.5 +/- 7.9 mm Hg), normoglycemia (plasma glucose concentration, 117 +/- 19 mg/dL), acute hypoxemia (PaO2 = 29.5 +/- 2.2 mm Hg), and acute hyperglycemia (plasma glucose concentration, 303 +/- 67 mg/dL). An H+ diffusion model was fitted to the outer retinal data to quantify photoreceptor H+ production. The inner retinal pH was also examined. RESULTS: Hypoxemia induced a mean acute panretinal acidification of 0.16 pH units that originated from a 2.55-fold increase in net photoreceptor H+ production. Hyperglycemia induced an acute panretinal acidification of 0.12 pH units; however, photoreceptor H+ production levels remained unchanged. Retinal pH changes followed the course of arterial PaO2 and blood glucose changes. CONCLUSIONS: The increase in photoreceptor H+ production during hypoxemia confirms the importance of glycolysis in the retina. Hyperglycemia-induced pH changes resulted from either increased inner retinal H+ production or decreased H+ clearance/neutralization. Clinical Relevance The hyperglycemia-induced acidification that originates in the inner retina suggests that retinal acidosis may contribute to the development of diabetic retinal disease.

Acidosis↗