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PubMed1982

Tissue oxygen delivery in lambs: effect of postnatal age and acute hypoxemia.

Organ tissue arterial oxygen delivery in relation to postnatal age and acute hypoxemia (arterial pO2 34 +/- 5 Torr for 30 min) was studied in chronically catheterized, non anesthetized lambs 2-38 days of age. Baseline tissue oxygen delivery to heart and skeletal muscle correlated significantly with postnatal age. Acute hypoxemia induced significantly decreased oxygen delivery to kidney, spleen, ileum, jejunum and skeletal muscle without significant relation to postnatal age. Hypoxemia also induced increased arterial oxygen capacity and hemoglobin concentration which correlated significantly with postnatal age. These results suggest that baseline organ tissue oxygen delivery and response to hypoxemia remain constant during early postnatal maturation. Furthermore, hypoxemia may induce an apparent shift of fluid from the intravascular compartment which is greater in older lambs.

Acute Disease↗

PubMed1991

Umbilical artery pulsatility index and placental vascular resistance during acute hypoxemia in fetal lambs.

The effect of hypoxemia on the pulsatility index (PI) of the umbilical artery flow velocity waveform and placental vascular resistance was studied. Fetal hypoxemia was induced by maternal breathing of a low-oxygen gas mixture. Umbilical venous blood flow was measured with an electromagnetic flowmeter. Placental vascular resistance (PVR) was defined as the ratio perfusion pressure (mean arterial pressure minus umbilical venous pressure) and umbilical blood flow. Umbilical artery velocity waveforms were obtained by a 5-MHz pulsed Doppler device around one umbilical artery in 4 lambs and by a transcutaneous 4-MHz continuous wave Doppler transducer in 3 lambs. Fetal arterial oxygen content was lowered from 2.28 +/- 0.18 to 0.93 +/- 0.15 mM (p less than 0.05), while pCO2 and pH remained unchanged. Control values of the hemodynamic variables were compared with values during deepest hypoxemia. Fetal heart rate, mean arterial and umbilical venous pressure, PVR and the umbilical artery PI did not significantly change, whereas umbilical blood flow increased from 436 +/- 64.7 to 491 +/- 65.9 ml/min (p less than 0.05) during deepest hypoxemia. Individual regression analysis, however, showed a significant inverse correlation of umbilical venous pressure whereas PVR had a positive correlation with actual oxygen content. It is concluded that acute fetal hypoxemia slightly decreases PVR, but does not affect the umbilical artery PI in sheep. Decreasing fetal oxygenation is associated with an increase in pressure in the umbilical vein.

Animals↗

PubMed1991

Role of intrarenal angiotensin II and alpha-adrenoceptors in renal vasoconstriction with acute hypoxemia and hypercapnic acidosis in conscious dogs.

To evaluate our previous observation of renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied 13 conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 meq/day for 4 days). Five dogs were studied during combined acute hypoxemia (PaO2, 37 +/- 1 mm Hg) and hypercapnic acidosis (PaCO2, 59 +/- 1 mm Hg; pH 7.20 +/- 0.01). Each dog was studied during infusion of 1) the intrarenal vehicle (n = 5), 2) the intrarenal alpha 1-antagonist prazosin (0.2 micrograms.kg-1.min-1, n = 5), 3) intrarenal [Sar1,Ala8]angiotensin II (70 ng.kg-1.min-1, n = 5), and 4) intrarenal prazosin and [Sar1,Ala8]angiotensin II (n = 4). Immediate induction of combined hypoxemia and hypercapnic acidosis after control measurements during intrarenal vehicle infusion resulted in a decrease in effective renal plasma flow and glomerular filtration rate, increase in renal vascular resistance, and decrease in filtered sodium load in the first 20 minutes of the blood gas derangement. Intrarenal administration of [Sar1,Ala8]angiotensin II failed to reverse the effects of the combined blood gas derangement on renal function. In contrast, intrarenal prazosin administration either alone or in combination with [Sar1,Ala8]angiotensin II abrogated the increase in renal vascular resistance, decrease in glomerular filtration rate, and fall in filtered sodium load. These studies identify a major role for alpha 1-adrenoceptors in the renal vasoconstriction during combined hypoxemia and hypercapnic acidosis.

Acidosis↗

PubMed1985

Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome.

Although right heart failure is a recognized complication of obstructive sleep apnea, the incidence and pathogenesis of this complication have not been established. We therefore studied 50 consecutive patients with obstructive sleep apnea to determine the incidence of right heart failure and the factors involved in its development. Six patients (12%) were found to have right heart failure. There were no differences in the number of apneas between those with right heart failure (mean +/- SE, 30 +/- 10 per h sleep) and those without right heart failure (33 +/- 4 per h sleep). In contrast, mean nocturnal oxygen saturation was lower in patients with right heart failure (76 +/- 3%) than in those without right heart failure (90 +/- 1%; p less than 0.001). Furthermore, patients with right heart failure also had a substantially lower awake arterial PO2 (52 +/- 4 mmHg versus 75 +/- 2 mmHg; p less than 0.001) and a higher PCO2 (51 +/- 2 mmHg versus 36 +/- 1 mmHg; p less than 0.001) than those without right heart failure. Severe nocturnal hypoxemia in the absence of diurnal hypoxemia was not associated with right heart failure. Daytime hypoxemia in the patients with right heart failure was associated with a higher residual volume (p less than 0.001) and lower forced expiratory volume in one second (p less than 0.001) than in the patients without right heart failure. The findings suggest that sustained hypoxemia and/or hypercapnia over a 24-h period is a necessary prerequisite for the development of right heart failure in patients with obstructive sleep apnea, and that diffuse airway obstruction plays a major role in causing such hypoxemia.

Circadian Rhythm↗

PubMed1987

Nocturnal increase of urinary uric acid:creatinine ratio. A biochemical correlate of sleep-associated hypoxemia.

Sleep-associated hypoxemia may result in tissue hypoxia and increased production and excretion of adenosine triphosphate (ATP) degradation intermediates and uric acid. Urinary uric acid:creatinine(UA:Cr) ratio is a convenient method for estimating uric uric acid excretion. We measured the overnight changes in urinary UA:Cr ratio in 17 patients with documented sleep-associated hypoxemia, 13 control patients who remained normoxemic during polysomnography, and 14 normal volunteers. The urinary UA:Cr ratio increased overnight in patients with sleep-associated hypoxemia (+31.2 +/- 10.9%), whereas it decreased in the control patients with negative sleep studies (-13.6 +/- 4.6%; p less than or equal to 0.01) and in the normal volunteers (-23.2 +/- 5.8%). Repeat polysomnography revealed interval resolution of sleep-associated hypoxemia in 2 patients and significant improvement in a third. In every case, this clinical improvement was accompanied by a decrease in the overnight change in UA:Cr ratio. We report that urinary UA:Cr ratio increased overnight in a nonhomogeneous group of patients with sleep-associated hypoxemia.

Adult↗

PubMed1985

Influence of vagal activity on the neonatal ventilatory response to hypoxemia.

The sustained increase in ventilation (V1) that occurs during acute hypoxemia in adults is not characteristic of the neonate as V1 falls to or below baseline values soon after onset of the hypoxic stimulus. Associated with this decline in V1 is a decrease in tidal volume, lung compliance, inspiratory duration, and an increase in functional residual capacity and respiratory frequency. We hypothesized that hypoxemia induced small airway constriction and pulmonary time constant inequalities resulting in a frequency dependent fall in lung compliance and tidal volume and retention of lung volume. In seven newborn subhuman primates, responses to acute hypoxemia were measured prior to and after administration of atropine methyl bromide to prevent vagally mediated narrowing of peripheral airways. The increase in frequency and fall in inspiratory duration characteristic of the ventilatory decline during hypoxemia was eliminated by the drug but functional residual capacity and lung compliance were unaffected. Also, the initial rise in V1 was blunted or blocked in all subjects. Bilateral vagotomy caused V1 to fall significantly requiring oxygen supplementation but responses to hypoxemia were still biphasic in nature. These findings suggest that cholinergically mediated mechanisms in the airways do not alter effective lung distensibility related to respiratory rate. Acetylcholine may be important at the peripheral chemosensor since cholinergic blockade eliminated the initial ventilatory increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Temporal response of immunoreactive erythropoietin to acute hypoxemia in fetal sheep.

Acute hypoxemia was produced in chronically catheterized sheep fetuses to determine the response time necessary to increase plasma immunoreactive erythropoietin (Ep) concentration. Sodium nitrite (0.2 mM) was infused via a fetal vein to induce fetal hypoxemia. The resultant fetal methemoglobinemia was associated with a predictable, incremental decrease in arterial oxygen content. Twelve nitrite infusions were performed in eight fetal sheep preparations (gestational ages 115-146 days). Mean methemoglobin level increased to 33% of total Hb after 1-2 h of NaNO2 infusion. These results were compared to those obtained in nine control studies in eight fetuses in which no change was observed for plasma Ep, arterial oxygen content, PaO2, pHa, or whole blood lactate. In the nitrite infused group, however, a significant and progressive increase in mean plasma Ep level over baseline levels was observed during the 4th and 5th h of hypoxemia (p less than 0.01). This change in Ep was significantly greater compared to the control group. These results, however, were confounded by the concomitant development of a lactic acidemia secondary to the fetal hypoxemia. To examine the theoretic possibility that lactic acidemia may primarily affect fetal Ep levels, an additional group of five fetuses was infused with L-lactic acid for the same time period. Although the decrements in pHa and whole blood lactate levels achieved in these fetuses were in excess of those observed during the nitrite infusions, this possibility was ruled out since no change in fetal plasma Ep levels occurred. We conclude that during the 4th h of acute fetal hypoxemia a predictable, progressive increase in plasma Ep level is observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1989

Beta-adrenergic influence on increased myocardial oxygen consumption during hypoxemia in awake newborn lambs.

The purpose of this investigation was to determine the role of increased beta-adrenergic activity in regulating the increase in myocardial oxygen consumption that occurs during hypoxemia in unanesthetized newborn lambs. Through a left thoracotomy, fluid-filled catheters were placed in the ascending aorta, coronary sinus and left atrium, a pressure transducer was introduced into the left ventricle, and pacing wires were sutured onto the left atrium. The lambs were studied 3 d later by making intermittent measurements of aortic and coronary sinus blood oxygen saturations and Hb concentrations, left ventricular myocardial blood flow, cardiac output, heart rate, left atrial and aortic blood pressures, the maximal first derivative of left ventricular pressure, aortic and coronary sinus blood oxygen contents, the arteriovenous difference of oxygen across the left ventricular myocardium, myocardial oxygen consumption, and external cardiac work (aortic mean blood pressure times cardiac output). In nine lambs with an intact beta-adrenergic nervous system (group 1), the above measurements were made during a control period and during hypoxemia (FiO2 = 0.08-0.10) with spontaneous tachycardia. In another group of 12 lambs (group 2), the measurements were made during a control period, after beta-blockade (1.5 mg/kg intravenous propranolol) with pacing at the control heart rate, during hypoxemia with pacing at the control heart rate, and during hypoxemia with pacing-induced tachycardia. In the group 2 lambs, beta-blockade completely inhibited the increase in heart rate, maximal first derivative of left ventricular pressure, cardiac output and cardiac work that occurred during hypoxemia in the group 1 lambs that had an intact beta-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Alterations in postnatal intestinal function during chronic hypoxemia.

Growth failure is a major complication of chronic hypoxemia, as seen in infants and children with cyanotic congenital heart disease. To determine whether chronic hypoxemia during infancy affects the gastrointestinal tract, we examined small intestinal growth and digestive enzyme activities in chronically hypoxemic newborn lambs and in age-matched controls. Chronic hypoxemia was produced by placing an inflatable occluder around the main pulmonary artery and performing a balloon atrial septostomy. Aortic oxygen saturation was reduced to 60-74% for 2 wk, after which the small intestine was removed for analysis. During chronic hypoxemia, somatic growth rate was decreased to 60% of control (hypoxemic, 135 +/- 20 versus control, 216 +/- 26 g/d, p less than 0.02). No differences in caloric intake were found (hypoxemic, 129 +/- 4 versus control, 128 +/- 4 kcal/kg/d). Chronic hypoxemia did not alter small intestinal growth, as measured by jejuno-ileal weight, jejuno-ileal length, mucosal weight, or mucosal protein or DNA contents. However, sp act of lactase, the principal disaccharidase of the infant lamb intestine, were significantly decreased (hypoxemic, 0.08 +/- 0.01 versus control, 0.146 +/- 0.03 units of enzyme activity/mg DNA, p less than 0.05), as were the total small intestinal contents of lactase (hypoxemic, 61.7 +/- 7.0 versus control, 120.6 +/- 21.7 units of enzyme activity, p less than 0.01). There also were decreases in specific and total activities of other digestive enzymes such as maltase, amino-oligopeptidase, and alkaline phosphatase in hypoxemic intestine that did not achieve statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Naloxone does not alter the arousal response decrement after repeated exposure to hypoxemia during sleep in lambs.

Experiments were done to determine if endogenous opiates cause the arousal response decrement that follows repeated exposure to hypoxemia during sleep in lambs. Five lambs were anesthetized and instrumented for sleep staging and measurement of arterial Hb oxygen saturation. No sooner than 3 d after surgery, measurements were made in quiet sleep and active sleep during control periods when the lambs were breathing 21% oxygen and during experimental periods when the lambs were breathing 5% oxygen. The experimental period was terminated during each epoch by changing the inspired gas mixture back to 21% oxygen, once the lamb aroused from sleep. After each lamb had been exposed to 5% oxygen during 100 consecutive epochs of sleep, naloxone--an opiate antagonist--was given i.v. in a dose of 3 mg/kg as a bolus. The animals continued to be exposed to 5% oxygen during six more epochs of sleep after the administration of naloxone. Arousal occurred from both sleep states during rapidly developing hypoxemia but was delayed in active sleep compared to quiet sleep. The arterial Hb oxygen saturation at arousal was significantly lower, and the time to arousal was significantly longer with repeated exposure to hypoxemia during both quiet sleep and active sleep. Naloxone did not alter this arousal response decrement to hypoxemia. Thus, our data provide evidence that endogenous opiates do not play a major role in causing the arousal response decrement that follows repeated exposure to hypoxemia during sleep in lambs.

Animals↗

PubMed1993

Hypoxanthine, xanthine, and uric acid concentrations in plasma, cerebrospinal fluid, vitreous humor, and urine in piglets subjected to intermittent versus continuous hypoxemia.

Infants with sudden infant death syndrome have higher hypoxanthine (Hx) concentrations in their vitreous humor than infants with respiratory distress syndrome and other infant control populations. However, previous research on piglets and pigs applying continuous hypoxemia has not been able to reproduce the concentrations observed in infants with sudden infant death syndrome. To test whether intermittent hypoxemia could, in part, explain this observed difference, Hx, xanthine (X), and uric acid were measured in vitreous humor, urine, plasma, and cerebrospinal fluid in newborn piglets during intermittent hypoxemia (IH) or continuous hypoxemia (CH) of equal degree and duration. Urinary Hx excretion was significantly higher (p < 0.04) in the IH group after 60 min of hypoxemia. The vitreous humor Hx increase was significantly higher in the IH group (from 21.0 +/- 7.8 to 44.1 +/- 25.5 mumol/L, p < 0.01 versus baseline) than in the CH group (from 16.4 +/- 4.2 to 23.2 +/- 7.3 mumol/L, p < 0.05 versus baseline) (p < 0.05 IH versus CH). X increased significantly more (p < 0.05) in vitreous humor in the IH group than in the CH group. No differences between the two groups were found in plasma and cerebrospinal fluid for either Hx, X, or uric acid. We conclude that vitreous humor Hx and X increases more during IH than during CH.

Animals↗

PubMed2004

Pituitary-adrenal responses to acute hypoxemia during and after maternal dexamethasone treatment in sheep.

The effects of maternal dexamethasone treatment on hypothalamic-pituitary-adrenal axis function were determined during basal and hypoxemic conditions in maternal and fetal sheep. Under halothane, ewes and their fetuses were catheterized at 117 d gestation (term = 145 d). Starting at 124 d, the ewes received i.m. injections of two doses of either dexamethasone (12 mg) or saline at 24-h intervals. All animals experienced one episode of hypoxemia when the dexamethasone was present in the maternal and fetal circulations [125 +/- 1 d (H1)] and a second episode of hypoxemia when the steroid was no longer detectable in either the maternal or fetal circulations [128 +/- 1 d (H2)]. The fall in partial pressure of oxygen in arterial blood in response to hypoxia was similar in the two episodes in both the fetal and the maternal blood. Maternal dexamethasone treatment diminished maternal and fetal basal plasma cortisol but not ACTH during the normoxic period of H1 but not H2. In control animals, hypoxemia induced increases in fetal but not maternal ACTH and cortisol concentrations. In dexamethasone-treated animals, maternal ACTH and cortisol concentrations also remained unchanged from baseline in both H1 and H2. In contrast, fetal plasma ACTH and cortisol responses to hypoxemia were significantly suppressed during H1 but not H2. Correlation of fetal plasma ACTH and cortisol concentrations suggested diminished cortisol output without a change in adrenocortical responsiveness in dexamethasone-treated fetuses during H1 but not H2. Maternal treatment with dexamethasone transiently suppressed maternal and fetal basal hypothalamic-pituitary-adrenal axis function and the fetal plasma ACTH and cortisol responses to acute hypoxemia in sheep.

Acute Disease↗

PubMed1984

Adrenal secretion of catecholamines during hypoxemia in fetal lambs.

A new method for quantifying adrenal secretory function in chronically catheterized fetal lambs was developed. This preparation included insertion of a catheter distally into the fetal left renal vein and placement of a remotely operated, hydraulically controlled choker around the renal vein at its junction with the vena cava. With the choker open, adrenal venous blood flowed into the renal vein and then into the vena cava. With the choker closed, adrenal blood flowed into the catheter so that timed samples of adrenal venous effluent could be obtained. With this technique, left adrenal secretory rates of norepinephrine and epinephrine were determined across a spectrum of oxygen concentrations in five near-term fetal lambs. There was a rapid rise in norepinephrine secretion after induction of hypoxemia. Maximum secretory rates occurred at about 5 min, concomitantly with the lowest attained fetal arterial partial pressure of oxygen (PO2s). There was an inverse exponential relation between these catecholamine secretion rates and fetal arterial PO2 (P less than 0.001). Norepinephrine secretion appeared to increase in response to lesser degrees of hypoxemia than did epinephrine, although a longer time delay between stimulation and epinephrine response may have been a factor. Overall, norepinephrine secretion was greater than that of epinephrine. The ratios of norepinephrine to epinephrine in individual adrenal samples varied considerably and in some instances were less than one. These ratios did not correlate significantly with the degree of hypoxemia. During 25 min of a relatively steady state of hypoxemia, norepinephrine secretion declined markedly after about 5 min, although it remained above control levels throughout. Epinephrine secretion rose more gradually but then was relatively stable during the remaining period of hypoxemia.

Adrenal Glands↗

PubMed1991

Nocturnal hypoxemia as a determinant of vigilance impairment in sleep apnea syndrome.

In sleep apnea syndrome (SAS), vigilance impairment is typically associated with highly disrupted sleep, but recently, nocturnal hypoxemia has also been identified as a second pathogenetic factor in patients with a high degree of desaturation. However, although sleep disruption has been demonstrated to play a role in both the propensity to fall asleep and the capacity to stay awake, the role of nocturnal hypoxemia has been implicated only in the latter. In the present study, both sleep disruption and nocturnal hypoxemia were assessed in 20 moderately to severely apneic patients. During the day, vigilance was assessed both by the multiple sleep latency test (MSLT), as a measure of the propensity to fall asleep, and by the four-choice reaction time test (FCRTT), as a measure of the capacity to stay awake in a performance task. Severity of nocturnal hypoxemia was found to predict performance on the MSLT, as well as on the FCRTT, but sleep disruption was found to predict performance only on the FCRTT. These results suggest that in moderately to severely affected SAS patients, nocturnal hypoxemia may play a primary role in the pathogenesis of vigilance impairment.

Adult↗

PubMed1991

Hypoxemia vs sleep fragmentation as cause of excessive daytime sleepiness in obstructive sleep apnea.

To determine the effects of intermittent hypoxemia on daytime sleepiness in the clinical setting of obstructive sleep apnea syndrome, we enrolled seven patients in a prospective, randomized, crossover study. We had two experimental conditions with NCPAP treatment as follow: (1) to correct apneas, sleep fragmentation, and hypoxemia; and (2) to correct apneas and sleep fragmentation and at the same time, induce intermittent hypoxemia. The outcome variable, daytime sleepiness, was measured objectively with the multiple sleep latency test following completion of baseline and each treatment condition. Compared with sleep latencies in the untreated condition, both experimental treatment arms prolonged sleep latencies (p less than 0.05). We found no statistically significant differences between mean MSLT scores obtained after NCPAP treatment under hypoxemic and nonhypoxemic conditions. In summary, two nights of intermittent nocturnal hypoxemia during NCPAP treatment for OSAS did not diminish the objective improvement in daytime somnolence seen with NCPAP treatment in the absence of nocturnal hypoxemia. Results lend further support to the hypothesis relating excessive daytime sleepiness to sleep fragmentation.

Adult↗

PubMed1997

Developmental regulation of preproenkephalin (PENK) gene expression in the adrenal gland of the ovine fetus and newborn lamb: effects of hypoxemia and exogenous cortisol infusion.

Development of the fetal adrenal gland is crucial not only for maturation of several fetal organ systems and the initiation of parturition, but also for the development of the fetal response to stress. The enkephalin-related peptides are present in the chromaffin cells of the fetal adrenal medulla and are secreted in response to stress and with sympathetic stimulation. However, changes in expression of preproenkephalin (PENK) with gestation and in response to stress have not been studied in detail. Therefore we examined the developmental pattern of PENK gene expression in the adrenal gland of fetal and newborn lambs, and of adult sheep. We also determined whether levels of PENK mRNA in the fetal adrenal gland changed in response to exogenous glucocorticoids in late gestation, or in response to hypoxemia. Adrenal glands were removed from fetal sheep, lambs and adult sheep at different stages of development for measurement of PENK mRNA. Cortisol was infused (5 micrograms/min) for 12, 24 or 96 h beginning on day 124-129 of gestation. Moderate hypoxemia was induced for 48 h beginning on day 126-130, or at day 134-136 of gestation, by lowering the maternal fractional inspired oxygen. At the end of the treatment periods, the ewes and fetuses were euthanized. Adrenal PENK mRNA were measured by Northern blot analysis. PENK mRNA levels in fetal adrenals were significantly higher (P < 0.05) on days 140-141 of gestation than earlier in pregnancy, and then decreased significantly with the onset of parturition (days 142-146). After cortisol infusion to the fetus for 96 h there was a significant reduction in adrenal PENK mRNA levels. Hypoxemia resulted in a significant increase in PENK mRNA levels in fetuses at day 126-130 of gestation, but not at the later time in pregnancy when endogenous plasma cortisol concentrations were higher. We conclude that there is a decrease in levels of PENK mRNA in the fetal adrenal gland before parturition at the time of the endogenous prepartum rise in plasma cortisol. Hypoxemia led to an elevation of PENK mRNA levels in fetuses at less than 130 days, but after that time, when the basal and stimulated cortisol responses had risen, there was no significant effect of hypoxemia on PENK mRNA. Cortisol infusion to the fetus at this stage of pregnancy resulted in a decrease in adrenal PENK mRNA levels. We suggest that cortisol may play an important role in the regulation of fetal adrenal PENK mRNA levels and enkephalin synthesis by the adrenal gland of the fetal sheep.

Adrenal Glands↗

PubMed1983

Renal oxygen delivery and consumption during progressive hypoxemia in the anesthetized dog.

The relationship between renal oxygen delivery (RDO2) and function was evaluated during progressive hypoxemia. Seven anesthetized, spontaneously breathing dogs were given progressively lower oxygen concentrations to breathe while monitoring renal O2 consumption (RVO2), renal hemodynamic and excretory function. In addition, basal RVO2 was determined in three models of kidneys without filtration. RDO2 averaged 3648 mumole O2/min/100 g during normoxia. Basal RVO2 averaged 100 mumole O2/min/100 g kidney while total RVO2 was 466 mumole O2/min/100 g kidney during normoxia, leaving 366 mumole O2/min/100 g consumed by those processes involved in tubular transport. During hypoxemia, all renal parameters were well maintained until the lowest PaO2 (24.2 Torr). At this level, total RVO2 and RDO2 were significantly reduced. However, RDO2 remained well above RVO2 throughout hypoxemia. The reduction in RVO2 was a direct result of decreased O2 demand, as glomerular filtration and tubular load were also reduced. This associated decrease in O2 demand and RVO2 was indicated by the fact that the renal (a - v)O2 difference remained low and unchanged (1.9 vol%), fractional sodium excretion was unchanged, and the ratio of tubular sodium reabsorption to RVO2 also remained unchanged (30.8 meq Na/mmole O2). It was concluded that hypoxemia, while reducing both RDO2 and RVO2 at the lowest PaO2 (24.2 Torr), did not functionally impair renal excretory function by limiting RDO2 to the tubular transport processes. A reduction in RBF is far more likely to compromise the RDO2 needed to sustain basal and active transport processes than hypoxemia itself.

Animals↗

PubMed2003

[Meta-analysis on the effectiveness of interventions applied to preventing endotracheal suction-induced hypoxemia].

PURPOSE: This study was conducted to investigate the effects of the suction-induced hypoxemia interventions. METHOD: 30 suction-induced hypoxemia interventions were reviewed for the purpose of meta-analysis. RESULT: The study showed that both preoxygenation and insufflation were the most frequently examined oxygenation time periods, and hyperoxygenation combined with hyperinflation was the most commonly applied oxygenation method in order to prevent suction-induced hypoxemia. The greatest effect was obtained by providing oxygenation before and after suctioning, whereas negative effect(the contrary results from the study hypotheses) was frequently obtained by applying insufflation only. Applying hyperoxygenation combined with hyperinflation had the greatest effect over that of applying hyperoxygenation only, even though the difference between effect sizes of both methods were statistically significant. CONCLUSION: The results of meta-analysis showed that the occurrence rate of hypoxemia after suctioning was significantly reduced with the overall interventions for hypoxemia (decreasing 40% of occurrence rate), independent with time periods or methods for providing oxygenation.

English Abstract↗