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PubMed1996

Role of nitric oxide in the hypoxemia-induced renal dysfunction of the newborn rabbit.

The current study was performed in 30 anesthetized and mechanically ventilated newborn rabbits to investigate the role of the endothelium-derived relaxing factor nitric oxide (NO) in the renal vasoconstriction observed during hypoxemia. Renal blood flow (RBF) and GFR were determined by the clearance of p-aminohippuric acid and inulin, respectively. In nine newborn rabbits (group 1), acute hypoxemia induced a significant decrease in RBF (-17 +/- 7%) and GFR (-11 +/- 6%). A second group of nine animals was used to determine the role of NO in regulating renal hemodynamics of the immature kidney in physiologic conditions. N omega-Nitro-L-arginine methyl ester (L-NAME), a NO synthesis inhibitor, significantly increased the renal vascular resistance by 31 +/- 9% and decreased RBF and GFR (-20 +/- 6% and -13 +/- 5%, respectively). Acute hypoxemia was induced in 12 additional newborn rabbits during L-NAME infusion (group 3) to define the role of NO in the renal vasoconstriction observed during hypoxemia. The changes in renal hemodynamics were greater in this group than in those induced by hypoxemia alone. The present results suggest that: 1) endogenous NO has a crucial role in maintaining basal renal perfusion, 2) the activity of NO synthase is maintained during acute hypoxemia, and 3) NO could blunt the effects of acute hypoxemia in the immature newborn rabbit kidney.

Animals↗

PubMed2000

Low doses of dexamethasone suppress pituitary-adrenal function but augment the glycemic response to acute hypoxemia in fetal sheep during late gestation.

Despite the widespread use of antenatal glucocorticoid therapy in obstetric practice, little is known about the effects of synthetic glucocorticoids on the fetal capacity to respond to episodes of acute hypoxemia, such as may occur during labor and delivery. This study investigated the effects of prolonged fetal exposure to low concentrations of dexamethasone on the fetal ACTH, cortisol, and glycemic responses to an episode of acute hypoxemia during the period of dexamethasone treatment in sheep. At 118 d of gestation (term is approximately 145 d), 11 fetal sheep had catheters implanted under halothane anesthesia. From 124 d, five fetuses were infused i.v. continuously with dexamethasone (1.80 +/- 0.15 microg x kg(-1) x h(-1) in 0.9% saline at 0.5 mL/h) for 48 h, and the other six fetuses received saline solution i.v. at the same rate. At 45 h of infusion, acute hypoxemia was induced in all fetuses for 1 h by reducing the maternal inspired fraction of oxygen. During glucocorticoid treatment, fetal plasma dexamethasone concentrations increased to 3.9 +/- 0.2 nM by 24 h and remained elevated for the rest of the infusion period. During hypoxemia, a similar fall in fetal arterial PO2 occurred in both saline-infused and dexamethasone-treated fetuses. In control fetuses, significant increases in plasma ACTH and cortisol concentrations and in blood glucose concentrations occurred during hypoxemia. Dexamethasone treatment prevented the increases in fetal plasma ACTH and cortisol, and augmented the blood glucose response, induced by hypoxemia. These data indicate that prolonged fetal exposure to low concentrations of dexamethasone suppresses pituitary-adrenal function, but augments the glycemic response, to acute hypoxemia in fetal sheep during late gestation.

Acid-Base Equilibrium↗

PubMed2005

The role of calcitonin gene-related Peptide in the in vivo pituitary-adrenocortical response to acute hypoxemia in the late-gestation sheep fetus.

This study tested the hypothesis that calcitonin gene-related peptide (CGRP) has a role in mediating the in vivo fetal adrenal glucocorticoid response to acute stress. The hypothesis was tested by investigating the effects of fetal treatment with a selective CGRP antagonist on plasma ACTH and cortisol responses to acute hypoxemia in the late-gestation sheep fetus. Under anesthesia, six fetuses at 0.8 of gestation were surgically instrumented with vascular catheters. Five days later, fetuses were subjected to 0.5-h hypoxemia during treatment with either iv saline or a CGRP antagonist, in randomized order, on different days. Treatment started 30 min before hypoxemia and ran continuously until the end of the challenge. Arterial blood samples were collected for plasma ACTH and cortisol measurements (RIA) and blood gas monitoring. CGRP antagonism did not alter basal arterial blood gas or endocrine status. During hypoxemia, similar falls in arterial partial pressure of oxygen occurred in all fetuses. During saline infusion, acute hypoxemia induced significant increases in fetal ACTH and cortisol concentrations. During CGRP antagonism, the pituitary-adrenal responses were markedly attenuated. Correlation of paired plasma ACTH and cortisol values from all individual fetuses during normoxia and hypoxemia showed positive linear relationships; however, neither the slope nor the intercept of the peptide-steroid relationship was affected by CGRP antagonism. These data support the hypothesis that CGRP is involved in the in vivo regulation of fetal adrenocortical steroidogenesis during acute hypoxemia. In addition, the data reveal that CGRP may have a role in the control of other components of the hypothalamo-pituitary-adrenal axis during stimulated conditions in fetal life.

Acid-Base Equilibrium↗

PubMed1998

Chemoreflex contribution to adrenocortical function during acute hypoxemia in the llama fetus at 0.6 to 0.7 of gestation.

This study tested the hypothesis that the fetal llama, a species adapted to the chronic hypoxia of life at high altitude, demonstrates a potent carotid chemoreflex influence on adrenocortical responses during acute hypoxemia. Plasma ACTH and cortisol concentrations, and mesencephalic and adrenal blood flows were measured during a 1-h period of acute hypoxemia in six intact and four carotid sinus-denervated llama fetuses at 0.6-0.7 of gestation. Fetal PaO2 was reduced from approximately 23 to about 14 mm Hg in both intact and carotid-denervated groups during acute hypoxemia. During hypoxemia, fetal plasma ACTH, adrenal blood flow, and, therefore, delivery of ACTH to the adrenals increased to similar extents in both intact and carotid-denervated fetal llamas. Despite this, the increase in plasma cortisol in hypoxemia in intact fetuses was absent in carotid-denervated fetuses. In addition, the increase in delivery of cortisol to the mesencephalon calculated in intact fetuses during hypoxemia did not occur in the carotid-denervated group. These data suggest that the integrity of the carotid chemoreceptors is indispensable to cortisol release during acute hypoxemia in the llama fetus, even at 0.6-0.7 of gestation.

Adrenal Cortex↗

PubMed1985

Hypoxemia in acute pulmonary embolism.

Most patients with severe, acute pulmonary embolism (PE) have arterial hypoxemia. To further define the respective roles of ventilation to perfusion (VA/Q) mismatch and intrapulmonary shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean PaO2, 67 +/- 11 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVA/QT 16.6 +/- 5.1 percent) was present in all patients. The relative contributions of VA/Q mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study. Although all patients had some degree of VA/Q mismatch, the two patients studied early (ie, less than 48 hours following acute PE) had normal chest x-ray film findings and no significant shunt; VA/Q mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 +/- 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute PE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops.

Acute Disease↗

PubMed1998

Posthyperventilation hypoxemia after methacholine inhalation.

The hypothesis of this study was that hypoxemia after methacholine (MTH) inhalation is related not only to ventilation/perfusion inhomogeneity, but also to posthyperventilation hypoxemia. To test the hypothesis, we paid special attention to changes in gas exchange and ventilation parameters after MTH inhalation. Six stable asthma patients were investigated, and SaO2, minute ventilation (V.E), oxygen uptake rate in the lung (V.O2), carbon dioxide output rate in the lung (V.CO2), and respiratory exchange ratio (R) were measured. The SaO2 level decreased from a baseline level (before MTH inhalation) of 96.8 +/- 1.0% (mean +/- SD) to the lowest level (the nadir SaO2) of 89.8 +/- 2.1% (p < 0.01) in 200 +/- 50 s after MTH inhalation and gradually increased toward the baseline level. V.CO2 increased just after MTH inhalation (post-MTH) with increased V.E, and decreased at the nadir SaO2 with baseline V.E and PaCO2, indicating a decrease in breath-by-breath V.A and an increase in dead space minute ventilation at the nadir SaO2, but V.O2 remained close to constant. R increased post-MTH, decreased at the nadir SaO2, and thereafter increased gradually toward the baseline level with a time constant of 5.6 min. The addition of CO2 to inspired air partially suppressed hypoxemia. The consensus is that hypoxemia after MTH is solely attributable to the ventilation/perfusion inhomogeneity, but posthyperventilation hypoxemia is another reasonable interpretation of the hypoxemia after MTH with decreased V.A, V.CO2, and R. It is speculated that posthyperventilation normoventilation in respect to V.CO2 with baseline PaCO2 after MTH inhalation resulted in posthyperventilation hypoxemia as a result of relative hypoventilation in respect to V.O2.

Administration, Inhalation↗

PubMedDate not supplied

Magnesium sulfate and fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin in response to acute hypoxemia in goats.

OBJECTIVE: We measured fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin during acute hypoxemia in goats and tested whether hypermagnesemia altered these endocrine responses. METHODS: Five chronically catheterized goat fetuses at 124-129 days' gestation were used. After 4 hours of infusion (magnesium or vehicle as controls), 30 minutes of hypoxemia was induced by infusing nitrogen gas through a maternal tracheal catheter. Fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin were measured before and during hypoxemia. Both magnesium sulfate and vehicle infusions were performed in each animal. Repeated-measures analysis of variance (ANOVA) and two-way ANOVA with post hoc test were used to determine statistical significance. RESULTS: During hypoxemia, fetal PO(2) decreased significantly from 30 to 14 mmHg with no significant changes in fetal pH or PCO(2) in both groups. Fetal heart rate was reduced significantly by hypoxemia, but to a lesser extent in the magnesium group (change in decrease in fetal heart rate: 41 beats per minute [bpm] in controls versus 26 bpm with magnesium). Mean blood pressure did not change significantly during hypoxemia in both groups. Fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin significantly increased from the prehypoxemic values both with magnesium and in controls. There were no significant differences in these hormone concentrations between magnesium and the controls. CONCLUSION: Magnesium sulfate had no effect on fetal plasma concentrations of vasopressin, epinephrine, and norepinephrine during acute hypoxemia.

Animals↗

PubMed1991

Hemodynamic responses to alpha-adrenergic blockade during hypoxemia in the fetal lamb.

The mechanisms responsible for the increase in umbilical venous and hepatic vascular resistance during hypoxemia are poorly understood. To assess the relative importance of alpha-adrenergic receptors, we produced an acute, severe hypoxemia in chronically instrumented fetal sheep. While fetal arterial oxygen saturation was maintained at the same level, we then injected phentolamine, a selective alpha-adrenoreceptor blocker. We found that the hypoxemia-induced vasoconstriction of the umbilical veins and hepatic vasculature was reversed by alpha blockade. Thus, alpha-adrenergic stimulation is necessary to maintain vasoconstriction of the umbilical veins and hepatic vasculature during acute fetal hypoxemia. Furthermore, alpha-adrenergic stimulation is responsible for the hypoxemia-induced vasoconstriction of the gut, spleen, and lower carcass. Thus, the alpha-adrenergic system mediates important fetal hemodynamic adaptations to acute hypoxemia. However, the alpha-adrenergic system is not responsible for the hypoxemia-induced constriction of the renal vasculature.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Hypoxemia in attack free asthmatic children: relationship with lung volumes and lung mechanics.

In 113 asthmatic children (mean age +/- SD = 11.0 +/- 2.8 years), the presence of hypoxemia was evaluated during an attack free period. Blood gases were measured in arterialized blood samples. 71% of the patients were hypoxemic. Hypoxemia was defined as partial pressure of O2 (PaO2) below 90% of the mean value for normal children. In a first step, the relationship between hypoxemia and frequency of asthma attacks was examined: frequency of attacks appeared to be a poor predictor of hypoxemia in an attack free period. In a second step, the relationship between hypoxemia and 9 pulmonary function test variables was examined. The static lung volumes considered were: functional residual capacity (FRC: helium dilution technique); thoracic gas volume (TGV: body plethysmography technique) and trapped gases (TG: difference between TGV and FRC). TG was expressed as a percentage of 1) measured FRC (TG/FRCmeas), 2) measured TGV (TG/TGVmeas), 3) predicted FRC (TG/FRCpred). Lung mechanics variables were determined by the oesophageal catheter technique: lung resistance (RL) and dynamic lung compliance (CLdyn). RL and CLdyn were expressed 1) in absolute terms, 2) as a percentage of the index of distension (ID: TGV/FRCpred). All variables are expressed as a percentage of predicted values except for TG/FRCmeas and TG/TGVmeas. Considering lung volumes, hypoxemia was found when TG was present. When lung mechanics were altered, hypoxemia was also present. The relationship between PaO2 and PFT variables was best expressed by the following equation: PaO2 (%) = 85.393 + 0.121 CLdyn/ID--0.151 TG/FRCpred--0.026 RL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

[Severe hypoxemia during cesarean section].

We describe three cases in which severe hypoxemia occurred during cesarean section. The first and second patients showed low oxygen saturation (91, 90%, respectively) on their arrival at the operation room, and hypoxemia deteriorated rapidly after the induction of anesthesia. During surgery low oxygen saturation, ranging from 90 to 95%, persisted until the beginning of spontaneous respiration. In the third patient, oxygen saturation fell suddenly to 93% after the delivery of a neonate, and the arterial blood gas analysis revealed Pao2 68.5 mmHg with 38% oxygen. Hypoxemia was transient and resolved at the end of operation. Parturients have been reported to be likely to develop hypoxemia physiologically. Apnea for a short interval during tracheal intubation may cause severe hypoxemia in parturients compared with normal subjects. Ritodrine, a beta 2 stimulator, which was administered in the first and second patients just prior to operation, may be one of the factors leading to hypoxemia because of its inhibition of hypoxic pulmonary vasoconstriction. Venous air embolism (VAE) may occur frequently during cesarean section, especially during repair of the uterus. VAE may have caused hypoxemia in the third patient. In conclusion, parturients should be monitored carefully with pulse oximetry during cesarean section.

Adult↗

PubMed1984

Hypoxemia associated with feeding in the preterm infant and full-term neonate.

Polygraphic monitoring studies were performed on more than 150 older preterm infants (postconceptional ages of 36 weeks or more) and full-term neonates to evaluate unexplained or persistent apnea. During polygraphic monitoring, 16 infants were observed to have hypoxemia associated with feedings. The feeding hypoxemia was accompanied by irregular respiratory effort and preceded any associated bradycardia. A comparison group of eight infants with similar gestational and postconceptional ages, but without feeding hypoxemia, was selected retrospectively from other infants referred for evaluation of persistent or unexplained apnea. The group with feeding hypoxemia showed evidence of CNS compromise as manifested by significant elevations of the maximum end-tidal carbon dioxide pressure during sleep and abnormal computed tomograms (7/11 v 0/5 in the comparison group). There was no relationship between feeding hypoxemia and sleep apnea or gastroesophageal reflux. Clinical follow-up showed that the feeding hypoxemia resolved with maturation.

Apnea↗

PubMed1985

Effect of hypoxemia on sodium and water excretion in chronic obstructive lung disease.

To determine the role of hypoxemia in the pathogenesis of impaired sodium and water excretion in advanced chronic obstructive lung disease, 11 clinically stable, hypercapneic patients requiring long-term supplemental oxygen were studied. The renal, hormonal, and cardiovascular responses to sodium and water loading were determined during five-and-a-half-hour studies on a control day (arterial oxygen tension = 80 +/- 6 mm Hg) and on an experimental day under hypoxic conditions (arterial oxygen tension = 39 +/- 2 mm Hg). Hypoxemia produced a significant decrease in urinary sodium excretion but did not affect urinary water excretion. Hypoxemia also resulted in concomitant declines in mean blood pressure, glomerular filtration rate, and filtered sodium load. Renal plasma flow and filtration fraction were unchanged whereas cardiac index rose. On the control day, plasma renin activity and norepinephrine levels were elevated whereas aldosterone and arginine vasopressin levels were normal; none of these four hormones was affected by hypoxemia. Renal tubular function did not appear to be altered by hypoxemia as there was no significant change in fractional reabsorption of sodium. The concurrent decreases in glomerular filtration rate, filtered sodium load, and mean blood pressure at constant renal plasma flow suggest that the reduction in urinary sodium excretion was due to an effect of hypoxemia on glomerular function, possibly related to impaired renovascular autoregulation.

Aged↗

PubMed1988

Circulatory responses to prolonged hypoxemia in fetal sheep.

Experiments were conducted in 11 chronically catheterized pregnant sheep to determine the distribution of blood flow within the fetus during prolonged (48 hours) hypoxemia secondary to the restriction of uterine blood flow. Uterine blood flow was mechanically restricted with a polytetrafluoroethylene vascular clamp placed around the maternal common internal iliac artery such that mean (+/- SEM) fetal arterial oxygen tension decreased from 23.4 +/- 1.9 to 17.3 +/- 0.8 mm Hg at 1 hour of hypoxemia and remained low for 48 hours. There was an initial increase in fetal arterial carbon dioxide pressure from 48.5 +/- 0.9 mm Hg during the control period to 56.2 +/- 2.3 mm Hg at 1 hour; this parameter subsequently returned to control values, whereas base excess showed a transient decrease. Fetal cerebral, myocardial, and adrenal blood flows were significantly increased at 1, 24, and 48 hours of hypoxemia. In contrast, there was no change in nuchal muscle or renal blood flows with hypoxemia of this magnitude. Cotyledonary blood flow increased transiently by 38% at 1 hour of hypoxemia, but was not changed from control at 24 and 48 hours. These experiments demonstrate that the sheep fetus is able to maintain the normal protective circulatory adjustments seen with acute hypoxemia for up to 48 hours in the absence of progressive metabolic acidemia.

Animals↗

PubMed1993

Effects of long-term, high-altitude hypoxemia on ovine fetal cardiac output and blood flow distribution.

OBJECTIVE: We sought to determine the effects of long-term hypoxemia on fetal cardiac output and flow distribution. STUDY DESIGN: We exposed six pregnant sheep to high altitude (3820 m) hypoxia from 30 to 135 days' gestation (term 146 days). Ten to 14 days after surgery we determined fetal cardiac output and organ blood flows by means of the radiolabeled microsphere technique during a baseline period and also during an additional 30-minute period of more severe added acute hypoxemia. RESULTS: Baseline maternal arterial PO2 was 60.7 +/- 1.7 torr and fell to 35.1 +/- 3.0 torr during the added acute hypoxemia. Fetal arterial PO2 decreased from 18.5 +/- 1.1 to 11.4 +/- 1.5 torr during added acute hypoxemia. Baseline fetal cardiac output was 351 +/- 55 ml/min/kg, which was significantly lower than previously reported values in low-altitude fetuses. Blood flow to critical organs such as the heart and brain was maintained at levels found in low-altitude fetuses, but flow to the carcass was significantly lower (-49%) than the mean value reported in the literature for low-altitude fetuses. Oxygen delivery was also maintained at normal levels to the brain and heart but was reduced in the kidneys (-31%), gastrointestinal tract (51%), and carcass (-58%). During added acute hypoxemia cardiac output did not change significantly; however, blood flow to the brain, heart, and adrenal glands increased 112%, 135%, and 156% (p < 0.05), respectively. CONCLUSION: We conclude that during long-term hypoxemia redistribution of fetal cardiac output is maintained favoring the brain and heart.

Adrenal Glands↗

PubMed1984

Cutaneous venodilation in response to systemic hypoxemia in dogs.

Experiments were performed in chloralose anesthetized dogs to test if the saphenous vein (a cutaneous vein) participates in the cardiovascular response to systemic hypoxemia. The saphenous vein was perfused at constant flow with cooled blood (32 degrees C) from the terminal aorta. Sixteen paralyzed (gallamine triethiodide) animals were ventilated with 10% O2 in N2 for 4-min episodes; arterial PO2 was 49 +/- 4 mm Hg after 4 min of ventilation with this gas mixture. Hypoxemia caused a 29% decrease in saphenous vein perfusion pressure (interpreted as a dilation) and an 8% increase in aortic pressure. The hypoxemia induced saphenous venous dilation was abolished by (1) section of the vagus nerves and denervation of the carotid chemoreceptors (afferent pathways), or (2) section of the lumbar sympathetic chain (efferent pathway). These data demonstrate that systemic hypoxemia causes a neurally mediated dilation of the saphenous vein that is dependent upon intact carotid chemoreceptors and/or vagus nerves. It is concluded that saphenous vein dilation is part of the integrated cardiovascular response to hypoxemia in anesthetized dogs. This reflex effect may represent a decompensatory mechanism that compromises cardiac output during hypoxemia in animals with hypothermic extremities.

Animals↗

PubMed2006

Magnesium sulfate exposure increases fetal blood flow redistribution to the brain during acute non-acidemic hypoxemia in goats.

BACKGROUND: It is still controversial that intrapartum exposure to magnesium may or may not reduce brain damage in premature infants in human and animal models. AIMS: We investigated the effect of hypoxemia alone under magnesium exposure on fetal cardiovascular changes in chronically catheterized goat fetuses. STUDY DESIGN: We performed a 3-day experimental protocol with control (10% glucose) on day 1, recovery on day 2, and magnesium on day 3. Magnesium sulfate was directly infused to fetuses in a bolus dose of 270 mg/kg followed by 80 mg/kg/h. Hypoxemia was induced by maternal inhalation of nitrogen gas on day 1 and on day 3. Cerebral blood flow was measured by colored microsphere techniques. Repeated measure ANOVA and Bonferroni's/Dunn's test were used for comparison. SUBJECTS: Six Japanese Saanen goats at 0.85 gestation. OUTCOME MEASURES: Fetal heart rate, blood pressure, and cerebral blood flow. RESULTS: Ionized magnesium concentrations were significantly increased. Fetal PO2 decreased significantly from 30 mmHg to 14 mmHg without acidemia. Magnesium exposure significantly attenuated hypoxemia-induced bradycardia but did not affect blood pressure. Hypoxemia significantly increased fetal brain blood flow from the pre-hypoxic levels on day 1. Magnesium exposure further increased hypoxemia-induced brain blood flow on day 3, but statistical significance was limited to the cerebral cortex. CONCLUSION: In near-term, initially healthy goat fetuses, brain blood flow during acute hypoxemia was significantly increased with magnesium sulfate exposure.

Animals↗

PubMed2004

Redistribution of power spectrum of heart rate variability during acute umbilical artery embolism and hypoxemia in late-gestation fetal sheep.

OBJECTS: Fetal heart rate variability (HRV) is subject to a number of factors, including fetal distress. The aim of this study was to investigate the power spectral distribution of fetal heart rate variability during acute hypoxemia following umbilical artery embolism and to test the hypothesis that the relative proportion of frequency domains in total power of HRV, reflects the changes in HRV during hypoxemia more closely than the absolute values. METHODS: Acute hypoxemia was induced in seven catheterized late-gestation fetal sheep by repeated injections of microspheres to cause umbilical artery embolism. The very-low, low-, middle- and high-frequency domains (0-0.025, 0.025-0.125, 0.125-0.20, and 0.20-0.50 cycles/beat, respectively) were determined by power spectral analysis. RESULTS: Umbilical artery embolism induced marked fetal hypoxemia, hypercapnia and acidosis, accompanied by an increase in heart rate and a decrease in arterial blood pressure. These changes were associated with the increase in power over the entire frequency range and in the relative power in the low-frequency range (P<0.01), and with decrease in the relative power in the high-frequency range (P<0.05). Correlations were found between the relative power in the low- and high-frequency ranges and PO2 and between the relative power in these ranges and mean arterial blood pressure (P<0.05), but not PCO2 or pH. CONCLUSIONS: The present study indicates that acute hypoxemia induced by umbilical artery embolism leads to the redistribution of power spectral density of fetal HRV and that the relative proportion of individual frequency domains may reflect the changes in HRV during acute hypoxemia more closely than the absolute power values.

Animals↗

PubMed2005

Chronic hypoxemia increases myocardial cytochrome oxidase.

OBJECTIVE: Cyanotic patients have potentially decreased tissue oxygen tension. Cytochrome oxidase catalyzes the reduction of oxygen and is integral to adenosine triphosphate production. Cytochrome oxidase subunit I, the active site, is encoded by mitochondrial DNA. Using a newborn swine model of chronic hypoxemia, we evaluated ventricular cytochrome oxidase subunit I mRNA and protein expression and assessed cytochrome oxidase activity. METHODS: Thirty-two newborn piglets underwent thoracotomy and placement of a pulmonary artery-to-left atrium shunt or sham operation. Two weeks later, partial pressure of arterial oxygen, hematocrit, and left ventricular shortening fraction values were compared with baseline values. Northern blot hybridization and protein immunoblotting for ventricular cytochrome oxidase subunit I were performed. Cytochrome oxidase kinetic activity was measured. Heme a,a3 content and turnover number were determined. Significance was assessed with a t test. RESULTS: Baseline partial pressure of arterial oxygen and hematocrit values were similar. Hypoxemic piglets had a lower partial pressure of arterial oxygen of 38 +/- 10 mm Hg (P < .001) and higher hematocrit value of 31.4% +/- 2.9% (P < .001) compared with a partial pressure of arterial oxygen of 140 +/- 47 mm Hg and hematocrit value of 24.6% +/- 3.9% after the sham operation. Baseline and postprocedure left ventricular shortening fraction were similar within and between groups. Chronic hypoxemia increased right ventricular and left ventricular cytochrome oxidase I mRNA and protein by more than 1.4-fold. Cytochrome oxidase activity increased significantly in hypoxemia by 2.5-fold compared with that seen after the sham operation. Heme a,a3 content and turnover number increased by 1.5-fold during hypoxemia. CONCLUSIONS: Chronic hypoxemia increases cytochrome oxidase I message, protein expression, and activity. The increase in kinetics was due to increased enzyme content and catalytic activity. This is a possible adaptive mechanism that might preserve organ function during chronic hypoxemia.

Animals↗