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PubMed1997

Effects of hypoxemia and reoxygenation with 21% or 100% oxygen in newborn piglets: extracellular hypoxanthine in cerebral cortex and femoral muscle.

OBJECTIVE: To determine whether reoxygenation with an FIO2 of 0.21 (21% oxygen) is preferable to an FIO2 of 1.0 (100% oxygen) in normalizing brain and muscle hypoxia in the newborn. DESIGN: Prospective, randomized, animal study. SETTING: Hospital surgical research laboratory. SUBJECTS: Twenty-six anesthetized, mechanically ventilated, domestic piglets, 2 to 5 days of age. INTERVENTIONS: The piglets were randomized to control or hypoxemia groups. Hypoxemia was induced by ventilating the piglets with 8% oxygen in nitrogen, which was continued until mean arterial pressure decreased to <20 mm Hg. After hypoxemia, the piglets were further randomized to receive reoxygenation with an FIO2 of 0.21 (21% oxygen group, n = 9) or an FIO2 of 1.0 for 30 mins followed by an FIO2 of 0.21 (100% oxygen group, n = 9), and followed for 5 hrs. The piglets in the control group were mechanically ventilated with 21% oxygen (n = 8). MEASUREMENTS AND MAIN RESULTS: We measured extracellular concentrations of hypoxanthine in the cerebral cortex and femoral muscle (in vivo microdialysis), plasma hypoxanthine concentrations, cerebral arterial-venous differences for hypoxanthine, acid base balances, arterial and venous (sagittal sinus) blood gases, and mean arterial pressures. The lowest pH values of 6.91 +/- 0.11 (21% oxygen group, mean +/- SD) and 6.90 +/- 0.07 (100% oxygen group) were reached at the end of hypoxemia and then normalized during the reoxygenation period. Plasma hypoxanthine increased during hypoxemia from 28.1 +/- 9.3 to 119.1 +/- 31.9 micromol/L in the 21% oxygen group (p < .001) and from 32.6 +/0- 14.5 to 135.0 +/- 31.4 micromol/L in the 100% oxygen group (p <.001). Plasma hypoxanthine concentrations then normalized over the next 2 hrs in both groups. In the cerebral cortex, extracellular concentrations of hypoxanthine increased during hypoxemia from 3.9 +/- 2.8 to 20.2 +/- 7.4 micromol/L in the 21% oxygen group (p < .001) and from 5.9 +/- 5.0 to 25.1 +/- 7.1 micromol/L in the 100% oxygen group (p < .001). In contrast to plasma hypoxanthine, extracellular hypoxanthine in the cerebral cortex increased significantly further during early reoxygenation, and, within the first 30 mins, reached maximum values of 24.9 +/- 6.3 micromol/L in the 21% oxygen group (p < .01) and 34.8 +/- 10.9 micromol/L in the 100% oxygen group (p < .001). This increase was significantly larger in the 100% oxygen group than in the 21% oxygen group (9.7 +/- 4.7 vs. 4.7 +/- 2.6 micromol/L, p < .05). There were no significant differences between the two reoxygenated groups in duration of hypoxemia, hypoxanthine concentrations in femoral muscle, plasma hypoxanthine concentrations, pH, or mean arterial pressure. The cerebral arterial-venous difference for hypoxanthine was positive both at baseline, at the end of hypoxemia, and after 30 mins and 300 mins of reoxygenation, and no differences were found between the two reoxygenated groups. CONCLUSIONS: Significantly higher extracellular concentrations of hypoxanthine were found in the cerebral cortex during the initial period of reoxygenation with 100% oxygen compared with 21% oxygen. Hypoxanthine is a marker of hypoxia, and reflects the intracellular energy status. These results therefore suggest a possibly more severe impairment of energy metabolism in the cerebral cortex or an increased blood-brain barrier damage during reoxygenation with 100% oxygen compared with 21% oxygen in this newborn piglet hypoxia model.

Animals↗

PubMed2004

Level of ventilation influences the cardiovascular response to hypoxemia in lambs.

Newborn animals of a number of species display a brisk increase in ventilation followed by a gradual drop toward or below baseline within minutes of exposure to acute hypoxemia. Heart rate and cardiac output (a determinant of systemic oxygen transport along with the arterial oxygen content) appear to follow a similar pattern, but whether or not the cardiovascular response is influenced by the respiratory response is unknown. We therefore carried out experiments in which the level of ventilation was controlled during normoxemia and hypoxemia to test the hypothesis that the level of ventilation influences the cardiovascular response to acute hypoxemia. Six lambs ranging in age from 17 to 22 days were anesthetized, tracheostomized, and instrumented for measurement of cardiovascular variables. A recovery period of at least 3 days was allowed before the study when each lamb was artificially ventilated with a mixture of 70% nitrous oxide and 30% oxygen in nitrogen. A control respiratory frequency (f) of 30 breaths per min was set and a control tidal volume (VT) was chosen to achieve normocapnia. Cardiovascular measurements were made during normoxemia and hypoxemia (FIO2 0.10) 5 min after f or VT was changed to simulate a decrease, no change, or an increase in ventilation. During normoxemia, the level of ventilation had little effect on the measured cardiovascular variables. At control levels of ventilation, hypoxemia caused an increase in cardiac output that was due solely to an increase in stroke volume as heart rate decreased; blood pressure was unchanged. Increasing ventilation during hypoxemia did not augment cardiac output or alter blood pressure as compared with that observed at control levels of ventilation. Decreasing ventilation during hypoxemia, however, decreased cardiac output due to a profound bradycardia; blood pressure increased significantly. Our data provide evidence that the level of ventilation significantly influences the cardiovascular response to hypoxemia in young lambs.

Animals↗

PubMed1983

Acute hypoxemia and hypercapnia: increase in plasma catecholamines in conscious dogs.

To systemically evaluate the effects of acute hypoxemia and hypercapnic acidosis on the sympathetic nervous system, five unanesthetized mongrel dogs were studied during acute hypoxemia [arterial O2 tension (PaO2) 33 +/- 2 Torr], acute hypercapnic acidosis [arterial CO2 tension (PaCO2) 53 +/- 1 Torr; pH, 7.19 +/- 0.02], and combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 Torr; PaCO2, 52 +/- 1 Torr; pH, 7.18 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis resulted in increased mean arterial pressure, cardiac output, and heart rate. Moreover, combining acute hypoxemia and hypercapnic acidosis acted synergistically to increase circulating norepinephrine and epinephrine. Acute hypoxemia alone and acute hypercapnic acidosis alone resulted in reversible increases in mean arterial pressure, cardiac output, heart rate, and circulating norepinephrine. Although plasma epinephrine concentrations increased during acute hypoxemia, circulating epinephrine was unchanged during acute hypercapnic acidosis. These data indicate that acute hypoxemia and hypercapnic acidosis result in synergistic increase in circulating catecholamines.

Acidosis↗

PubMed2001

Purinergic contribution to circulatory, metabolic, and adrenergic responses to acute hypoxemia in fetal sheep.

This study investigated the effects on femoral vascular resistance, blood glucose and lactate levels, and plasma catecholamine concentrations of fetal treatment with an adenosine receptor antagonist during acute hypoxemia in fetal sheep during late gestation. Under anesthesia, seven fetal sheep were instrumented between 117 and 118 days gestation (term is approximately 145 days) with vascular and amniotic catheters and an ultrasonic probe around a femoral artery. Six days after surgery, all fetuses were randomly subjected to a 3-h experiment consisting of 1 h of normoxia, 1 h of hypoxemia, and 1 h of recovery. This was done during either intravenous infusion of vehicle or the adenosine receptor antagonist [8-(p-sulfophenyl)-theophylline; 8-SPT] dissolved in vehicle. During vehicle infusion, all fetuses responded to hypoxemia with bradycardia, an increase in arterial blood pressure, and femoral vasoconstriction. Increases in blood glucose and lactate concentrations and in plasma epinephrine and norepinephrine concentrations also occurred in all fetuses during hypoxemia. Fetal treatment with 8-SPT markedly attenuated the bradycardic, hypertensive, vasoconstrictor, glycemic, and adrenergic responses to hypoxemia, but it did not affect the increase in blood lactate concentrations during hypoxemia. These data show that adenosine is involved in the mechanisms mediating fetal cardiovascular, metabolic, and adrenergic responses to hypoxemia in fetal sheep. Fetal treatment with 8-SPT mimics the effects of carotid sinus nerve section on fetal cardiovascular function during hypoxemia, suggesting a role for adenosine in mediating fetal cardiovascular chemoreflexes.

Animals↗

PubMed1986

Effects of renal denervation on renal responses to hypoxemia in fetal lambs.

The role of renal nerves in mediating renal hemodynamics and renal function during normal physiological conditions and following moderate hypoxemia was studied in chronically catheterized fetal lambs (125-141 days of gestation) following unilateral renal denervation. Base-line values for renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), urinary flow rate (UFR), urinary electrolyte (Na+, K+, and Cl-) excretion rate, and urine osmolality (Uosm) were similar in both intact and denervated kidneys. Hypoxemia was associated with a significant rise in mean arterial blood pressure and a significant decrease in heart rate. Hypoxemia produced a similar decrease in GFR and similar increases in urinary Na+ and Cl- excretion rates in both intact and denervated kidneys. However, the effect of hypoxemia on renal hemodynamics differed between intact and denervated kidneys. Hypoxemia produced a continuous and progressive decrease in RBF and increase in RVR in the intact kidney. On the other hand, renal denervation was associated with an early renal vasodilation and attenuated the reduction in RBF and the rise in RVR during hypoxemia; this early renal vasodilation was blunted following prostaglandin synthesis inhibition. Taken together, these results suggest that fetal renal denervation is not associated with significant changes in renal hemodynamics or renal function during normal physiological conditions but that renal denervation partially inhibited the renal vasoconstriction associated with fetal hypoxemia. Finally, it was found that endogenous prostaglandins counteract the renal vasoconstriction associated with fetal hypoxemia.

Animals↗

PubMed1986

Baroreceptor control of pressure-flow relationships during hypoxemia.

In the absence of peripheral chemoreceptors, the effects of graded hypoxemia on the carotid sinus control of central and regional hemodynamics were studied in anesthetized mongrel dogs. Baroreceptor stimulation was effected by carotid sinus isolation and perfusion under controlled pressure. Blood flows were measured in the aorta and the celiac, mesenteric, left renal, and right iliac arteries. Carotid sinus reflex set-point pressures were well maintained until hypoxemia was severe. Carotid sinus reflex set-point gain was maximal during mild hypoxemia. Reflex operating point regional flows were unaffected by hypoxemia. A factorial analysis of overall reflex increases in mean aortic pressure, flow, and power during reduced baroreceptor stimulation showed potentiation by increasing hypoxemia. Corresponding effects of baroreceptor stimulation and hypoxemia on aortic resistance and heart rate were additive. Celiac, renal, and iliac blood flows increased during both hypoxemia and reduced baroreceptor stimulation. Only in the celiac bed were blood flow changes independent of concomitant changes in cardiac output. Thus, at maximum sympathetic stimulation (low carotid sinus pressure) during hypoxemia, the cardiovascular system maintained both central and regional blood flows at high systemic blood pressures independent of the peripheral chemoreceptors.

Animals↗

PubMed1987

Ventral medullary extracellular fluid pH and PCO2 during hypoxemia.

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].

Acid-Base Equilibrium↗

PubMed1988

Plasma adenosine and hypoxemia in patients with sleep apnea.

Severe hypoxemia causes ATP depletion and increased adenosine production in many body tissues. Therefore we hypothesized that patients with sleep apnea and severe hypoxemia during sleep have higher adenosine production and higher plasma adenosine levels than patients without hypoxemia. Twelve patients with sleep apnea and six normal volunteers had plasma adenosine levels measured by high-performance liquid chromatography. Each patient with sleep apnea had a polysomnograph sleep study with oxyhemoglobin saturation continuously recorded. Five of 12 patients with sleep apnea had both sleep apnea and severe hypoxemia during sleep. These patients with severe nocturnal hypoxemia had significantly higher plasma adenosine levels (means +/- SD 9.7 +/- 5.5 X 10(-8) M) than either a group of six normal volunteers (3.5 +/- 0.7 X 10(-8) M) or a group of seven patients with sleep apnea without hypoxemia at night (3.1 +/- 1.5 X 10(-8) M) (P less than 0.01). In addition plasma adenosine levels were significantly correlated with two indexes of nocturnal hypoxemia (desaturation index rs = 0.79, and median oxyhemoglobin saturation during sleep rs = -0.75, P less than 0.01). Plasma adenosine markedly fell to a normal level in the only two patients with sleep apnea who had successful treatment of their multiple apneas and accompanying severe hypoxemia during sleep.

Adenosine↗

PubMed1989

Does acute hypoxemia blunt sympathetic activity in hyperthermia?

Sympathetic alpha-adrenergic function is depressed by hypoxemia per se; does addition of another sympathoexcitatory stimulus elicit normal responses in other sympathetic effector pathways? We activated by hyperthermia four sympathetic pathways: alpha-adrenergic [norepinephrine (NE) release], beta-adrenergic [plasma renin activity (PRA)], cholinergic (sweating), and peptidergic (active vasodilation). In the first test, five normothermic men were exposed to hypoxemia for 10 min (control), then hypoxemia plus heat for 30 min, and then heat with normoxia for 8-10 min over a continuous 48- to 50-min period. Heating was controlled with a water-perfused suit. Time courses and magnitudes of heat-induced increments in body temperature, forearm blood flow, and sweat rate were normal during hypoxemia and unaffected by switching to normoxia. Hypoxemia exaggerated increases in plasma NE, epinephrine, PRA, and heart rate but had no additional effects on blood pressure. In a second 50-min test (2 men) with normoxic control (10 min), heating plus normoxia (20 min), and heating plus hypoxemia (20 min), effects of hypoxemia on all variables were as in the first test. Thus, acute moderate hypoxemia did not blunt active cutaneous vasodilation or sweating and exaggerated increases in catecholamines and heart rate, indicating maintained peripheral autonomic function.

Acute Disease↗

PubMed1994

Effect of maternal hypoxemia on behavior in unanesthetized normoxic or mildly hyperoxic fetal lambs.

To determine whether hypoxemia inhibits fetal activity by substances from the mother or placenta, six fetal lambs were chronically instrumented at 128-132 days gestation for extra-corporeal membrane oxygenation (ECMO). Severe maternal hypoxemia (arterial PO2 decreased to 6.00 +/- 0.60 kPa) was produced while fetal arterial PO2 was maintained normoxic or mildly hyperoxic using ECMO. The incidences of fetal breathing movements were 34.8 +/- 3.1% (SE) during baseline before ECMO, 36.8 +/- 3.4% during baseline with ECMO, and 21.4 +/- 3.5% (P < 0.05 compared with baseline with ECMO) during maternal hypoxemia. The durations of periods of breathing were 9.8 +/- 1.2 min before ECMO, 9.3 +/- 1.1 min with ECMO, and 10.5 +/- 1.7 min (P = NS) during maternal hypoxemia. In 7 of 14 maternal hypoxemia experiments, breathing activity stopped too late (7-23 min) to be attributed to maternal hypoxemia. Fetal electrocorticographic activity (P = NS), nuchal electromyographic activity (P = NS), and eye movements were normal before ECMO, with ECMO, and during maternal hypoxemia. Fetal blood pressure and heart rate did not change. We conclude that the inhibition of fetal activity during maternal hypoxemia does not seem to be mediated by release of factors from the maternal side of the placenta or the ewe.

Animals↗

PubMed2000

Age-dependent core temperature responses of conscious rabbits to acute hypoxemia.

Experiments were carried out on chronically instrumented newborn and older rabbits to characterize their core temperature (T(c)) responses to acute hypoxemia and to differentiate "forced" vs. "regulated" thermoregulatory responses. Three age ranges of kits were studied: 4-6, 9-11, and 28-30 days of age. During an experiment, T(c), selected ambient temperature (T(a)), and oxygen consumption were measured from kits studied in a thermocline during a control period of normoxemia, an experimental period of normoxemia or hypoxemia (fraction of inspired oxygen 0.10), and a recovery period of normoxemia. We reasoned that no change or a decrease in T(a) while T(c) decreased during hypoxemia would indicate a regulated thermoregulatory response, whereas an increase in T(a) while T(c) decreased during hypoxemia would indicate a forced thermoregulatory response. T(c) decreased during acute hypoxemia in the older kits but not in the 4- to 6-day-old kits; the decrease in T(c) was accentuated on postnatal days 28-30 compared with postnatal days 9-11. T(a) decreased or stayed the same during exposure to acute hypoxemia. Our data provide evidence that postnatal maturation influences the T(c) response of rabbits to acute hypoxemia and that the decrease in T(c) during hypoxemia in the older kits results from a regulated thermoregulatory response.

Acute Disease↗

PubMed2001

Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses.

Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial PCO2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial PO2 values were significantly (P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar PO2, as arterial PCO2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.

Animals↗

PubMed1987

Acidemia potentiates the plasma catecholamine response to hypoxemia in fetal sheep.

Though hypoxemia has been shown to stimulate adrenal medullary catecholamine (CA) release and raise plasma CA concentrations, the extent to which concomitant acidosis influences the magnitude of this response is unclear. Eleven chronically catheterized late gestation (0.8 term) fetal lambs in utero were investigated during a baseline control period and following the onset of umbilical cord constriction-induced hypoxemia (PO2 = 5-15 Torr). Plasma CA rose in response to hypoxemia in all animals but was potentiated by the development of acidemia. Baseline norepinephrine (NE = 487 +/- 113 pg/cm3 and increased to 1,386 +/- 127 pg/cm3 (p less than 0.001) in response to hypoxemia. Hypoxemia combined with acidemia promoted an even greater rise in NE to 6,726 +/- 1,289 pg/cm3 (p less than 0.05). Plasma epinephrine (E) = 99 +/- 36 pg/cm3 during baseline observations and increased to 512 +/- 81 pg/cm3 (p less than 0.001) in response to hypoxemia. However, an additional 9-fold increase (p less than 0.05) was noted when hypoxemia was combined with acidemia (E = 4,311 +/- 1,449 pg/cm3). Thus, acidosis significantly potentiates the magnitude of the plasma CA response to hypoxemia in the late gestation fetus.

Acidosis↗

PubMed1994

Cerebral blood flow autoregulation after moderate hypoxemia in the newborn piglet.

The isotope-labelled microsphere method was used to study blood flow autoregulation in the brainstem (BS), cerebellum (CBL), cerebrum (CBR) and choroid plexus (ChPl) in 21 newborn piglets exposed to hypoxemia and/or hypovolemia. One group of piglets (n = 7) was made hypoxemic by breathing 10% O2 for 10 min, a second group (n = 8) was studied during hypoxemia (10% O2, 10 min), followed by hypovolemia (bleeding 20% of estimated blood volume). A third group of piglets (n = 6) was made hypovolemic by bleeding 20%. Hypoxemia significantly impaired the autoregulatory capacity in CBL and CBR resulting in a pressure-passive flow pattern. Hypovolemia alone did not produce any significant cerebral vascular response in BS, CBL and CBR, not even when hypovolemia was preceded by hypoxemia, indicating a rapid restoration of the autoregulatory capacity of the cerebral vasculature after hypoxemia of moderate duration. The hypotension seen both during hypoxemia and hypovolemia was gradually compensated for and normalized within 60 min. However, animals exposed to both hypoxemia and hypovolemia were still hypotensive 60 min after the hypoxemic insult. Cardiac output (CO) was not affected by hypoxemia, but was consistently reduced in hypovolemia. We therefore speculate that in the newborn a reduced CO might be a more specific parameter for hypovolemia than a low blood pressure.

Animals↗

PubMed1981

Developmental aspects of the renal response to hypoxemia in the lamb fetus.

The effects of fetal hypoxemia on renal hemodynamics and renal function were studied in two groups of chronically catheterized young (< 120 days of gestation) and near-term lamb fetuses (> 130 days). Fetal hypoxemia produced, in both groups, a significantly decrease in renal blood flow (RBF) and a significant increase in the filtration fraction. However, the glomerular filtration rate (GFR) did not change significantly suggesting that the renal vasoconstriction associated with fetal hypoxemia was more important at the efferent than at the afferent arteriolar level. In the group of near-term fetuses, the decrease in RBF correlated closely with changes in plasma renin activity (PRA) (r = 0.77). No changes in PRA were observed during hypoxemia in the group of young fetuses. After hypoxemia, reactive hyperemia associated with a significant increase in urinary prostaglandin excretion (PGE and PGF2 alpha) was observed in near-term fetuses but not in young fetuses. It also was demonstrated that fetal hypoxemia produced a significant increase in fetal plasma concentrations of vasopressin associated with an antidiuresis in all but one near-term fetus and in 50% of the young fetuses, suggesting that the ability of the fetal kidney to reabsorb free water is more developed in near-term fetuses. Finally, fetal hypoxemia had no effect on mean arterial pressure and heart rate in young fetuses; however, in near-term fetuses, a significant increase in blood pressure and a decrease in heart rate were observed. In summary, it appears that the response of the fetal kidney to hypoxemia depends on the degree of fetal maturation.

Animals↗

PubMed1973

Effects of splenectomy and beta-adrenoceptor blockade on cardiac output response to acute hypoxemia.

Acute hypoxemia produced by the inhalation of 8% and 5% oxygen increased cardiac output in intact anesthetized dogs by 38% and 62%, respectively. Although practolol, a cardioselective beta-adrenergic blocking agent, reduced the increase in cardiac output in dogs subjected to severe hypoxemia (5% O(2) breathing) from 62% to 43%, it only slightly reduced the cardiac output rise in dogs subjected to moderate hypoxemia (8% O(2) breathing). Splenectomy, on the other hand, abolished the increase in cardiac output produced by moderate hypoxemia except for a small initial rise, but it reduced the increase in cardiac output during severe hypoxemia only to 37%. The entire increase, except for a small initial rise, disappeared only when splenectomized dogs were pretreated with practolol. Sham operation did not affect the cardiac output response to hypoxemia. It is concluded that an intact spleen is required for a significant portion of the increased cardiac output that occurs during both moderate and severe hypoxemia and that catecholamines do not participate in the regulation of cardiac output unless severe hypoxemia occurs.

Adrenergic beta-Antagonists↗

PubMed1991

Vascular lactic acid infusions do not alter the incidence of fetal breathing movements or their inhibition by acute hypoxemia.

Hypoxemia transiently inhibits the incidence of fetal breathing movements (FBM), but their incidence returns to normal after several hours despite maintained hypoxemia. We hypothesized that the lactic acidosis associated with prolonged systemic hypoxemia might mediate the adaptation of the hypoxemic inhibition of FBM. In sheep fetuses, the incidence of FBM was measured in a control hour and during 6 h of i.v. infusion of L-lactic acid, which raised the blood lactate concentrations to levels seen with moderate hypoxemia. FBM were observed at the same incidence as during control during each of the first 4 h (all approximately 40%). In the 5th h of lactic acid infusion, fetal hypoxemia was induced by lowering maternal inspired oxygen fraction and FBM occurred only 8 +/- 1% (SEM) of that hour. In a subsequent normoxemic recovery hour, the incidence of FBM remained below control levels. In the same animals on a different day, a similar hypoxemia induced without the acid infusion caused a comparable inhibition of FBM, but the incidence of FBM returned to the control level in a subsequent recovery hour. A moderate peripheral lactic acidosis does not blunt the inhibition of FBM evoked by acute hypoxemia and is not a likely explanation for the return of FBM during prolonged hypoxemia but actually might mediate some of the inhibition.

Acidosis, Lactic↗

PubMed1998

Pulmonary hemodynamics and plasma endothelin-1 during hypoxemia and reoxygenation with room air or 100% oxygen in a piglet model.

The immediate effect on the pulmonary circulation of reoxygenation with either room air or 100% O2 was studied in newborn piglets. Hypoxemia was induced by ventilation with 8% O2 until base excess was <-20 mmol/L or mean arterial blood pressure was <20 mm Hg. Reoxygenation was performed with either room air (n = 9) or 100% O2 (n = 9). Mean pulmonary artery pressure increased during hypoxemia (p = 0.012). After 5 min of reoxygenation, pulmonary artery pressure increased further from 24 +/- 2 mm Hg at the end of hypoxemia to 35 +/- 3 mm Hg (p = 0.0077 versus baseline) in the room air group and from 27 +/- 3 mm Hg at the end of hypoxemia to 30 +/- 2 mm Hg (p = 0.011 versus baseline) in the O2 group (NS between groups). Pulmonary vascular resistance index increased (p = 0.0005) during hypoxemia. During early reoxygenation pulmonary vascular resistance index decreased rapidly to values comparable to baseline within 5 min of reoxygenation in both groups (NS between groups). Plasma endothelin-1 (ET-1) decreased during hypoxemia from 1.5 +/- 0.1 ng/L at baseline to 1.2 +/- 0.1 ng/L at the end of hypoxemia (p = 0.003). After 30 min of reoxygenation plasma ET-1 increased to 1.8 +/- 0.3 and 1.5 +/- 0.2 ng/L in the room air and O2 groups, respectively (p = 0.0077 in each group versus end hypoxemia; NS between groups). We conclude that hypoxemic pulmonary hypertension and plasma ET-1 normalizes as quickly when reoxygenation is performed with room air as with 100% O2 in this hypoxia model with newborn piglets.

Acid-Base Equilibrium↗