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Results for “hypoxemia”

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PubMed2000

Secondary hypoxemia exacerbates the reduction of visual discrimination accuracy and neuronal cell density in the dorsal lateral geniculate nucleus resulting from fluid percussion injury.

The purpose of this study was to determine the impact of secondary hypoxemia on visual discrimination accuracy after parasagittal fluid percussion injury (FPI). Rats lived singly in test cages, where they were trained to repeatedly execute a flicker-frequency visual discrimination for food. After learning was complete, all rats were surgically prepared and then retested over the following 4-5 days to ensure recovery to presurgery levels of performance. Rats were then assigned to one of three groups [FPI + Hypoxia (IH), FPI + Normoxia (IN), or Sham Injury + Hypoxia (SH)] and were anesthetized with halothane delivered by compressed air. Immediately after injury or sham injury, rats in groups IH and SH were switched to a 13% O2 source to continue halothane anesthesia for 30 min before being returned to their test cages. Anesthesia for rats in group IN was maintained using compressed air for 30 min after injury. FPI significantly reduced visual discrimination accuracy and food intake, and increased incorrect choices. Thirty minutes of immediate posttraumatic hypoxemia significantly (1) exacerbated the FPI-induced reductions of visual discrimination accuracy and food intake, (2) further increased numbers of incorrect choices, and (3) delayed the progressive recovery of visual discrimination accuracy. Thionine stains of midbrain coronal sections revealed that, in addition to the loss of neurons seen in several thalamic nuclei following FPI, cell loss in the ipsilateral dorsal lateral geniculate nucleus (dLG) was significantly greater after FPI and hypoxemia than after FPI alone. In contrast, neuropathological changes were not evident following hypoxemia alone. These results show that, although hypoxemia alone was without effect, posttraumatic hypoxemia exacerbates FPI-induced reductions in visual discrimination accuracy and secondary hypoxemia interferes with control of the rat's choices by flicker frequency, perhaps in part as a result of neuronal loss and fiber degeneration in the dLG. These results additionally confirm the utility of this visual discrimination procedure as a sensitive, noninvasive means of assessing behavioral function after experimental traumatic brain injury.

Animals↗

PubMed1996

A comparative study of early postoperative hypoxemia in infants, children, and adults undergoing elective plastic surgery.

To determine the influence of age on postoperative hypoxemia, we studied postoperative hypoxemia in 1152 patients, from infants to adults, ASA physical status I, undergoing elective plastic surgery. Subjects were divided into four groups on the basis of age: Group 1, infants aged 1 yr or less (n = 108); Group 2, children aged 1-3 yr (n = 240); Group 3, children aged 3-14 yr (n = 482); and Group 4, adults aged 14-58 yr (n = 322). Arterial oxygen saturation (Spo2) levels were recorded while patients were breathing room air in the postanesthesia recovery room shortly after arrival (0 min), and 5, 10, 15, 20, 30, 40, 50, 60, 120, and 180 min thereafter. Younger patients showed lower Spo2 levels and a higher incidence of hypoxemia during the early postoperative period. The incidences of hypoxemia (Spo2 = 86%-90%) and severe hypoxemia (Spo2 < or = 85%) in the recovery room were 30.6% and 16.7%, respectively, in Group 1, 20.0% and 10.0% in Group 2, 14.1% and 3.3% in Group 3, and 7.8% and 0.6% in Group 4. Hypoxemia occurred most commonly within 1 h after anesthesia, particularly during the first 40 min in infants and during the first 15 min in older children and adults. A significant correlation was found by linear regression analysis between low Spo2 levels on admission to the recovery room and children's age. Thereafter, Spo2 levels and the incidence of hypoxemia during the early postoperative period were related only to infants' recovery scores.

Adolescent↗

PubMed1981

Respiratory and cardiovascular responses to hypoxemia and the effects of anesthesia.

The normoxic ventilatory drive contributes to the normal level of ventilation, and the hypoxic ventilatory drive contributes to the maintenance of adequate gas exchange in the presence of ventilation/blood flow maldistribution and increased mechanical load to breathing. This respiratory drive arises principally from stimuli at the carotid chemoreceptors. The reflex cardiovascular responses to hypoxia also contribute to the delivery of O2 to vital organs, and their efficacy depends on the integrity of the respiratory response and the autonomic nervous system as well as the function of the vascular system. Prolonged exposure to hypoxemia from altitude, cyanotic congenital heart disease, and chronic pulmonary disease impair the ventilatory response to hypoxia. In addition, the respiratory and cardiovascular responses to hypoxemia are impaired by familial or acquired abnormalities of the autonomic effector system. There is growing evidence that impaired respiratory response to hypoxemia is a major factor in recurrent respiratory failure in obesity, obstructive pulmonary disease, idiopathic or familial "hypoventilation," and contributes to disturbances in oxygenation during sleep [152, 189, 192, 202]. Although the ventilatory response to hypoxemia was traditionally thought to be resistant to the effects of inhalational anesthetics, barbiturates, and narcotics, there is abundant evidence that in fact the ventilatory response to hypoxia is more sensitive to depression by drugs than the ventilatory response to CO2. In addition, the hemodynamic responses to hypoxia are modified by anesthesia and anesthetic techniques. The clinical implications of these observations are wide. The ventilatory and cardiovascular response to hypoxemia will be altered, and usually depressed by age, disease processes, premedicant and anesthetic drugs, and autonomic blocking drugs. The cardiovascular responses will be modified indirectly by altered ventilatory control due to neuromuscular blocking drugs and controlled ventilation. Thus, not only will the responses to hypoxemia be depressed by anesthesia but the early clinical hemodynamic signs will be modified or absent, or indeed the cardiovascular response will further impair oxygen delivery. Furthermore, it is not only anesthetic doses that impair the reflex respiratory responses, but also subanesthetic doses of inhalational anesthetics and premedicant doses of barbiturates and narcotics. Hence the patient in the perioperative period continues to have impaired respiratory response to hypoxemia. As anesthetic and surgical care extends to older patients, patients with systemic disease, and recipients of cardiovascular peripheral and central drugs, the clinical implications of the impairment of ventilatory and cardiovascular responses to hypoxia, and the maintenance of organ and system function, escalate. Only a few hesitant steps have been taken into this vast arena of clinical and experimental research.

Age Factors↗

PubMed1997

Effects of hypoxemia on early postoperative course of liver transplantation in pediatric patients with intrapulmonary shunting.

Nine pediatric patients (mean age, 10 years) with biliary atresia, who had hypoxemia related to intrapulmonary shunting, underwent living related liver transplantation. The effects of hypoxemia during the early postoperative period after liver transplantation on cardiopulmonary and renal function, as well as on transplanted liver, were analyzed. Based on the degree of shunt ratio calculated by technetium-99m macroaggregated albumin scintigraphy, the nine patients were included in the moderate group (shunt ratio under 40%, n=4) or the severe group (shunt ratio over 40%, n=5). Partial pressure of arterial oxygen was maintained at normal range in the moderate group, while that in the severe group persistently had very low values (<50 mmHg), in spite of a high degree of oxygen supply. However, all patients in the severe group maintained stable cardiopulmonary vital signs, including systemic blood pressure, heart rate, respiratory rate, and cardiac index. They also demonstrated stable renal function. None of the patients died of cardiopulmonary or renal insufficiency after transplantation, but three patients died of portal vein thrombosis, sepsis, and intracranial hemorrhage (one each). The minimal adverse effect of hypoxemia on the transplanted liver was confirmed by a rapid increase of arterial ketone body ratio, low peak values (under 200 IU/L) of aspartate aminotransferase, and a steady decrease of serum total bilirubin. Four patients encountered surgical complications, including two bile leaks from the cut liver surface, two leaks from bilioenteric anastomosis, and one intestinal perforation. Six patients suffered from bacterial infections, including four wound infections, three right subphrenic abscesses, one cholangitis, and two systemic sepses. All patients in the moderate group recovered from hypoxemia, but four of five patients in the severe group have not recovered during the follow-up period between 4 and 9 months. It was concluded that the adverse effects of hypoxemia on cardiopulmonary and renal function and transplanted liver were minimal, so that patients with severe hypoxemia could tolerate the stress of liver transplantation without special management. However, the high incidence of surgical complication and infection suggested the adverse effects of hypoxemia on wound healing and resistance to bacteria infection.

Adolescent↗

PubMed1986

Intestinal blood flow and O2 uptake during hypoxemia in the newborn piglet.

Previous work has indicated that the neonatal intestinal circulation responds to hypoxemia with vasoconstriction and subsequent intestinal ischemia. This work was carried out in newborn lambs, a ruminant species, and may not be representative of all newborns. Therefore, we measured intestinal blood flow, vascular resistance, tissue O2 uptake, and cardiac output during normoxemia and varying degrees of hypoxemia in newborn piglets, a nonruminant species. Hypoxemia was induced by adding N2 gas to the inspired gas mixture, and measurements were obtained over a wide range of arterial O2 contents (2.2-15.6 ml O2 X dl-1). Intestinal blood flow increased in response to moderate hypoxemia and decreased in response to severe hypoxemia. The changes in intestinal blood flow were primarily due to change in intestinal vascular resistance, not cardiac output. Intestinal O2 was independent of arterial O2 content until the latter decreased below approximately 6.5 ml O2 X dl-1. These data indicate that the response of the neonatal intestinal circulation to hypoxemia is species specific and that the nonruminant neonatal intestine is capable of vasodilation in response to moderate hypoxemia.

Animals↗

PubMed2006

Development of the ovine fetal cardiovascular defense to hypoxemia towards full term.

We tested the hypothesis that fetal cardiovascular responses to hypoxemia change close to full term in relation to the prepartum increase in fetal basal cortisol and investigated, in vivo, the neural and endocrine mechanisms underlying these changes. Fetal heart rate and peripheral hemodynamic responses to 1 h of hypoxemia were studied in 25 chronically instrumented sheep within three narrow gestational age ranges: 125-130 (n = 13), 135-140 (n = 6), and >140 (n = 6) days (full term approximately 145 days). Chemoreflex function and plasma concentrations of vasoconstrictor hormones were measured. Reductions in fetal arterial Po(2) during hypoxemia were similar at all ages. At 125-130 days, hypoxemia elicited transient bradycardia, femoral vasoconstriction, and increases in plasma concentrations of catecholamines, neuropeptide Y (NPY), AVP, ACTH, and cortisol. Close to full term, in association with the prepartum increase in fetal basal cortisol, there was a developmental increase in the magnitude and persistence of fetal bradycardia and in the magnitude of the femoral constrictor response to hypoxemia. The mechanisms mediating these changes close to full term included increases in the gain of chemoreflex function and in the magnitudes of the fetal NPY and AVP responses to hypoxemia. Data combined irrespective of gestational age revealed significant correlations between fetal basal cortisol and fetal bradycardia, femoral resistance, chemoreflex function, and plasma AVP concentrations. The data show that the fetal cardiovascular defense to hypoxemia changes in pattern and magnitude just before full term because of alterations in the gain of the neural and endocrine mechanisms mediating them, in parallel with the prepartum increase in fetal basal cortisol.

Acid-Base Equilibrium↗

PubMed1982

Fetal myocardial oxygen and carbohydrate consumption during acutely induced hypoxemia.

Two days after catheter placement we measured the heart rate, arterial blood pressure, myocardial blood flow, and the myocardial consumption of oxygen, glucose, lactate, and pyruvate in 11 fetal sheep in utero. We then administered 8-10% oxygen to the ewe, producing a 50% decrease in oxygen content in the fetal ascending aortic blood. After 15 min of hypoxemia we repeated the measurements. Oxygen content in the fetal coronary sinus blood decreased significantly, but the arteriovenous difference of oxygen across the left ventricle also decreased during hypoxemia. Fetal myocardial blood flow increased 160% above the control level, and the myocardial oxygen consumption did not change. The systolic arterial blood pressure increased and the heart rate decreased, but cardiac work, as estimated by the rate-pressure product, was unchanged. As both fetal myocardial oxygen consumption and cardiac work did not change, myocardial oxygenation, the relationship between oxygen consumption and cardiac work, appears to be unchanged during this degree of hypoxemia. Although arterial blood glucose, lactate, and pyruvate concentrations increased significantly during hypoxemia, only the myocardial consumption of pyruvate increased; the arteriovenous difference of glucose and lactate decreased in proportion to the increase in myocardial blood flow. During hypoxemia, glucose consumption did not change, and lactate continued to be consumed rather than produced; thus it is apparent that fetal myocardial metabolism continued to be aerobic during this degree of hypoxemia. Complete oxidative combustion of the quantities of carbohydrates that were consumed would supply all of the substrate necessary to meet fetal myocardial energy demands both at rest and during hypoxemia.

Animals↗

PubMed1995

Hypoxemia in the absence of blood loss or significant hypotension causes inflammatory cytokine release.

Although hemorrhagic shock causes a significant elevation of circulating levels of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6], it remains unknown whether hypoxemia per se in the absence of blood loss activates macrophages (Mø) to release increased amounts of these mediators. To study this, hypoxemia was induced in C3H/HeN mice by placing them in a plastic box that was flushed with a gas mixture containing 95% N2-5% O2 for 60 min, followed by return of the mice to room air. For control animals, the plastic box was flushed with room air. At 0, 2, or 24 h thereafter, blood samples were obtained, plasma was separated, and then peritoneal Mø (pMø) and Kupffer cells (KC) were isolated and incubated at 37 degrees C for 24 h with lipopolysaccharide. The Mø supernatants, as well as plasma samples, were assayed for TNF-alpha, IL-1 beta, and IL-6 with the use of specific bioassays. Hypoxemia induced a significant (P < 0.05) increase in plasma TNF-alpha levels during the entire study period while circulating IL-6 was elevated by 313% (P < 0.01) at 24 h after hypoxemia compared with shams. Moreover, the release of TNF-alpha, IL-1 beta, and IL-6 by pMø and KC was markedly increased after hypoxemia compared with shams. Thus, hypoxemia in itself, in the absence of any blood loss or tissue injury, induces release of proinflammatory cytokines, which may contribute to systemic inflammation following hypoxemia.

Animals↗

PubMed2003

Enhanced umbilical blood flow during acute hypoxemia after chronic umbilical cord compression: a role for nitric oxide.

BACKGROUND: The continuing incidence of intrapartum morbidity may be partly due to antenatal compromise, which influences the fetal defense to labor and delivery. We have shown that antenatal exposure of the ovine fetus to partial compression of the umbilical cord suppresses femoral vasoconstriction during subsequent acute hypoxemia through elevated nitric oxide (NO) activity. This study investigated whether elevated NO activity in cord-compressed fetuses enhanced the vasodilator response to hypoxemia in circulations in which blood flow is known to increase during acute hypoxemia, such as the umbilical vascular bed. METHODS AND RESULTS: Fifteen fetal sheep were chronically instrumented between 117 and 120 days of gestation with vascular catheters and an umbilical flow probe. In 8 of these fetuses, umbilical blood flow was reduced by 30% for 3 days between 125 and 128 days. The remaining 7 fetuses acted as sham-operated controls. Between 2 and 7 days after umbilical cord/sham compression, fetuses were exposed to 2 episodes of acute hypoxemia, on separate days, during infusion with either saline or treatment with a combination of NG-nitro-l-arginine methyl ester and sodium nitroprusside. The data show that umbilical cord compression significantly enhances the umbilical hyperemia through NO-dependent mechanisms during a subsequent episode of acute hypoxemia. CONCLUSIONS: Increased fetal NO activity after chronic cord compression has opposing effects in circulations that either constrict or dilate during subsequent acute hypoxemia. The data imply that antenatal compromise switches the fetal strategy to withstand episodes of subsequent acute hypoxemia of the type that may occur during labor and delivery from a reliance on vasoconstrictor mechanisms to those promoting NO-dependent vasodilation.

Acute Disease↗

PubMed1979

Prostaglandin control of the renal circulation in response to hypoxemia in the fetal lamb in utero.

We studied the effects of 10-minute periods of hypoxemia in unanesthetized fetal lambs in utero instrumented for measurements of arterial pressure and renal and iliac blood flows. Fetal hypoxemia, induced by delivering a hypoxic gas mixture to the ewe, was characterized by a reduction in fetal PaO2 from 20.1 +/- 1.4 to 8.8 +/- 1.0 mm Hg (mean +/- SE). The fetus responded with bradycardia and persistent vasoconstriction in the iliac bed throughout the 10-minute period. In contrast, renal resistance rose significantly only at the end of the hypoxemic period. After 5-7 minutes of hypoxemia, when iliac flow had fallen by 40 +/- 4% and iliac resistance had risen by 86 +/- 13%, renal flow and resistance were not changed significantly from control; in fact, we found that renal flow rose substantially at this time in several fetal lambs. After blockade of prostaglandin synthesis with either indomethacin or meclofenamate, renal flow fell after 5-7 minutes of hypoxemia by 36 +/- 5%. The reduction in renal flow and increases in renal resistance were significantly greater than was observed prior to blockade of prostaglandin synthesis. Thus, fetal hypoxemia elicits bradycardia and intense peripheral vasoconstriction reflected by the changes in the iliac bed, with relative sparing of the reanl bed. The relative protection of the renal bed during fetal hypoxemia appears to be related to a mechanism involving prostaglandins, since after blockade of prostaglandin synthesis, hypoxemia results in intense renal vasoconstriction.

Animals↗

PubMed1981

Postnatal age-related renal responses to hypoxemia in lambs.

The role of normocapnic hypoxemia (arterial PO2 33 +/- 7 torr for 30 minutes) in asphyxial renal failure and its modification by maturation of renal function was studied in 50 chronically catheterized, unanesthetized lambs of 2-38 days postnatal age. Arterial pH and PCO2 did not change significantly in response to hypoxemia in these lambs. Normocapnic hypoxemia was associated with (1) significant percent increases in arterial serum osmolality (1.82 +/- 2.96%, P = 0.0001), arterial blood lactate concentration (1009 +/- 2092%, P = 0.0018), arterial blood hematocrit (6 +/- 12%, P = 0.0016), arterial hemoglobin concentration (4.6 +/- 6.5%, P = 0.0004), arterial plasma vasopressin (2370 +/- 3340%, P = 0.0001), arterial plasma renin activity (153 +/- 230%, P = 0.0001), arterial plasma aldosterone (91.3 +/- 143%, P = 0.0001), and fractional sodium excretion rate (120 +/- 240%, P = 0.007); and (2) significant percent decline in glomerular filtration rate (-22.6 +/- 32.6%, P = 0.0003). Several responses to hypoxemia correlated significantly with postnatal age, including (1) positive correlation of postnatal age with percent change in blood osmolality (r = 0.36, P = 0.010), hematocrit (r = 0.48, P = 0.0005), hemoglobin (r = 0.59, P = 0.0004), and lactate (r = 0.72, P = 0.0001), suggesting greater water movement from the intravascular compartment in response to hypoxemia in more mature lambs; and (2) positive correlation of postnatal age with change in urinary flow rate (r = 0.66, P = 0.0001), urinary sodium excretion rate (r = 0.65, P = 0.0001), and osmolar clearance rate (r = 0.60, P = 0.0002), suggesting a greater effect of hypoxemia on the renal tubules to decrease sodium reabsorption in more mature kidneys. Thus, normocapnic hypoxemia may play a role in asphyxial renal failure, and the immature kidney does not have increased susceptibility to this condition.

Aging↗

PubMed1986

The effect of furosemide during normoxemia and hypoxemia.

The effect of furosemide infusion was studied in 6 normal subjects and 6 patients with severe COPD and right ventricular failure during normoxemia and hypoxemia. In normal subjects, hypoxemia alone caused an insignificant (p less than 0.15) fall in plasma aldosterone concentrations (PAC). Intravenously administered furosemide resulted in significant (p less than 0.05) increases in PAC during both normoxemia and hypoxemia. After furosemide treatment mean arterial pressure (MAP) was significantly lower and arginine vasopressin (AVP) was significantly higher (p less than 0.05) with hypoxemia than with normoxemia. These changes in MAP and AVP were strongly correlated (r = -0.84). Urinary losses of water and sodium were similar after furosemide treatment with hypoxemia and normoxemia. In patients with right ventricular failure, neither changes in oxygenation nor furosemide infusion affected the markedly elevated baseline PRA and PAC levels. Arginine vasopressin levels were significantly higher with hypoxemia than with normoxemia, but urinary losses of water and salt did not differ between the 2 study days. We conclude that hypoxemia does not affect the PAC increase or urinary volume and sodium response to furosemide.

Adult↗

PubMed1982

Power spectral analysis of the neonatal primate electroencephalogram during acute hypoxemia.

The effect of acute graded hypoxemia on the electroencephalogram (EEG) of five prematures and five full term Macaca nemestrina in the neonatal period was determined using power spectral analysis--a technique that obviates the limitations of visual inspection. The EEG of selected epochs was analyzed by a Fast Fourier Transform program (POWER) during the 20 min of each trial of hypoxemia and compared with simultaneous arterial oxygen tensions. Levels of hypoxemia were graded as profound (PaO2=15-25 Torr); severe (PaO2=26-35 Torr), moderate (PaO2=36-50 Torr), or mild (PaO2=51-75 Torr). The EEG during normoxemia had a band width of 0.5 to 10 Hz and a peak power at 1-3 Hz. During mild hypoxemia, an increase in power in the delta range (0-3.5 Hz) occurred in the oldest animals. At moderate hypoxemia, the youngest animals showed a depression of absolute power in the delta band. A slowing of the EEG and decrease in power in the theta frequency range (4-8 Hz) followed when severe hypoxemic levels are reached. During profound hypoxemia, all animals at each postnatal age exhibited a significant decrease in EEG power at the delta and theta frequencies (P less than 0.025) except 3-wk-old full term animals in which there was no significant change in the delta band. These results clarify and extend previously reported effects of hypoxemia on the neonatal EEG.

Animals↗

PubMed1983

Effects of ambient temperature on oxygen consumption and the circulation in newborn lambs at rest and during hypoxemia.

To assess the effects of environmental temperature on responses to hypoxemia, we studied five unsedated lambs in the first week after birth. We catheterized the carotid artery and pulmonary artery (via the jugular vein). After recovery of at least 1 day, we measured pH, blood gases, arterial and mixed venous blood O2 content, oxygen consumption (VO2), heart rate, carotid and pulmonary arterial pressures, and cardiac output in both warm (25 degrees C) and cool (17.4 +/- 1.1 degree C) environments. In the cool environment, with no shivering, VO2 increased 40% (14.9 to 20.8 ml/kg/min). There were also increases of arteriovenous blood O2 content difference of 19%, cardiac output of 18%, and heart rate of 14%. In four lambs, we studied the same variables during hypoxemia (FiO2 = 0.09 for 1 h) at both temperatures. In the cool environment, hypoxemia produced a greater fall of VO2 (26% versus 6%) and arteriovenous oxygen differences (30% versus 19%) and a smaller increase of cardiac output (8% versus 14%) and heart rate (26% versus 43%). Also in the cool environment, core temperature decreased more (2.1 versus 0.4 degree C), but base deficit was the same (-6 versus -5 mEq/liter). Despite the greater fall in VO2 during hypoxemia in the cool environment, the lowest value achieved was still higher than the level during normoxemia in the warm environment. Similarly, cardiac output during hypoxemia was greater in the cool than in the warm environment. These findings may explain the variability in reported normal resting values and responses to hypoxemia. Contrary to previous reports, they also indicate that during severe hypoxemia neonates have a decreased reserve of metabolic and cardiovascular responses in a cool compared with a warm environment.

Animals↗

PubMed1984

Factors controlling aldosterone secretion during hypoxemia in fetal lambs.

Factors modulating the fetal aldosterone response to hypoxemia were studied in three groups of chronically catheterized fetal lambs between 131 and 143 days of gestation (term, 145 days). One group (control group) received an infusion of 5% dextrose in water; the second group (captopril-treated group) was given captopril, an inhibitor of angiotensin-converting enzyme; the third group (captopril plus dexamethasone-treated group) received dexamethasone in addition to captopril. In all groups of fetuses, hypoxemia was associated with a significant increase in plasma K+ concentration (+0.7 +/- 0.1 meq/liter). In control fetuses, changes in plasma aldosterone concentration during hypoxemia correlated closely with changes in plasma K+ concentration r = 0.79; P less than 0.001) and with changes in plasma angiotensin II concentration (r = 0.77; P less than 0.001). In the captopril-treated fetuses, the rise in plasma aldosterone concentration during hypoxemia correlated closely with plasma K+ (r = 0.79; P less than 0.001) but not with plasma angiotensin II values (r = 0.17). No significant correlation was found between percent changes in maternal aldosterone and percent changes in fetal aldosterone during hypoxemia and following recovery (r = 0.36; P greater than 0.1) in captopril-treated fetuses. Administration of dexamethasone to fetuses receiving captopril completely inhibited the rise in plasma aldosterone associated with hypoxemia. Taken together, the present results suggest that the rise in plasma aldosterone during hypoxemia is not related to the level of activity of the renin-angiotensin system but depends probably on the increased secretion of adrenocorticotrophin by the fetus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1988

Renal hemodynamic responses to hypoxemia during development: relationships to circulating vasoactive substances.

Chronically catheterized fetal lambs (n = 11, gestational age 111-139 days) and neonatal lambs (n = 20, postnatal age 4-30 days) were studied to explore during development the relationship of renal hemodynamic responses during hypoxemia to plasma epinephrine concentration (E), plasma norepinephrine concentration (NE), plasma arginine vasopressin concentration (AVP), and plasma renin activity (PRA). A low oxygen gas mixture (11.1 +/- 0.1% O2) was administered for 30 min to the pregnant ewe or neonatal lamb to induce hypoxemia with maintenance of normal arterial pCO2 and pH. Arterial blood pressure was recorded continuously and renal blood flow (RBF) was determined by the radiolabeled microsphere technique. Moderate hypoxemia (pO2 16 +/- 2 torr and 33 +/- 6 torr in fetus and neonate, respectively) induced increases in E, NE (measured by radioenzymatic assay), and AVP (measured by radioimmunoassay) in both fetus and neonate. PRA (measured by radioimmunoassay) also increased in response to hypoxemia in neonatal lambs. The change in mean arterial pressure with hypoxemia (delta MAP) was significant in fetuses (delta MAP 8 +/- 14%, p less than 0.05) but not in lambs (delta MAP 1 +/- 10%, p greater than 0.5). Similarly, the change in renal blood flow with hypoxemia (delta RBF) was significant (delta RBF -51 +/- 24%, p less than 0.001) in fetuses but not in neonatal lambs (delta RBF -9 +/- 38%, p greater than 0.1). These results reflected a change in renal vascular resistance with hypoxemia (delta RVR) that was significant in fetal lambs (delta RVR 169 +/- 168%, p less than 0.01) but not in neonatal lambs (delta RVR 51 +/- 180%, p greater than 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1988

Effect of beta-adrenergic receptor blockade on responses to acute hypoxemia in lambs.

We studied the effects of beta-adrenergic receptor blockade on general circulatory and metabolic responses to moderate (FIO2 = 0.09) acute hypoxemia in newborn (protocol 1) and 3-wk-old (protocol 2) lambs, and on regional blood flow distribution in newborn lambs (protocol 1). Via a left thoracotomy we placed an electromagnetic flow transducer around the ascending aorta and inserted various vascular catheters. After 2 days of recovery, the lambs were studied. In protocol 1, we measured cardiovascular variables and regional blood flow distribution during control conditions, after 45 min of acute hypoxemia, and after 0.5 mg/kg of propranolol during acute hypoxemia. In protocol 2, we measured cardiovascular variables during control conditions and after 45 min of acute hypoxemia with and without propranolol pretreatment. In both groups, propranolol limited the increase in cardiac output and heart rate caused by hypoxemia, and thus decreased oxygen delivery. However, propranolol also decreased oxygen consumption so that pulmonary arterial pO2 was either higher (protocol 1) or the same (protocol 2) as during acute hypoxemia alone. Neither metabolic acidosis nor hypothermia ensued. In protocol 1, propranolol decreased renal, carcass, and most importantly, myocardial blood flows. However, myocardial O2 consumption also fell, coronary sinus pO2 increased, and blood was redistributed toward the subendocardium, suggesting that myocardial perfusion improved. Thus, beta-adrenergic receptor blockade during acute moderate hypoxemia may have a beneficial effect by reducing total body and myocardial oxygen demand in excess of the reduction in oxygen delivery.

Acute Disease↗

PubMed1993

Carotid, not aortic, chemoreceptors mediate the fetal cardiovascular response to acute hypoxemia in lambs.

The fetal cardiovascular response to acute hypoxemia consists of a decrease in heart rate, a variable change in mean arterial pressure, and an increase in peripheral vascular resistance. This response is mediated by the arterial chemoreceptors. To determine whether chemoreceptors in the carotid artery or in the aorta mediate the fetal cardiovascular response to acute hypoxemia, we studied the response to acute hypoxemia in fetal lambs at 125 to 130 d of gestation after selective carotid (six fetuses) or aortic (five fetuses) denervation. One to 3 d after insertion of catheters, hypoxemia was induced by inflating a balloon occluder around the ewe's hypogastric artery or by giving the ewe 95% N2 and 5% O2 to breathe. The chemoreflex response was measured as decrease in heart rate per decrease in Hb O2 saturation. To validate our results, we also studied the response to chemical stimulation of the chemoreceptors by injection of sodium cyanide into the inferior vena cava. We found that carotid denervation abolished the heart rate and peripheral vascular resistance responses to hypoxemia but that aortic denervation did not. Responses after injection of sodium cyanide were similar to those seen during acute hypoxemia. We conclude that the carotid chemoreceptors, and not the aortic chemoreceptors, mediate the fetal cardiovascular response to acute hypoxemia.

Animals↗