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PubMed2002

Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats.

In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague-Dawley rats with UCAL were studied during 20 min periods of baseline (FI(O(2))=30%), hypoxemia (FI(O(2))=9.5%) and recovery (FI(O(2))=30%): mean arterial pressure of oxygen (PA(O(2))) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37+/-0.14 and 2.85+/-0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09+/-0.20 Hz (mean+/-S.E.M.) during baseline, which was not reversed during recovery (3.27+/-0.11 Hz) (ANOVA, P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.

Animals↗

PubMedDate not supplied

Effects of adaptation level and hypoglycemia on function of the cat retina during hypoxemia.

Acute hypoxemia (low PaO2) leads to changes in oxygen consumption and electrical responses of the outer retina of cats, but inner retinal ERG components and ganglion cell responses have been shown to be quite resistant to hypoxemia. The purpose of this study was to determine whether the resistance of the inner retina depends on (1) the stimulus conditions, specifically the degree of light adaptation; and (2) the ability of the photoreceptors to increase glycolysis during hypoxemia. To address these issues, recordings of single ganglion cell action potentials and of the b-wave and scotopic threshold response (STR) of the electroretinogram (ERG) were made from the eyes of anesthetized cats during hypoxemia alone and hypoxemia plus hypoglycemia. Ganglion cells appeared to be equally resistant to hypoxemia at high and low backgrounds (3.3 to 9.7 log equivalent quanta(555 nm)-deg-2(-s)-1), and the STR, recorded with dim stimuli during dark adaptation, when photoreceptor oxygen consumption is most susceptible to hypoxemia, was unchanged until PaO2 was below 30 mm Hg. The amplitude of the b-wave was similarly resistant to hypoxemia when the animal was normoglycemic. During hypoglycemia, however, both the b-wave and the STR became more sensitive to hypoxemia, beginning to change at PaO2s as high as 50 mm Hg when blood glucose was 40-50 mg/dl. It is argued that hypoglycemia limits or prevents the increased glycolytic ATP production that would ordinarily occur when the photoreceptor oxygen supply decreases, and that increased photoreceptor glycolysis is essential in the protection of the retina against mild hypoxemia.

Acute Disease↗

PubMed1998

Hypoxemia decreases the shivering threshold in rabbits anesthetized with 0.2 minimum alveolar anesthetic concentration isoflurane.

UNLABELLED: Shivering has been proposed as an etiology of postoperative hypoxemia. The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3 degrees C/h by perfusing water at 10 degrees C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7 degrees C at 130 mm Hg to 35.4 degrees C at 50 mm Hg (threshold = PaO2.0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold >1 C. A 1 C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia. IMPLICATIONS: Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia.

Anesthesia, Inhalation↗

PubMed1999

The influence of surgical sites on early postoperative hypoxemia in adults undergoing elective surgery.

UNLABELLED: To determine the influence of the surgical sites on early postoperative hypoxemia, we studied postoperative hypoxemia in 994 patients, ASA physical status I or II, aged 18-68 yr, scheduled for various types of elective surgery. Patients were divided into three groups on the basis of the surgical sites: Group 1 = elective superficial plastic surgery (n = 288); Group 2 = upper abdominal surgery (n = 452); and Group 3 = thoracoabdominal surgery (n = 254). Anesthesia was maintained with 1%-2% enflurane and 67% nitrous oxide in oxygen; thiopental or fentanyl was given IV as required. SpO2 levels were recorded while patients breathed room air shortly after arrival in the recovery room (0 min) and 5, 10, 15, 20, 30, 40, 50, 60, 120, and 180 min thereafter. The results showed that during the early postoperative period, the degree of arterial desaturation and the incidences of hypoxemia (SpO2 86%-90%) and severe hypoxemia (SpO2 85%) were closely related to the operative sites and were greatest for thoracoabdominal operations, less for the upper abdominal operation, and least for the peripheral surgery. The incidence of hypoxemia and severe hypoxemia in the recovery room was 7% and 0.7%, respectively, in Group 1, 38% and 3% in Group 2, and 52% and 20% in Group 3. Mild airway obstruction and hypothermia in the postanesthesia recovery unit (PAR) were the predictive factors of early postoperative hypoxemia. We conclude that during the early postoperative period, there were significant differences in SpO2 levels and incidences of hypoxemia and severe hypoxemia among the three groups. IMPLICATIONS: We found that the severity of arterial desaturation and the incidence of hypoxemia during the early postoperative period are closely related to the surgical sites and are strongest for thoracoabdominal surgery, less for upper abdominal surgery, and least for peripheral surgery.

Abdomen↗

PubMed1989

Arginine vasopressin mediates cardiovascular responses to hypoxemia in fetal sheep.

Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1996

Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus.

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.

Acid-Base Equilibrium↗

PubMed1986

Acute alterations in diastolic left ventricular chamber distensibility: mechanistic differences between hypoxemia and ischemia in isolated perfused rabbit and rat hearts.

Changes in diastolic chamber distensibility (DCD) during hypoxemia and ischemia were studied in isolated-buffer-perfused rabbit hearts. Two minutes of hypoxemia (low PO2 coronary flow) resulted in a shift of the diastolic pressure-volume curve to the left, i.e., distensibility was decreased (hypoxemic contracture). In contrast, 2 minutes of ischemia (zero coronary flow) resulted in an initial shift of the diastolic pressure-volume curve to the right indicating increased distensibility, which was followed by a later (30 minutes) shift to the left (ischemic contracture). Two minutes of ischemia superimposed on hypoxemia caused complete reversal of contracture. A quick stretch and release applied to the myocardium reversed late ischemic contracture but did not effect early hypoxemic contracture. The role of intracellular pH in modulating changes in DCD during hypoxia and ischemia was studied using phosphorus-31 nuclear magnetic resonance spectroscopy of isolated-buffer-perfused rat hearts that demonstrated changes in DCD similar to rabbit hearts during hypoxemia and ischemia. Intracellular pH decreased from 7.03 +/- 0.02 to 6.87 +/- 0.03 (p less than .01) during 2 minutes of ischemia but did not change significantly during 4 minutes of hypoxemia. When 2 minutes of ischemia were superimposed on hypoxemia, pH decreased from 6.99 +/- 0.01 during hypoxemia to 6.88 +/- 0.02 after 2 minutes of ischemia (p less than .01), concomitant with the complete reversal of hypoxemic contracture. These results suggest different mechanisms for late ischemic and early hypoxemic contracture and also suggest an explanation for the opposite initial changes in DCD seen after brief periods of ischemia and hypoxemia. The early development of contracture during hypoxemia and rapid redevelopment of diastolic tension after quick stretching are consistent with the hypothesis that hypoxemic contracture results from persistent Ca++-activated diastolic tension secondary to impaired calcium resequestration by the sarcoplasmic reticulum. In contrast, the late development of contracture during global ischemia and reversal by quick stretching is compatible with rigor bond formation. The initial increase in distensibility during early ischemia and the reversal of hypoxemic contracture by a brief period of superimposed ischemia probably is the result of two factors present during ischemia but not during hypoxemia: the collapse of the coronary vasculature and loss of the "erectile" effect and, the rapid development of intracellular acidosis, which has been shown to affect myofibrillar calcium sensitivity, and this may lead to a decrease in Ca++ activated diastolic tension.

Acidosis↗

PubMed2004

Maternally administered dexamethasone at 0.7 of gestation suppresses maternal and fetal pituitary and adrenal responses to hypoxemia in sheep.

Women who are at risk of preterm delivery are treated with antenatal steroids to facilitate fetal lung maturation. During this period, there is a potential for fetal or maternal hypoxemia to occur. Fetal responses to hypoxemia in sheep are well documented. However, less is known regarding maternal responses to hypoxemia. Therefore, we determined the effects of dexamethasone (DM) on maternal and fetal responses to hypoxemia in sheep. Ewes received four i.m. injections of DM or saline at 12-h intervals beginning at 103 d of gestation. Samples for ACTH, cortisol, and glucose were collected at 0900 h. At 105 d of gestation, hypoxemia was induced for 1 h by maternal nitrogen gas inhalation. Samples for ACTH, cortisol, and glucose were collected at 15-min intervals before, during, and after the hypoxemia challenge. Fluorescent microspheres were administered to the mother and the fetus before and during hypoxemia to measure organ perfusion. DM suppressed basal fetal and maternal cortisol and ACTH concentrations but increased glucose levels. DM also increased fetal but not maternal blood pressure. In control subjects, hypoxemia elevated fetal and maternal cortisol and ACTH concentrations. These responses were obliterated by DM. Hypoxemia increased blood pressure in DM-exposed fetuses but not in control subjects. In addition, hypoxemia decreased fetal adrenal vascular resistance in saline but not DM fetuses or ewes from either treatment group. In summary, maternal administration of a low dose of DM at 0.7 of gestation suppresses maternal and fetal adrenal function and changes fetal responses to hypoxemic stress to resemble those observed later in gestation.

Adrenal Glands↗

PubMed2000

Age-dependent metabolic effects of repeated hypoxemia in piglets.

The aim of this study was to determine whether repeated exposure to hypoxemia would modify the response to hypoxemia during maturation. We exposed piglets to three 1-h cycles of hypoxemia (PaO2 = 30 to 35 mmHg; 1 mmHg = 133.3 Pa) at 1 week (n = 9), 2-3 weeks (n = 10), and 4-5 weeks of age (n = 10). O2 consumption (V(O2)) and CO2 production (V(CO2)) were measured, and alveolar ventilation (V(A)) was derived from V(CO2) and PaCO2. Levels of lactic acid (lactate) and serum catecholamines were also measured. With hypoxemia, time had a significant effect on V(O2) and body temperature in an age-dependent fashion: that is, whereas the 1 week group and the 4-5 week group showed both variables decreasing over time, the 2-3 week group showed no drop in V(O2) and a small increase in body temperature over time. Lactate levels increased with hypoxemia in all animals during the first exposure. However, with repeated exposures to hypoxemia, only the 2-3 week group continued to increase its lactate levels. Furthermore, the changes in lactate levels paralleled the changes in epinephrine levels with hypoxemia. We found, too, that although V(A) increased significantly with hypoxemia in all animals, this change was not modified by age or repeated exposures. No significant effects of age or repeated exposures were found in the cardiovascular response to hypoxemia. We concluded that, from a metabolic viewpoint, after repeated exposures to hypoxemia the 2-3 week animals responded differently.

Aging↗

PubMed2000

Effects of hypoxemia on the a- and b-waves of the electroretinogram in the cat retina.

PURPOSE: Slow components of the electroretinogram (ERG) are sensitive to even mild hypoxemia (60 < P(a)O(2) < 100 mm Hg) in the cat eye. However, the electrical responses of the inner retina remain unchanged until P(a)O(2) is below 40 mm Hg. In this study, the effects of hypoxemia on photoreceptors, on which both slow ERG components and inner retinal activity depend, were examined by recording the a-wave of the ERG. METHODS: The ERG of dark-adapted, anesthetized cats was recorded between an Ag-AgCl electrode in the vitreous humor and a reference electrode near the eye. Responses to bright flashes of diffuse white light were recorded at 3-minute intervals during hypoxemic episodes lasting 15 minutes to 2 hours. RESULTS: The cat a-wave was well described by the Lamb and Pugh a-wave model during normoxia and hypoxemia. During mild hypoxemia (P(a)O(2) of 50-60 mm Hg), small changes in a-wave amplitude were detected but did not become greater during severe hypoxemia. The mean decrease in the a-wave amplitude during severe hypoxemia (P(a)O(2) of 20-30 mm Hg) was 8.9% from the mean amplitude during air breathing. The effects of hypoxemia were more severe on the b-wave amplitude. The mean decrease in the b-wave was 35% at P(a)O(2) of 20-30 mm Hg. CONCLUSIONS: The a-wave is more resistant to severe hypoxemia than the b-wave. This implies that photoreceptor transduction works almost normally during hypoxemia and that failure of inner retinal PO(2) regulation causes the decrease in the b-wave. Previously observed changes in the amplitudes of slow ERG components during hypoxemia may result from changes in the ionic environment, rather than a failure of photoreceptor energy metabolism.

Animals↗

PubMed1990

[Effects of volatile anesthetics on the cervical sympathetic nerve activity during acute hypoxemia or hypercarbia in dogs].

Either hypoxemia or hypercarbia produces a significant change in the autonomic nervous system activity. Responses of the cervical sympathetic nerve activity (CSA) to acute hypoxemia and/or hypercarbia were studied in the absence and the presence of either halothane (H), enflurane (E), isoflurane (I) or sevoflurane (S). Multifiber potentials of CSA, EEG, ECG, heart rate, arterial blood pressure, arterial oxygen saturation (SaO2) and endtidal carbon dioxide concentration (FETCO2) were continuously monitored. CSA increased responding to acutely induced hypoxemia at a speed of -6-9% (SaO2)/min. The response of CSA was estimated in two ways as a function of SaO2; the threshold was determined at which CSA increased by 3% over the base level and the gain was determined by the slope of CSA increase divided by the SaO2 span. They were 92% and -1. 88 (Mean) in the absence of volatile anesthetics, respectively. The threshold and the gain decreased markedly in the presence of volatile anesthetics in a dose dependent fashion. They were 89.2% and -1.16; 81% and -0.74; 84.2% and -1.16 and 86.2% and -0.94 with 1MAC of H, E, I and S. At 1MAC, E and S suppressed CSA response significantly compared to equipotential H and I. CSA also increased responding to acutely induced hypercarbia at FETCO2 of 10%. The peak level increased 34% above the control value responding to hypercarbia in the absence of volatile anesthetics, though it was less than a half value of that induced by hypoxemia. The tonic levels of CSA were suppressed with increasing concentrations of volatile anesthetics. The base level and the peak level were 68.3% and 75%; 50.7% and 51.8%; 70.3% and 76.7%, and 55.5% and 63.2% with 1MAC of H, E, I and S. The inhibitory effects of 1MAC E on the CSA was significantly stronger than that of equipotential H or I. CSA did not respond against hypoxemia following bilateral sinus nerve block with 2% lidocaine 4 ml. Since EEG was silent while SaO2 was lower than 30%, vigorous CSA at these levels of hypoxemia should be maintained by strong afferent activity of the chemoreceptor site. These combined stimulation of both acute hypoxemia and hypercarbia seem to suggest that CSA response are additive each other. In conclusion, it is indicated that the depressant effects of volatile anesthetics on the CSA responses to acutely induced hypoxemia and hypercarbia can cause depression of the control activity on the autonomic nervous system against hypoxemia and hypercarbia, and conceal the manifestation of clinical signs of hypoxemia and hypercarbia, per se.

Acute Disease↗

PubMed1994

Anesthesia related hypoxemia. The effect of pulse oximetry monitoring on perioperative events and postoperative complications.

The objectives of the present investigation were to evaluate the extent of perioperative hypoxemia and to investigate the impact of pulse oximetry monitoring on the extent of hypoxemia and on perioperative morbidity in adults. To accomplish these objectives a number of prospective studies were carried out. The incidence, duration, and severity of hypoxemia were evaluated in two single blinded observer studies in the operating room (N = 296) (I) and in the Postanesthesia Care Unit (N = 200) (II). Pulse oximetry monitoring's effect on the extent of hypoxemia was evaluated in a randomized blinded observer study of 200 patients (III). The impact of pulse oximetry on the frequency of perioperative events, changes in patient care, and post-operative complications were studied in a randomized evaluation of 20,802 patients (IV-V). Finally, a subgroup of 736 patients already included in the randomized evaluation was psychologically evaluated pre- and postoperatively (VI). In the observer studies in the OR and PACU mild hypoxemia (SpO2 86-90%) was recorded in 53% and 55% of the patients, respectively. Severe hypoxemia with SpO2 values < 81% was recorded in 20% and 13% of the patients, respectively. In the randomized blinded observer study, patients with pulse oximeter data available had a significantly reduced incidence of perioperative hypoxemia when compared to patients where the data were unavailable. Most noteworthy was that in the available group extreme hypoxemia (SpO2 < 76%) was not encountered in the OR and both severe (SpO2 76-80%) and extreme hypoxemia were not observed in the PACU. In the randomized evaluation of pulse oximetry significantly more patients in the oximetry group experienced at least one respiratory event than did control patients in both the OR and in the PACU. This was a result of a 19 fold increase in the incidence of diagnosed hypoxemia in the oximetry group than in the control group. In the OR cardiovascular events were observed in a similar number of patients in both groups, except myocardial ischemia, which was detected in 12 patients in the oximetry group and in 26 patients in the control group (P < 0.03). Several changes in PACU care were observed in association with the use of pulse oximetry. These included higher flow rates of supplemental oxygen (P < 0.00001), increased use of supplemental oxygen at discharge (P < 0.00001), and increased use of naloxone (P < 0.02). One or more postoperative complications occurred in 10% of the patients in the oximetry group and in 9.4% in the control group (NS).(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia↗

PubMedDate not supplied

Vasopressin and catecholamine responses to 24-hour, steady-state hypoxemia in fetal goats.

The purpose of the present study was to determine the effect of prolonged hypoxemia without acidemia on fetal stress hormones. Twenty-four-hour hypoxemia was conducted in nine chronically catheterized pregnant goats to determine fetal plasma concentrations of arginine vasopressin (AVP), epinephrine (E), and norepinephrine (NE). Nine experiments were performed. Six resulted in nonacidemic, steady-state hypoxemia, and three incidentally resulted in hypoxemia with progressive acidemia. In steady-state hypoxemia, fetal PO2 decreased significantly from 28.1 +/- 2.4 Torr to 18.8 +/- 2.5 Torr, fetal PCO2 also decreased significantly by about 5 Torr, and pH values did not change significantly. Fetal plasma concentrations of AVP, E, and NE were significantly increased at 1 h of hypoxemia. As hypoxemia continued, AVP returned to control level by 24 h, while E and NE remained elevated throughout the hypoxemic period. In the three experiments with progressive acidemia, AVP, E, and NE increased further as fetal acidosis progressed. We conclude that fetal AVP acts as a shorter-term stress hormone than E and NE in steady-state hypoxemia. This adaptive response is present without progressive acidosis. We also conclude that accompanying acidemia is a more potent stimulus for AVP, E, and NE than isolated hypoxemia during longer-term studies.

Acidosis↗

PubMed2001

Effects of acute hypoxemia on force and surface EMG during sustained handgrip.

Data on the consequences of acute hypoxemia on the strength of contraction are often contradictory. In healthy subjects, we tested the effects of hypoxemia (PaO(2) = 56 mmHg), maintained for a 30-min period, on static handgrip elicited by voluntary effort or direct electrical muscle stimulation, in order to separate the consequences of hypoxemia on central or peripheral factors, respectively. Force was measured during maximal voluntary contractions (MVCs), 60% MVCs sustained until exhaustion, and 1-min periods of electrical muscle stimulation at 60 HZ. The evoked compound muscle action potential (M wave) was recorded in resting muscle and after each period of 60-HZ stimulation or sustained 60% MVC. Power spectrum analysis of surface electromyogram (EMG) was performed during sustained 60% MVC. Compared to normoxemia, acute hypoxemia lowered MVC (-12%, P < 0.01) but enhanced (+38%, P < 0.01) the peak force elicited by electrical muscle stimulation. In resting muscle, hypoxemia had no influence on the M-wave amplitude but lengthened the neuromuscular transmission time(+740 micros, P < 0.05). Hypoxemia did not alter the M wave measured after 60 HZ stimulation and 60% MVC. During sustained 60% MVC, hypoxemia markedly depressed the EMG changes, abolishing the leftward shift of power spectra. These data show that acute hypoxemia reduces MVC through depression of the central drive, whereas it improves the peripheral muscle response to electrical stimulation. In addition, hypoxemia reduces the recruitment of slow firing motor unit, which are highly oxygen-dependent. This could constitute an adaptative muscle response to a reduced oxygen supply.

Action Potentials↗

PubMed1986

Plasma adrenocorticotropic hormone and cortisol and adrenal blood flow during sustained hypoxemia in fetal sheep.

We examined the effect of sustained hypoxemia with progressive acidemia on pituitary-adrenal endocrine function (adrenocorticotropic hormone, cortisol) and on adrenal blood flow in fetal sheep. Hypoxemia was induced by the maternal sheep breathing a gas mixture containing 9% oxygen, with 3% carbon dioxide added. Induced hypoxemia resulted in a progressive fetal metabolic acidosis but with little change in maternal pH. During induced hypoxemia there was little change in maternal plasma adrenocorticotropic hormone or cortisol level. Fetal adrenocorticotropic hormone and cortisol increased to peak values within 2.8 hours of induced hypoxia but by 7.2 hours had begun to fall to values that were not significantly different from those at 1.4 hours. Fetal adrenal blood flow (microsphere technique) also increased significantly and remained elevated throughout the duration (7.2 hours) of hypoxemia. The maximum fetal adrenal blood flow achieved during hypoxemia was significantly correlated with the basal (prehypoxemia) flow to the adrenals. We conclude that the changes in fetal adrenocorticotropic hormone, cortisol, and adrenal blood flow seen in short-term hypoxemia are reproduced during sustained hypoxemia with acidemia. Furthermore, the noted rise in the fetal adrenocorticotropic hormone level may be an important factor contributing to the increase in adrenal blood flow during hypoxemia.

Adrenal Glands↗

PubMed1997

Severe hypoxemia in the absence of blood loss depresses hepatocellular function and up-regulates IL-6 and PGE2.

Although hepatocellular function is depressed early after trauma and hemorrhage (which are associated with low flow conditions and tissue hypoxemia), it remains unknown whether hypoxemia without blood loss, produces hepatocellular dysfunction and, if so, whether IL-6 and PGE2 are associated with this dysfunction. To study this, rats were placed in a plastic box which was flushed with a gas mixture containing 6.3% O2:93.7% N2 or room air for 60 min, followed by their return to room air. At 0 and 4 h after hypoxemia, hepatocellular function (i.e., maximum velocity of indocyanine green clearance (Vmax) and the efficiency of the transport (Km)) was measured using an in vivo hemoreflectometer. Cardiac output was assessed by dye dilution technique. Tissue microvascular blood flow was determined by laser Doppler flowmetry. Plasma IL-6 and PGE2 were measured by bioassay and radioimmunoassay, respectively. The results indicate that hypoxemia produced a depression in hepatocellular function (i.e., decreased Vmax by 44-50% and Km by 55-68%) despite stable cardiac output and hepatic microcirculation at 0 and 4 h after hypoxemia. Moreover, hypoxemia resulted in a significant increase in plasma IL-6 (by 372%-389%) as well as PGE2 (by 38% at 0 h post-hypoxemia). Thus, hypoxemia observed after trauma and hemorrhagic shock appears to be responsible for producing hepatocellular dysfunction possibly through the up-regulation of IL-6 and PGE2. In view of this, long-lasting hypoxemia in trauma victims should be avoided, perhaps by early intubation and ventilation so that the potential additional proinflammatory cytokine and PGE2 release can be prevented.

Animals↗

PubMed1997

Early neuropathologic effects of mild or moderate hypoxemia after controlled cortical impact injury in rats.

Hypoxemia has detrimental effects after traumatic brain injury (TBI) in both experimental models and humans. The purpose of this study was to determine the effect of mild or moderate hypoxemia on early histologic and motor functional outcome after controlled cortical impact (CCI) in rats. Anesthetized rats underwent CCI and were randomized to receive mild (FiO2 = 13%, n = 6), moderate (FiO2 = 11%, n = 9), or no (FiO2 = 33%, n = 6) hypoxemia for 30 min after trauma. Sham-operated rats without hypoxemia (n = 7) were used as controls. Motor function (beam balance latency) was assessed on days 0-5. Rats were killed 7 days after injury and their brains removed for assessment of survival of hippocampal neurons and contusion volume. Terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick end labeling (TUNEL) was performed on brain sections from rats killed at 6, 24, and 72 h after CCI and moderate hypoxemia to assess DNA fragmentation in situ. Mild and moderate hypoxemia augmented motor function deficits after CCI in a dose-dependent manner. Moderate hypoxemia after CCI reduced 7-day survival of CA3 neurons but not CA1 neurons vs. sham (55 [46-86] vs. 99 [95-130], p < 0.05, and 79 [63-86] vs. 101 [81-123], NS, respectively; % uninjured hemisphere, median [range]). The addition of mild or moderate hypoxemia did not increase contusion volume. TUNEL-positive neurons were seen in ipsilateral cortex and dentate gyrus at 6, 24, and 72 h after trauma, and in ipsilateral CA3 hippocampal neurons and thalamus at 24 and 72 h. Moderate hypoxemia augments CA3 neuronal death and early motor functional deficits after CCI. The pattern of DNA fragmentation in selectively vulnerable neurons suggests that apoptosis may play a role in the delayed neuronal death seen after TBI.

Analysis of Variance↗

PubMed1998

Effects of hyperventilation and hypocapnic/normocapnic hypoxemia on renal function and lithium clearance in humans.

BACKGROUND: Using the renal clearance of lithium as an index of proximal tubular outflow, this study tested the hypothesis that acute hypocapnic hypoxemia decreases proximal tubular reabsorption to the same extent as hypocapnic normoxemia (hyperventilation) and that this response is blunted during normocapnic hypoxemia. METHODS: Eight persons were studied on five occasions: (1) during inhalation of 10% oxygen (hypocapnic hypoxemia), (2) during hyperventilation of room air leading to carbon dioxide values similar to those with hypocapnic hypoxemia, (3) during inhalation of 10% oxygen with the addition of carbon dioxide to produce normocapnia, (4) during normal breathing of room air through the same tight-fitting face mask as used on the other study days, and (5) during breathing of room air without the face mask. RESULTS: Hypocapnic and normocapnic hypoxemia and hyperventilation increased cardiac output, respiratory minute volume, and effective renal plasma flow. Glomerular filtration rate remained unchanged on all study days. Calculated proximal tubular reabsorption decreased during hypocapnic hypoxemia and hyperventilation but remained unchanged with normocapnic hypoxemia. Sodium clearance increased slightly during hypocapnic and normocapnic hypoxemia, hyperventilation, and normocapnic normoxemia with but not without the face mask. CONCLUSIONS: The results indicate that (1) respiratory alkalosis with or without hypoxemia decreases proximal tubular reabsorption and that this effect, but not renal vasodilation or natriuresis, can be abolished by adding carbon dioxide to the hypoxic gas; (2) the increases in the effective renal plasma flow were caused by increased ventilation rather than by changes in arterial oxygen and carbon dioxide levels; and (3) the natriuresis may be secondary to increased renal perfusion, but application of a face mask also may increase sodium excretion.

Adult↗