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PubMed1998

Effect of allopurinol on NMDA receptor modification following recurrent asphyxia in newborn piglets.

The present study tests the hypothesis that repeated episodes of asphyxia will lead to alterations in the characteristics of the N-methyl-d-aspartate (NMDA) receptor in the brain cell membrane of newborn piglets and that pre-treatment with allopurinol, a xanthine oxidase inhibitor, will prevent these modifications. Eighteen newborn piglets were studied. Six untreated and six allopurinol treated animals were subjected to eight asphyxial episodes and compared to six normoxic, normocapneic controls. Brain cell membrane Na+,K+-ATPase activity was determined to assess membrane function. Na+,K+-ATPase activity was decreased from control following asphyxia in both the untreated and treated animals (47.7+/-3.2 vs. 43.0+/-2.2 and 41.0+/-5.3 micromol Pi/mg protein/h, p<0.05, respectively). 3H-MK-801 binding studies were performed to measure NMDA receptor binding characteristics. The receptor density (Bmax) in the untreated asphyxia group was decreased compared to control animals (0.80+/-0.11 vs. 1.13+/-0.33, p<0.05); furthermore, the dissociation constant (Kd) was also decreased (3.8+/-0.7 vs. 9.2+/-2.2, p<0.05), indicating an increase in receptor affinity. In contrast, Bmax in the allopurinol treated asphyxia group was similar to control (1. 06+/-0.37); and Kd was higher (lower affinity) than in the untreated group (6.5+/-1.4, p<0.05). The data indicate that recurrent asphyxial episodes lead to alterations in NMDA receptor characteristics; and that despite cell membrane dysfunction as seen by a decrease in Na+,K+-ATPase activity, allopurinol prevents modification of NMDA receptor-ion channel binding characteristics induced by repeated episodes of asphyxia.

Allopurinol↗
PubMed2000

Effect of repetitive asphyxia on leukocyte-vessel wall interactions in the developing chick intestine.

BACKGROUND/PURPOSE: Information on leukocyte-vessel wall interactions (LVWI) during development of the immature intestine is scarce. The authors designed an experimental model for studying the microcirculation in the developing intestine of chick fetuses at days 13 (n = 12), 15 (n = 17), and 17 (n = 19) of incubation (0.6, 0.7, and 0.8 of the incubation time, respectively) using intravital microscopy. METHODS: The authors investigated whether episodes of asphyxia increase LVWI and induce tissue damage in the developing intestine. Asphyxia was induced by clamping of the chorioallantoic vein for 6 periods of 5 minutes each, with 5-minute intervals, whereas in sham groups a sham procedure was performed. Video recordings were made before as well as 10, 20, and 30 minutes after the end of the asphyxia or sham protocol. RESULTS: Baseline number of rolling leukocytes per minute significantly increased (P < .001) from 0 at 0.6 incubation to 1.5 and to 4 at 0.7 and 0.8 incubation time, respectively. At 0.6 and 0.7 incubation no adherent leukocytes were observed under baseline conditions, whereas at 0.8 incubation single leukocytes adhered to the venular wall. LVWI variably increased during the course of the experiments. Asphyxia neither enhanced LVWI nor induced histological damage in the intestine. CONCLUSIONS: These findings indicate that (1) leukocyte-vessel wall interactions mature during fetal development, and (2) repetitive episodes of asphyxia induce neither an inflammatory response nor histological tissue injury in the developing intestine from 0.6 to 0.8 incubation. The authors hypothesize that immaturity of leukocyte-vessel wall interactions, as part of the nonspecific host defense to invading bacteria, might play a role in the development of necrotizing enterocolitis in premature neonates.

Animals↗
PubMed1980

Neonatal asphyxia. I. Relationship of obstetric and neonatal complications to neonatal mortality in 38,405 consecutive deliveries.

The requirement of greater than one minute of positive pressure ventilation was prospectively used to identify infants suffering from asphyxia at birth in 38,405 consecutive deliveries. Multivariate analysis of high-risk factors associated with increased risk of asphyxia showed the prematurity was the most significant predictor of asphyxia. Asphyxia occurred in 62.3% of infants less than 27 weeks' gestation and decreased to 0.4% in infants greater than 38 weeks' gestation. Presence of asphyxia was associated with significant increase in neonatal mortality of infants greater than 36 weeks' gestation. Of the asphyxiated neonates, growth retardation, hypothermia, hyaline membrane disease, and seizures were significantly associated with an increased risk of death.

Asphyxia Neonatorum↗
PubMed1988

Perinatal asphyxia in infants of insulin-dependent diabetic mothers.

Infants of diabetic mothers are thought to be at risk for perinatal asphyxia. We hypothesized that the following are significant risk factors for perinatal asphyxia: poor third-trimester glycemic control, diabetic vascular disease (nephropathy, retinopathy) appearing in pregnancy, pregnancy-associated hypertension, smoking, prematurity, fetal macrosomia, and maternal hyperglycemia and hypoglycemia within 6 hours preceding delivery. We prospectively studied 162 infants born to 149 diabetic mothers (White classes B through R-T). Perinatal asphyxia was defined clinically as fetal distress during labor (late decelerations, persistent fetal bradycardia, or both), 1-minute Apgar score less than or equal to 6, or intrauterine fetal death. Forty-four infants (26.7%) had perinatal asphyxia. The presence of perinatal asphyxia did not correlate with third-trimester glycemic control, pregnancy-associated hypertension, smoking, fetal macrosomia, or maternal hypoglycemia before delivery, but it did correlate significantly with nephropathy appearing in pregnancy, maternal hyperglycemia before delivery, and prematurity. We speculate that (1) the appearance of diabetic vasculopathy (nephropathy) during pregnancy is accompanied by placental vascular disease and subsequently by fetal compromise and (2) in pregnancy complicated by diabetes, maternal and subsequently fetal hyperglycemia before delivery leads to fetal hypoxemia.

Adult↗
PubMed2000

Respiratory neural activity responses to chemical stimuli in newborn rats: reversible transition from normal to 'secondary' rhythm during asphyxia and its implication for 'respiratory like' activity of isolated medullary preparation.

To clarify a possible origin of 'respiratory like' rhythmic activities observed in in vitro brainstem preparation, the phrenic (Phr) and cranial nerve (XII or IX) inspiratory activities were analyzed in halothane-anesthetized, vagotomized and artificially ventilated newborn (2--6 days after birth) and young adult rats (30--50 days) during altered chemical stimuli and prolonged asphyxia at 25 degrees C. The newborn rat showed regular rhythmic inspiratory discharges of short duration, and their responses to CO(2) and hypoxia did not differ from those seen in adult rats. In the newborn rat the Phr and cranial nerve inspiratory discharges increased first, then respiratory frequency decreased and finally ceased completely for approximately 1--2 min during asphyxia. Thereafter, 'secondary' rhythmic inspiratory activity emerged at a slower rate with decremental inspiratory discharge profile, which persisted for a period more than 40 min of asphyxia. A normal respiratory activity recovered after resumption of artificial ventilation. Though young adult rats exhibited similar sequential changes in respiratory activity during asphyxia, the 'secondary' rhythmic activity persisted for a period of several min only. The pattern of 'secondary' respiratory activity corresponded well with that of rhythmic activities seen in the isolated medullary block preparation of newborn rat. 'Respiratory like' activity found in isolated medullary preparations of newborn animals may arise from a mechanism that generates 'secondary' (or so called 'gasping' type) rhythmic inspiratory activity during prolonged asphyxia in in vivo preparations.

Age Factors↗
PubMed2002

Apoptosis in the rat spinal cord during postnatal development; the effect of perinatal asphyxia on programmed cell death.

The aim of our study was to investigate the effect of perinatal asphyxia on developmental apoptosis in the cervical and lumbar spinal cord in the neonatal rat. Perinatal asphyxia was induced by keeping pups at term in utero in a water bath at 37 degrees C for 20 min, followed by resuscitation. Effects of this treatment on developmental apoptosis were studied on postnatal days 2, 5 and 8 using terminal deoxynucleotidyl transferase (TdT)-dUTP-biotin nick end labelling (TUNEL) and caspase-3 staining. TUNEL positive cells were identified using double immunostaining. On postnatal day 2 an increase of 215% in TUNEL positive cells was detected (P=0.005) in laminae IV-VII of the lumbar spinal cord of rats which underwent perinatal asphyxia compared to controls. An increase of 55% compared to controls (P=0.03) was seen in laminae I-III of the lumbar spinal cord at postnatal day 8. TUNEL positive cells could be partly identified as microglia cells (ED1 positive) and oligodendrocytes (O4 positive). The effect of perinatal asphyxia on programmed cell death in the neonatal rat spinal cord was mainly observed in the intermediate zone and dorsal horn of the lumbar spinal cord. We conclude that perinatal asphyxia has a pronounced effect on the survival of cells in a specific region of the spinal cord and thus may have a profound effect on the development of motor networks.

Animals↗
PubMed1999

Prediction of neurological outcome after birth asphyxia from early continuous two-channel electroencephalography.

OBJECTIVE: To determine whether two-channel continuous electroencephalography (EEG) applied within 12 h of birth can predict the severity of neurological complications and neurodevelopmental outcome following birth asphyxia. METHODS: A continuous two-channel EEG was performed within 12 h of birth in 22 infants suspected of having suffered birth asphyxia and 11 healthy control infants (22 infants at a general and 11 at a specialist paediatric unit). Criteria to categorise normal and abnormal EEG records were defined and compared with the severity of hypoxic/ischaemic encephalopathy (HIE) and with neurodevelopmental outcome, assessed at or after 12 months of age. RESULTS: EEG recordings were commenced at a median (range) of 2 h 50 min (1 h 45 min to 12 h) after birth. Technically satisfactory recordings were obtained in all but one infant. All control infants remained asymptomatic and had a normal EEG with discernible sleep/awake periods. 12 h after birth the EEG was normal in all 12 infants suspected of asphyxia who remained well or developed grade 1 HIE and was abnormal in six of nine infants with grade II or III HIE. Fifteen of 16 infants suspected of asphyxia with a normal neurodevelopmental outcome had a normal EEG at 12 h; transient abnormalities lasting not more than 8 h had been detected in three of these infants. All five infants who died or developed neurodevelopmental abnormalities had an abnormal EEG. At 12 h of age the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and likelihood ratio for predicting severe (grade II or III) HIE were: 67, 100, 100, 80% and infinity and for subsequent death or neurodevelopmental impairments: 100, 94, 83, 100 and 16%, respectively. Assessment of the EEG before 12 h of age altered prognostic accuracy: 4 h after birth the sensitivity, specificity, positive and negative predictive values and the likelihood ratio for poor neurodevelopmental outcome were 100, 71, 33%, 100 and 3.7%, respectively (16 infants). CONCLUSION: Continuous two-channel EEG is an accurate tool for assessing the severity of neurological insult soon after birth asphyxia.

Asphyxia Neonatorum↗
PubMed2000

Perinatal asphyxia results in changes in presynaptic bouton number in striatum and cerebral cortex-a stereological and behavioral analysis.

Deficits in cognitive function have been related to quantitative changes in synaptic population, particularly in the cerebral cortex. Here, we used an established model of perinatal asphyxia that induces morphological changes, i.e. neuron loss in the cerebral cortex and striatum, as well as behavioural deficits. We hypothesized that perinatal asphyxia may lead to a neurodegenerative process resulting in cognitive impairment and altered presynaptic bouton numbers in adult rats. We studied cognitive performance at 18 months and presynaptic bouton numbers at 22 months following perinatal asphyxia. Data of the spatial Morris water escape task did not reveal clear memory or learning deficits in aged asphyctic rats compared to aged control rats. However, a memory impairment in aged rats versus young rats was observed, which was more pronounced in asphyctic rats. We found an increase in presynaptic bouton density in the parietal cortex, whereas no changes were found in striatum and frontal cortex in asphyctic rats. An increase of striatal volume was observed in asphyctic rats, leading to an increase in presynaptic bouton numbers in this area. These findings stress the issue that volume measurements have to be taken into account when determining presynaptic bouton density. Furthermore, perinatal asphyxia led to region-specific changes in presynaptic bouton numbers and it worsened the age-related cognitive impairment. These results suggest that perinatal asphyxia induced neuronal loss, which is compensated for by an increase in presynaptic bouton numbers.

Adult↗
PubMed1998

[Definition of asphyxia neonatorum and incidence of neurologic and systemic complications in the full-term newborn].

PATIENTS AND METHODS: In a prospective multicentric study, 152 of 10,065 live term births had birth asphyxia, defined by the association of three indicators (fetal distress, depression at birth and metabolic acidosis). RESULTS: The incidence of birth asphyxia was 1.5% of live term births when birth asphyxia was defined by the presence of at least two indicators, and 1% of live term births when birth asphyxia was defined by the association of metabolic acidosis and another indicator. Neurological complications were observed in 66 cases (43%). The incidence of post-asphyxial encephalopathy (PAE) was 5.9/1000 of live term births (mild PAE: 3/1000; moderate PAE: 2.7/1000; severe PAE: 0.2/1000). Systemic complications were observed in 87 patients (57%). Renal injury and coagulopathy were associated with moderate or severe PAE. Respiratory complications (39%), infections (17%) and gastro-intestinal intolerance (15%) often complicated the course. Severe complications were never seen in the absence of significant metabolic acidosis at 30 minutes of life. CONCLUSION: Our study has many implications concerning the diagnosis of birth asphyxia and its complications. A terminology based on clinical observation and arterial pH evaluation is proposed in order to clarify the situation.

Acidosis↗
PubMed2003

NF-kappaB activation in peripheral blood mononuclear cells in neonatal asphyxia.

Neonatal asphyxia results in hypoxic-ischaemic encephalopathy. Previous studies have demonstrated that brain hypoxia and ischaemia lead to the production of proinflammatory cytokines, including tumour necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and IL-6. Transcription factor NF-kappaB is essential for the expression of these cytokines. We examined whether or not NF-kappaB is activated in peripheral mononuclear cells (PBMC) in neonatal asphyxia by flow cytometry. In addition, we examined the relationship between NF-kappaB activation in PBMC and the neurological prognosis. Flow cytometry analysis demonstrated that the level of NF-kappaB activation in CD14+ monocytes/macrophages of the patients with asphyxia who had neurological sequelae was significantly higher than in the controls, and in the patients with asphyxia who survived (31.7 +/- 7.2%versus 2.5 +/- 0.9%, P = 0.008, and versus 1.6 +/- 1.4%, P = 0.014, respectively). Our findings suggest that NF-kappaB activation in peripheral blood CD14+ monocytes/macrophages in neonatal asphyxia is important for predicting the subsequent neurological sequelae.

Asphyxia Neonatorum↗
PubMed2002

Consequences of intrauterine growth restriction on ventilatory and thermoregulatory responses to asphyxia and hypercapnia in the newborn guinea-pig.

The purpose of this study was to determine the effects of prenatal growth restriction on the ventilatory and thermoregulatory responses to asphyxia and hypercapnia in the newborn guinea-pig. Spontaneously growth-restricted (SGR) animals born to unoperated dams, and growth-retarded (GR) neonates born to dams in which a uterine artery had been ligated at mid gestation, were studied and compared with control neonates. Ventilatory responses to progressive asphyxia and steady-state hypercapnia were tested at 3-6 days of age using a barometric plethysmograph. The animals were then killed and the brains prepared for histological and immunohistochemical analysis. During progressive asphyxia, SGR neonates (n = 5) had a significantly increased minute ventilation compared with both control (n = 6) and GR (n = 5) neonates. Rectal temperature fell significantly in GR and SGR neonates after progressive asphyxia, but was unchanged in control neonates. The ventilatory responses to steady-state hypercapnia were not different in the GR, SGR and control neonates. The immunoreactive expression of glial fibrillary acidic protein, tyrosine hydroxylase, substance P and met-enkephalin in the medulla was also not different between the three groups. It was concluded that prenatal growth restriction is associated with alterations in the respiratory and thermoregulatory responses to asphyxia and hypercapnia, with greater effects observed when in utero growth restriction arises spontaneously, compared with that produced experimentally over approximately the last half of gestation.

Animals↗
PubMed1999

Inappropriately high plasma insulin levels in suspected perinatal asphyxia.

The aim of this study was to determine differences in levels of the major hormones responsible for glucose homeostasis (insulin and glucagon) in babies with acute neonatal encephalopathy secondary to perinatal asphyxia and to correlate these with outcome. In a prospective observational study, plasma insulin, C-peptide, glucagon and serum glucose levels were determined using standard techniques at specified times in term babies with a diagnosis on admission of perinatal asphyxia or acute neonatal encephalopathy. The setting comprised two university-affiliated, regional, tertiary level neonatal intensive care units. Thirty-one babies with a diagnosis of perinatal asphyxia or acute neonatal encephalopathy were entered into the study over 15 months and neurodevelopmental outcomes at 18 months of age for 28 babies were available for analysis. Babies with a poor neurodevelopmental outcome had significantly higher insulin and C-peptide levels than those who had a good outcome. Glucose delivery, serum glucose and glucagon levels did not differ significantly between the babies with a poor outcome and those with a good outcome. In conclusion, babies with significant foetal or neonatal asphyxia frequently have inappropriately high plasma insulin levels. This, either alone or in combination with other hormonal disturbances, may lead to the hypoglycaemia often associated with severe asphyxia and may predict a poor outcome.

Asphyxia Neonatorum↗
PubMed2005

Autoerotic asphyxia: part I.

Fatal autoerotic asphyxia refers to death during solitary sexual activity with self-induced asphyxiation meant to be brief and reversible. However, an unexpected fatality results from a failure of a release mechanism apparatus. The large majority of victims of autoerotic death are Caucasian males between the second and fourth decade. While autoerotic death may encompass a myriad of other means of achieving sexual gratification, which includes asphyxia by plastic bag or inhalation of noxious chemicals, the most common method is by ligature about the neck. This study presents a 9-year retrospective review of deaths due to autoerotic asphyxia, specifically ligature asphyxia, in Kentucky between 1993 and 2001. Of the sixteen victims, all were Caucasian males between the ages of 14 and 59 years, with a mean age of 38.3 years. Cross-dressing was a feature in 4 cases. A thorough review of the decedent's background, meticulous scene investigation, and complete postmortem examination may shed light on the mechanism and psychosocial predisposition associated with autoerotic asphyxia.

Adolescent↗
PubMed2005

Asphyxia by tracheobronchial thrombus.

Asphyxia secondary to airway obstruction has numerous underlying causes, both acute and chronic. Causes of chronic airway obstruction, such as neoplasms and tracheal scarring, are often clinically apparent well prior to asphyxia. Causes of acute airway obstruction may not be as obvious to clinicians or investigators. These include infections, anaphylactic reactions, status asthmaticus, inhalational injuries, and aspirations, which may result in acute obstruction and sudden death. We report the deaths of 2 individuals, a 43-year-old female and a 78-year-old female, both with adenocarcinoma. The 43-year-old was hospitalized with a stage III, poorly differentiated infiltrating ductal carcinoma of the breast metastatic to the lymph nodes. She was intubated to treat poor respiratory function and acidosis. A bronchoalveolar lavage was consistent with alveolar hemorrhage; no organisms were identified. Blood and "clot" were in her endotracheal tube, so the endotracheal tube was replaced. She became comatose and life support was withdrawn. At autopsy, a large red-gray thrombus obstructed the trachea and extended into the right bronchus. Microscopically, the entire clot was composed of fibrin, red blood cells, and some mucus. Findings of acute respiratory distress syndrome with hyaline membranes were identified. The cause of death was listed as acute respiratory distress syndrome with tracheobronchial thrombus. Experiencing a decline in mental status, the 78-year-old had metastatic adenocarcinoma of unknown primary. She developed sudden respiratory distress and an airway obstruction was discovered. After failure to relieve the obstruction, she decompensated and died. At autopsy, a large, red-gray thrombus obstructed the distal trachea and both bronchi. Microscopically, the thrombus was composed of fibrin, platelets, and red blood cells. The cause of death was asphyxia secondary to airway obstruction by thrombus. We present these 2 unusual cases of asphyxia and review of the literature focusing on asphyxia and the etiology of airway thrombi.

Adenocarcinoma↗
PubMed2001

Differential changes in insulin-like growth factors and their binding proteins following asphyxia in the preterm fetal sheep.

1. The purpose of this study was to examine the changes in circulating concentrations of insulin-like growth factor (IGF)-I, IGF-II, IGF-binding protein (IGFBP)-1, IGFBP-2 and insulin following asphyxia in utero. 2. Fetal sheep at 90-93 days gestation underwent either sham occlusion (n = 7) or asphyxia (n = 6) induced by complete umbilical cord occlusion for 30 min. Fetal blood samples were taken before occlusion and 4, 6, 24, 48 and 72 h post-occlusion. 3. During the early phase of recovery there was a substantial fall (80 %) in circulating plasma IGF-I concentrations by 6 h post-asphyxia (P < 0.001). This was associated with a rapid rise in IGFBP-1 (P < 0.001), but no change in IGF-II or IGFBP-2. Insulin was significantly reduced at 4 h (P < 0.001) and glucose slightly elevated (P < 0.05), but insulin values returned to baseline by 6 h. Between 24 and 72 h of recovery, IGF-I gradually increased, IGFBP-1 returned to control values, and there was an increase in IGFBP-2 after 24 h (P < 0.05) and in IGF-II by 72 h (P < 0.05) after asphyxia. 4. These data demonstrate a differential effect of asphyxia on the IGF axis of the premature fetal sheep. A key finding was the large fall in circulating IGF-I, but not IGF-II, during the early phase of recovery. IGF-I bioavailability was, in part, regulated by IGFBP-1, but maximal changes in IGF-I and IGFBP-1 were independent of plasma insulin and glucose.5. The impact of this substantial change in circulating IGF-I on the fetus is unknown. It may facilitate metabolic requirements by promoting catabolism. Alternatively, as IGFs play a role in wound repair, the acute changes in IGF-I and IGFBP-1 may reflect transport of IGF-I from the circulatory pool to injured tissues to promote wound repair.

Animals↗
PubMed1981

Metabolic effects of obstetric regional analgesia and of asphyxia in the newborn infant during the first two hours after birth. III. Adjustment of arterial blood gases and acid-base balance.

Effects of obstetric regional analgesia and of asphyxia on the arterial blood gases and acid-base balance in the first two hours after birth were investigated in 85 newborn infants divided into a control group, an asphyxia group and a continuous epidural, an intermittent epidural and a paracervical + pudendal block group. Lidocaine was the drug used in the analgesia groups. In the asphyxia group the metabolic acidosis decreased and pH was normalized to the level of the control group between 10 and 30 min after birth. During this period in the asphyxia group PaO2 was higher than and PaCO2 similar to the corresponding control values. Compared with the control group, in the regional analgesia groups the metabolic acidosis tended to be less extensive and PaO2 higher, whereas PaCO2 was similar. A lower packed red cell volume in the asphyxia and in the regional analgesia groups, probably due to differences in placental transfusion, may have had influence on the results. Within the regional analgesia groups infants with hyperglycemia showed signs of an increased metabolic acidosis while infants with hypoglycemia had low base deficit and lactate values supporting the assumption that neonatal blood glucose concentration may reflect perinatal distress.

Acid-Base Equilibrium↗
PubMed1994

Cerebral blood flow velocity in term newborns following intrapartum fetal asphyxia.

Twenty-six term newborns with intrapartum fetal asphyxia, determined biochemically (umbilical artery base deficit > 12 mmol/l), were compared with 59 normal newborns to determine the effect of intrapartum fetal asphyxia on newborn blood pressure and cerebral blood flow velocity following delivery. Cerebral blood flow velocity observations with concurrent measures of blood pressure and heart rate were obtained during the 24 h after delivery and after 24 h. After delivery, diastolic blood pressure in the newborns of the asphyxia group was significantly greater than that of the newborns of the normal group and this difference persisted after 24 h. Cerebral blood flow velocity in the newborns of the asphyxia group was of the same order as that of the newborns of the normal group during the 24 h after delivery. However, there was a significant increase in both peak systolic and end-diastolic blood flow velocity after 24 h. The duration of metabolic acidosis may be a factor in the occurrence of this delayed cerebral blood flow velocity response. Observations of cerebral blood flow velocity should be continued for more than 24 h following delivery to determine the effect of intrapartum fetal asphyxia.

Asphyxia Neonatorum↗
PubMed1969

Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex.

1. In the spontaneously breathing anaesthetized dog, the systemic circulation was perfused at constant blood flow; there was no pulmonary blood flow and the systemic arterial blood P(O2) and P(CO2) were controlled independently by an extracorporeal isolated pump-perfused donor lung preparation. The carotid and aortic bodies were separately perfused at constant pressure with blood of the same composition as perfused the systemic circulation.2. Apnoeic asphyxia, produced by stopping the recipient animal's lung movements and, at the same time, making the blood perfusing the systemic circulation and the arterial chemoreceptors hypoxic and hypercapnic by reducing the ventilation of the isolated perfused donor lungs, caused an increase in systemic vascular resistance.3. While the systemic arterial blood was still hypoxic and hypercapnic, withdrawal of the carotid and aortic body ;drive' resulted in a striking reduction in systemic vascular resistance. Re-establishing the chemoreceptor ;drive' immediately increased the vascular resistance again.4. Apnoeic asphyxia carried out while the carotid and aortic bodies were continuously perfused with oxygenated blood of normal P(CO2) had little or no effect on systemic vascular resistance.5. The systemic vasoconstrictor response produced by apnoeic asphyxia was reduced or abolished by re-establishing the recipient animal's lung movements, and this effect occurred in the absence of changes in the composition of the blood perfusing the systemic circulation and arterial chemoreceptors. This abolition of the vasoconstriction was due to a pulmonary reflex.6. Apnoeic asphyxia slowed the rate of the beating atria due to excitation of the carotid and aortic body chemoreceptors. This response can be over-ridden by an inflation reflex arising from the lungs.7. It is concluded that the cardiovascular responses observed in apnoeic asphyxia are due, at least in part, to primary reflexes from the carotid and aortic body chemoreceptors engendered by arterial hypoxia and hypercapnia. The appearance of these responses is, however, dependent upon there being no excitation of a pulmonary (inflation) vagal reflex.

Animals↗