SEARCH · Search PubMed

Results for “Asphyxia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources

PubMed2003

Time course of brainstem pathophysiology during first month in term infants after perinatal asphyxia, revealed by MLS BAER latencies and intervals.

Dynamic changes in electrophysiology of brainstem auditory neurons during the first month after birth were studied in 51 term infants after perinatal asphyxia using maximum length sequence brainstem auditory evoked responses. The responses were recorded on d 1, 3, 5, 7, 10, 15, and 30 after birth. On d 1, wave III and V latencies and all interpeak intervals increased significantly at all repetition rates of clicks used (91-910/s), especially the higher rates (ANOVA, p < 0.05-0.0001). On d 3, all these latencies and intervals increased further and differed more significantly from the normal control subjects. Thereafter, the latencies and intervals decreased progressively. On d 7, wave V latency and all intervals still differed significantly from the control subjects. These dynamic changes were more significant at higher rates of clicks than at lower rates. On d 10 and 15, all intervals decreased significantly. On d 30, all wave latencies decreased to the values in the normal control subjects on the same day. The intervals also approached normal values, although the III-V and I-V intervals still increased slightly. These results indicate that hypoxic-ischemic brain damage persists during the first week, with a peak on d 3, and recovers progressively thereafter. By 1 mo, the damage has largely returned to normal. Maximum length sequence brainstem auditory evoked responses results correlated well with the stage of hypoxic-ischemic encephalopathy during the first week. The present study revealed a general time course of brainstem pathophysiology after asphyxia, although there were individual variations. Our findings can be used as a reference to monitor cerebral function and help judge the value of neuroprotective or therapeutic interventions. The first week, particularly the first 3 d, is a critical period of hypoxic-ischemic brain damage, and early intervention may prevent or reduce deterioration of the damage.

Asphyxia↗

PubMed2004

Comparison of short- and long-duration oxygen treatment after cerebral asphyxia in newborn piglets.

We tested whether reoxygenation with 100% O(2) for 5 min after experimental asphyxia in newborn piglets was as efficient as 100% O(2) for 20 min compared with room air. Forty-one anesthetized piglets, 1-3 d old, were randomized to cerebral hypoxemia-ischemia-hypercapnia (HIH) or control (n = 5). HIH was achieved by ventilation with 8% O(2), temporary occlusion of the common carotid arteries, and adding of CO(2). After 25 min, reoxygenation-reperfusion was started with 100% O(2) for 20 min (group 1, n = 12), 100% O(2) for 5 min (group 2, n = 12), or 21% O(2) (group 3, n = 12). All piglets were observed for 2 h. During reoxygenation-reperfusion, significantly higher blood pressure and more complete restoration of microcirculation (laser Doppler flow) in the cerebral cortex was found in both groups reoxygenated with 100% O(2) compared with 21% O(2) (regional cerebral blood flow >or=100% versus 70% of baseline, p = 0.04). Reoxygenation with 100% O(2) for 5 min was as efficient as 20 min. Oxygen delivery in cortex was significantly higher in groups 1 and 2 compared with group 3 (p = 0.03), but there were no significant differences in cerebral metabolic rate for oxygen. In the striatum, no significant differences in flow or extracellular glutamate, glycerol, and lactate/pyruvate ratio were found between the groups. In conclusion, after experimental asphyxia, newborn piglets can be reoxygenated as efficiently with 100% O(2) for only 5 min as 100% O(2) for 20 min compared with room air.

Animals↗

PubMed1981

Prognostic importance of brainstem auditory evoked responses after asphyxia.

Brainstem auditory evoked responses were recorded after acute asphyxia in 126 infants, ages birth through 18 months. Of these, 21 had markedly abnormal amplitude ratios, and all infants with abnormal amplitude ratios had severe neurologic handicaps. An abnormal amplitude ratio predicts long-term neurologic sequelae of acute asphyxia in infants. Normal amplitude ratios did not, however, ensure normal neurologic outcome; 10 infants with normal responses were severely handicapped.

Asphyxia Neonatorum↗

PubMed1989

Use of 31P magnetic resonance spectroscopy to characterize evolving brain damage after perinatal asphyxia.

We investigated postasphyxial brain damage with 31P magnetic resonance spectroscopy (MRS) and correlated it with neurologic assessment and standard laboratory evaluation during the first 10 months of life in 1 infant, baby G. We compared these observations to 31P MRS data from 7 healthy term newborns, 1 normal infant examined serially over the first 8.5 months of life, and 5 other term infants following perinatal asphyxia. MRS noninvasively provides biochemical correlates of the evolution of brain damage following perinatal asphyxia and suggests that pH derived from the inorganic phosphate peak may serve as a marker for brain injury.

Asphyxia Neonatorum↗

PubMed2001

(1)H-MR spectroscopy is sensitive to subtle effects of perinatal asphyxia.

The authors performed neuropsychological and (1)H-MRS studies in 18 subclinical patients with antecedents of perinatal asphyxia (PA) and in 18 matched control subjects. Patients with PA showed reduced values of N-acetylaspartate (NAA) in both the basal ganglia and the midtemporal region (MTR) and reduced NAA/choline values in the MTR. Neuropsychological testing showed group differences in tasks related to attention and memory. These results indicate persistent dysfunctions in cerebral structures vulnerable to hypoxia and demonstrate the utility of MRS for the long-term evaluation of cerebral sequelae of neonatal asphyxia.

Adolescent↗

PubMed2002

Seizure-associated brain injury in term newborns with perinatal asphyxia.

BACKGROUND: There is controversy over whether seizures, the most common manifestation of neonatal brain injury, may themselves damage the developing brain. OBJECTIVE: To determine if neonatal seizures are independently associated with brain injury in newborns with perinatal asphyxia. METHODS: Ninety term neonates were studied with MRI and single-voxel (1)H-MRS on median day of life 6 (range 1 to 13 days). The severity of MR abnormality in the (1)H-MRS regions of interest was scored using a validated scale. Seizure severity was scored based on seizure frequency and duration, EEG findings, and anticonvulsant administration. Multivariable linear regression tested the independent association of seizure severity with impaired cerebral metabolism measured by lactate/choline and compromised neuronal integrity measured by N-acetylaspartate/choline in both regions. RESULTS: Clinical seizures occurred in 33 of 90 infants (37%). Seizure severity was associated with increased lactate/choline in both the intervascular boundary zone (p < 0.001) and the basal nuclei (p = 0.011) when controlling for potential confounders of MRI abnormalities and amount of resuscitation at birth. Each increase in seizure score was independently associated with a 21% increase in lactate/choline in the intervascular boundary zone (95% CI, 5.1-38.2%) and a 15% increase in the basal nuclei (95% CI, 0.1-31.7%). Seizure severity was independently associated with diminished N-acetylaspartate/choline in the intervascular boundary zone (p = 0.034). CONCLUSION: The severity of seizures in human newborns with perinatal asphyxia is independently associated with brain injury and is not limited to structural damage detectable by MRI.

Asphyxia Neonatorum↗

PubMed1995

Carbon dioxide euthanasia in rats: oxygen supplementation minimizes signs of agitation and asphyxia.

This paper records the effects of carbon dioxide when used for euthanasia, on behaviour, electrical brain activity and heart rate in rats. Four different methods were used. Animals were placed in a box (a) that was completely filled with carbon dioxide; (b) into which carbon dioxide was streamed at a high flow rate; (c) into which carbon dioxide was streamed at a low flow rate and (d) into which a mixture of carbon dioxide and oxygen was streamed at a fast rate. It was found that the cessation of behaviour was associated with an aberrant pattern of electrical brain activity together with an abnormally low heart rate. The time to reach this point was shortest in those animals placed in the box filled with pure carbon dioxide, longer when carbon dioxide was introduced at a high rate into the box, longer still when oxygen was added to the carbon dioxide gas, and longest when carbon dioxide was streamed slowly into the box. In the condition with pure carbon dioxide, signs of behavioural agitation and asphyxia were seen. This was also true for the two conditions in which carbon dioxide streamed into the box, but to a lesser degree. These signs occurred when some degree of consciousness may still have been present in the animals. Signs of agitation and asphyxia were almost completely absent in the condition where oxygen was added to the carbon dioxide. These results not only demonstrate the usefulness of behavioural criteria next to electrophysiological indices, but also demonstrate that the negative effects of carbon dioxide euthanasia can be prevented by an additional supply of oxygen.

Animal Welfare↗

PubMed1987

Consequences of asphyxia in surfactant deficiency.

Consequences of asphyxia in babies with surfactant deficiency are discussed. Several important points concerning transition from intra- to extrauterine life are underlined. In asphyxia large amounts of hypoxanthine are formed and in the postasphyxic period when high concentrations of oxygen are given large amounts of oxygen radicals are produced. Experimentally we have shown that such radicals produce lung engorgement, hemorrhage and edema. Further they inactivate surfactant. Oxygen radicals also reduce the lung compliance dramatically in animal experiments. Saline alone given intratracheally to animals ventilated artificially will also reduce lung compliance. It is therefore not recommended to give saline intratracheally as a placebo in surfactant trials.

Adenine Nucleotides↗

PubMed1989

Beta-2-microglobulin in the assessment of renal function in full term newborns following perinatal asphyxia.

In order to evaluate the clinical usefulness of serum and urinary beta 2 microglobulin (beta 2-m) determination as a marker of renal damage following perinatal asphyxia, twenty asphyxiated and twenty healthy full term newborns were studied. Renal function was monitored on the first and third day after birth by traditional tests such as creatinine (Cr), endogenous creatinine clearance (Ccr), and fractional Na excretion (FeNa), as well as by serum and urinary beta 2 microglobulin. The value of different tests for the diagnosis of oliguria and of acute renal failure was determined. Eleven asphyxiated neonates developed oliguria and five ARF in contrast to none of the controls. Both traditional tests of renal function, and determinations of beta 2-m with the exception of serum beta 2-m, were significantly different (p less than 0.01) between controls and asphyxiated neonates. When stratified analysis was performed, only serum cr, urinary beta 2-m/cr ratio, and Fe beta 2-m were able to discriminate oliguria from preserved diuresis on the first day of life. For ARF, only Ccr and Fe beta 2-m were different, again on the first day of life. Urinary beta 2-m/creatinine ratio and Fe beta 2-m appear to be more sensitive and specific for the early detection of proximal tubular renal dysfunction following perinatal asphyxia than usual tests of renal function.

Asphyxia Neonatorum↗

PubMed1997

Interleukin-6 in the cerebrospinal fluid after perinatal asphyxia is related to early and late neurological manifestations.

OBJECTIVES: To investigate if the concentration of interleukin-6 (IL-6) in the cerebrospinal fluid (CSF) is affected by perinatal asphyxia, and to examine the relation of IL-6 levels in the CSF to the severity of hypoxic-ischemic encephalopathy (HIE), to brain damage, and to the neurological outcome. METHODS: Asphyxiated term neonates were included. Cerebrospinal fluid IL-6 was measured by a sensitive enzyme-linked immunosorbent assay. RESULTS: Twenty neonates were studied: 3 had no HIE, 5 had stage 1, 6 had stage 2, and 6 had stage 3. CSF IL-6 levels (8 to 90 hours of life) were higher in neonates with HIE stage 3 (range, 65 to 2250 pg/mL) when compared with neonates with HIE stage 0 to 2 (<2 pg/mL in 12 neonates, 10 pg/mL in 1). According to neuroimaging techniques and/or pathological examination, 14 neonates were normal, and 5 showed signs of brain damage; 1 was not classified. CSF IL-6 levels were significantly higher in neonates with signs of brain damage. Finally, 5 neonates had adverse outcomes (4 died, 1 had cerebral palsy), 2 had mild motor impairment, and 13 had normal outcomes. CSF IL-6 levels were higher in neonates with adverse outcomes (range, 65 to 2250 pg/mL) compared with neonates with favorable outcomes. CONCLUSION: The magnitude of IL-6 response in the CSF after perinatal asphyxia is related to the severity of neonatal HIE, to brain damage, and to the neurological outcome. Our results suggest that IL-6 might play a role in neonatal hypoxic-ischemic brain damage.

Asphyxia Neonatorum↗

PubMed2000

A randomized, double-blind, placebo-controlled trial of the effects of prophylactic theophylline on renal function in term neonates with perinatal asphyxia.

BACKGROUND: The kidney is the most damaged organ in asphyxiated full-term infants. Experiments in rabbits and rats have shown that renal adenosine acts as a vasoconstrictive metabolite in the kidney after hypoxemia and/or ischemia, contributing to the fall in glomerular filtration rate (GFR) and filtration fraction. Vasoconstriction produced by adenosine can be inhibited by the nonspecific adenosine receptor antagonist, theophylline. Gouyon and Guignard performed studies in newborn and adult rabbits subjected to normocapnic hypoxemia. Their results clearly showed that the hypoxemia-induced drop in GFR could be avoided by the administration of low doses of theophylline. OBJECTIVE: This study was designed to determine whether theophylline could prevent and/or ameliorate renal dysfunction in term neonates with perinatal asphyxia. SETTING: Buenos Aires, Argentina. STUDY DESIGN: We randomized 51 severe asphyxiated term infants to receive intravenously a single dose of either theophylline (8 mg/kg; study group: n = 24) or placebo (control group: n = 27) during the first 60 minutes of life. The 24-hour fluid intake and the urine volumes formed were recorded during the first 5 days of life. Daily volume balances (water output/input ratio and weights) were determined. Severe renal dysfunction was defined as serum creatinine elevated above 1.50 mg/dL, for at least 2 consecutive days after a fluid challenge, or rising levels of serum creatinine (.3 mg/dL/day). The GFR was estimated during the second to third days of life by endogenous creatinine clearance (mL/minute/1.73 m2) and using Schwartz's formula: GFR (mL/minute/1.73 m2) =.45 x length (cm)/plasma creatinine (mg/100 mL) during the first 5 days of life. Tubular performance was assessed as the concentration of beta2-microglobulin (beta2M) determined by enzyme immunoassay, on the first voided urine 12 hours after theophylline administration. The statistical analysis for the evaluation of the differences between the groups was performed with Student's t and chi(2) tests as appropriate. RESULTS: During the first day of life, the 24-hour fluid balance was significantly more positive in the infants receiving placebo compared with the infants receiving theophyline. Over the next few days, the change in fluid balance favored the theophyline group. Significantly higher mean plasma values were recorded in the placebo group from the second to the fifth days of life. Severe renal dysfunction was present in 4 of 24 (17%) infants of the theophylline group and in 15 of 27 (55%) infants of the control group (relative risk:.30; 95% confidence interval:.12-.78). Mean endogenous creatinine clearance of the theophylline group was significantly increased compared with the creatinine clearance in infants receiving placebo (21.84 +/- 7.96 vs 6.42 +/- 4.16). The GFR (estimated by Schwartz's formula) was markedly decreased in the placebo group. Urinary beta2M concentrations were significantly reduced in the theophylline group (5.01 +/- 2.3 mg/L vs 11.5 +/- 7.1 mg/L). Moreover, 9 (33%) patients of the theophylline group versus 20 (63%) infants of the control group had urinary beta2M above the normal limit (<.018). There was no difference in the severity of the asphyxia between infants belonging to the theophylline and control groups in regards of Portman's score. Except for renal involvement, a similar frequency of multiorganic dysfunction, including neurologic impairment, was observed in both groups. The theophylline group achieved an average serum level of 12.7 microg/mL (range: 7.5-18.9 microg/mL) at 36 to 48 hours of live versus traces (an average serum level of .87 microg/mg) in the placebo group. CONCLUSIONS: Our data suggest that prophylactic theophylline, given early after birth, has beneficial effects on reducing the renal dysfunction in asphyxiated full-term infants. (ABSTRACT TRUNCATED)

Asphyxia Neonatorum↗

PubMed1998

[Perinatal asphyxia and heart problems].

PURPOSE: To evaluate the severity of cardiac complications of neonatal asphyxia in relation to the length and degree of hypoxia. METHODS: Ninety babies with an Apgar score < or = 6 were examined in the intensive care unit at our institution during seven years. Arterial blood for measuring pH, glucose, LDH and MB fraction of CK, together with serial electrocardiogram (ECG), echocardiogram and chest X rays was obtained. The fatal cases were studied with macro and microscopic examination. RESULTS: From a total of 90 cases, 73 were premature: 30 (41%) appropriate for gestation age (AGA) and 43 (59%) small for gestation age (SGA). Twenty one (23%) cases had arterial pH < 7.2. The most common clinical conditions were: pneumonia 28 (31%), anemia 24 (26%) and jaundice 12 (13%). The main cardiological findings were: systolic murmur in 46 (50%), signs of heart hypertrophy in 18 (20%) and heart failure in 8 (9%). On ECG the main findings were ST and T abnormalities. The echocardiogram showed a patent ductus arteriosus (PDA) in 20 (22%), tricuspid regurgitation in 6 (7%), pulmonary hypertension in 6 (7%), dyskinesia and ventricular dilatation in 4 (5%). Necropsy was performed in 23 cases and macro and microscopy obtained in 14; the most frequent findings were: myocite necrosis in 8 (54%), congestion, vacuolization and loss of striae in 4 (29%). CONCLUSION: In the majority of cases, patients had a benign course, even those presenting with severe acidemia. Many abnormal EKGs and echocardiograms became normal after a few weeks. Among those who had a fatal outcome, the severity of histological lesions was observed in babies who had suffered asphyxia for more prolonged periods.

Asphyxia Neonatorum↗

PubMed2002

Clinical value of color Doppler ultrasonography measurements of full-term newborns with perinatal asphyxia and hypoxic ischemic encephalopathy in the first 12 hours of life and long-term prognosis.

The cerebral blood flow velocities (CBFV) of infants with perinatal asphyxia and hypoxic ischemic encephalopathy (HIE) in the first 12 hours of their lives have been the chief focus of our concern in this study. Cerebral ischemia which can develop in the earlier hours of HIE, and the detection and diagnosis of this condition with color Doppler ultrasonography (cD-USG) will be put into discussion. Twenty-three full-term newborn infants who had perinatal asphyxia and HIE together with a control group constituting twenty full-term newborn infants who produced no problems, were included in our study. All of the infants underwent cD-USG in the postpartum period of the first 12 hours (mean 8.4 hours). Measurements being based upon peak systolic velocity (PSV), end diastolic velocity (EDV) and Pouecelout's resistive index (RI) in anterior and middle cerebral arteries were conducted. The infants, having been discharged from the unit they were followed up for mean 9.8 months in the outpatient clinic. PSV and EDV counts in the postpartum first 12 hours of 23 infants who were detected to have HIE were found to be significantly lower compared to the control group, whereas RI counts were found to be significantly higher (p < 0.05). The counts obtained from the right and left cerebral arteries of the infants with HIE were found to be corraleted with each others. The neonates in the patient group were observed to have gone through this prognosis: Three of them died, three of them had cerebral palsy, one of them had infantile spasms, and three of them had developmental retardation. When we compared the CBFV of the 10 neonates who had poor prognosis, retrospectively with the other 13 neonates who had good prognosis, PSV and EDV were found to be significantly lower and RI significantly higher (p < 0.05). In the light of the data we have obtained, cD-USG can be considered to be a highly practical device in evaluating CBVF of the infants with HIE. A skillful detection of the decrease in cerebral blood flow which can develop in the postasphyxial first 12 hours and the prospective treatments being based upon this approach would contribute to the diagnosis, treatment and prognosis of such cases.

Asphyxia Neonatorum↗

PubMed2005

Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs.

We examined the effect of the Ca(2+) concentration in the endolymph ([Ca](e)) or in the endolymphatic surface cells ([Ca](i)) on the endocochlear potential (EP) by using an endolymphatic or perilymphatic perfusion technique, respectively. (i) A large increase in [Ca](e) up to approximately 10(-3) M with a fall in the EP was induced by transient asphyxia ( approximately 2 min) or by the intravenous administration of furosemide (60 mg/kg), and a significant correlation was obtained between the EP and p[Ca](e) (= -log [Ca](e), r = 0.998). (ii) Perfusion of the endolymph with 10 mM EGTA for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP (DeltaEP(asp)), suggesting that neither [Ca](e) nor the Ca(2+) concentration gradient across the stria vascularis contributed directly to the generation of the EP in the condition of low [Ca](e). In contrast, endolymphatic perfusion with high Ca(2+) (more than 10 mM) produced a decrease in EP and a significant correlation was obtained between the EP and the Ca(2+) concentration of perfusion solution (r = 0.982), suggesting that Ca(2+) permeability may exist across the stria vascularis. (iii) The administration of a Ca(2+) chelator, EGTA-acetoxymethyl ester (AM, 0.3 mM), to the endolymph, which produced a gradual increase in EP, suppressed significantly, by 60-80%, DeltaEP(asp) or furosemide-induced changes in EP. In contrast, perilymphatic administration of 0.5 mM EGTA-AM caused no significant suppression of the DeltaEP(asp). These findings suggest that [Ca](i) plays an important role in generating/maintaining a large positive EP.

Animals↗

PubMedDate not supplied

Neonatal asphyxia, definitive markers and hearing loss.

A study of 56 severely asphyxiated infants (8 hearing impaired and 46 normally hearing) was designed to identify specific markers associated with asphyxia which could be related to hearing loss. Sixteen variables, including such items as: one- and five-minute Apgar scores, muscle tone, use of a ventilator, prolonged stay in the NICU, hypoxic-ischemic encephalopathy (HIE), other organ damage, and intra-uterine growth retardation (IUGR) were considered. Results suggested four factors related to asphyxia which are often found in the presence of hearing loss, but none of these was considered a definitive marker or predictor of such a disability. A combination of HIE, seizures, associated organ damage and IUGR should be considered a strong marker for the probability of a sensorineural hearing loss.

Apgar Score↗

PubMed1997

Perinatal asphyxia, hypoxia, ischemia and hearing loss. An overview.

Birth hypoxia, asphyxia and ischemia have often been thought to be major causes of early hearing loss or deafness. The purpose of the present review is to focus on the role of these particular factors for perinatal auditory disorders. On the whole, only a small proportion of neonatal hearing loss is caused by perinatal factors. The exact etiology of neonatal hearing loss in children with complicated deliveries is difficult to evaluate due to the large number of causative factors that might be involved. After reviewing the literature covering the past 15-20 years, it is not possible to say that we understand the relative importance of different factors and their interactions. However, in the majority of studies, birth asphyxia is not correlated with hearing loss in babies with complicated deliveries Prolonged artificial ventilation, the presence of severe hypoxic ischemic encephalopathy or persistent pulmonary hypertension are important factors. The brain is more susceptible to anoxia than the ear and both are more likely to be damaged after prolonged pre-, peri- and postnatal hypoxia-ischemia than pure hypoxia during delivery. Perinatal hypoxia is more likely to cause a temporary hearing loss than a permanent one. Preterm babies are more vulnerable than term babies. The total number of risk factors, e.g. medicated by total length of stay in the neonatal intensive care unit and length of artificial ventilation, is the best predictor of risk for hearing loss of perinatal origin. The similarities between hearing loss and cerebral palsy are pointed out; only 8% of the cases of cerebral palsy are considered to be caused by conditions during delivery.

Asphyxia Neonatorum↗

PubMed1983

Cortical oxidative metabolism under conditions of ischemia, hypoxia, and asphyxia in the rabbit.

The purpose of this investigation was to compare the effects of hypoxia, asphyxia, and ischemia on brain cortical oxidative metabolism. This study was carried out using 14 New Zealand White rabbits. The effects of episodic stress were measured simultaneously on brain functional metabolism by monitoring cortical oxygen tension (brain pO2), cortical cerebral blood flow (cCBF), cortical blood volume, and mitochondrial oxidative metabolism. During hypoxia (when the fraction of inspired O2 (FiO2) was reduced to 10%) and asphyxia (induced by turning the respirator off), there was a decrease of brain pO2 but an increase of cCBF and blood volume. Similarly, there was a reduction of cortical oxidative metabolism. In post-asphyxic conditions, an overshoot of brain pO2 and post-asphyxic oxidation of cytochrome (Cyt.) aa3 were usually shown. Under ischemic conditions (induced by sudden severe hypotension plus bilateral common carotid occlusion), cCBF and blood volume were decreased. There was also a decrease of brain pO2 and a reduction of Cyt. aa3 following ischemia. These techniques are applicable in intraoperative monitoring of patients.

Animals↗

PubMed1975

Evidence for beneficial effect of intravenous glucose on the hemodynamic response to acute asphyxia.

Anesthetized rabbits were subjected to two 4-min periods of asphyxia with a 15-min recovery period intervening. During the recovery period animals received an iv infusion of either isotonic glucose or mannitol. Results indicated that glucose had a beneficial effect on systolic blood pressure during the second period of asphyxia. A direct metabolic action of glucose on the myocardium is favored as the explanation, but other possibilities include peripheral or neurohumoral effects.

Acute Disease↗