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PubMed1986

Association of changes in bombesin immunoreactive neuroendocrine cells in lungs of newborn infants with persistent fetal circulation and brainstem damage due to birth asphyxia.

The pulmonary neuroendocrine (NE) cells, from 16 term infants dying at 1-4 days of age from birth asphyxia, were immuno stained for bombesin-like immunoreactivity by the immunoperoxidase method. The distribution and frequency of bombesin-immunoreactive NE cells were quantified morphometrically and correlated with the presence or absence of brainstem function and persistent fetal circulation (PFC). In infants with loss of brainstem function, the frequency of bombesin immunoreactive NE cells was significantly increased compared to infants with intact brainstem function, i.e. meconium aspiration with PFC. Infants with brainstem injury, with one exception, failed to develop PFC. Pathological changes in the tegmentum of the brainstem, i.e. containing the respiratory center, correlated in nine of 10 cases with loss of brainstem function. These data suggest an inverse relationship between brainstem function, release of bombesin-like peptide from the pulmonary NE cells and the functional state of the pulmonary vasculature. Intact brainstem function appears to be essential for both the release of bombesin-like peptide from the NE cells and for pulmonary vasoconstriction leading to PFC; absence of brainstem function is, on the other hand, associated with failure to release bombesin-like peptide and loss of PFC type reactivity in the pulmonary vasculature. However, it appears unlikely that bombesin itself is a direct mediator of pulmonary vasoconstriction.

Asphyxia Neonatorum↗
PubMed1995

The effect of asphyxia on the pharmacokinetics of ceftazidime in the term newborn.

The multiple-dose pharmacokinetics of ceftazidime (CAZ) (administered twice daily in a 50 mg/kg of body weight i.v. dose) were studied in 10 severely asphyxiated term infants with suspected septicemia on d 3 of life. Nine term infants with suspected septicemia but without asphyxia served as controls. Blood samples were collected from an arterial catheter at 0, 0.5, 1, 2, 4, 8, and 12 h after an i.v. bolus injection. A high performance liquid chromatography method was used to determine CAZ concentrations from serum. CAZ pharmacokinetics followed a one-compartment open model. The GFRs of all infants were simultaneously studied by means of the 24-h continuous inulin infusion technique. Elimination serum half-life (5.86 +/- 1.13 h versus 3.85 +/- 0.40 h) and serum trough concentrations (46 +/- 14 mg/L versus 23 +/- 7 mg/L) of CAZ were significantly (p < 0.001) increased in the asphyxiated newborn, whereas total body clearance of CAZ (128.4 +/- 25.1 mL/h versus 205.7 +/- 55.4 mL/h), CAZ clearance per kg (40.9 +/- 6.1 mL/h/kg versus 60.8 +/- 8.3 mL/h/kg), and the GFR expressed in mL/min (3.14 +/- 0.43 versus 4.73 +/- 0.89) were significantly (p < 0.001) decreased in the asphyxiated newborn. We conclude that twice daily administration of 50 mg/kg of body weight CAZ given to asphyxiated term newborns in the first days of life results in significantly higher serum trough levels in comparison with control infants. The impaired CAZ clearance is a result of a significantly decreased GFR.

Asphyxia Neonatorum↗
PubMed1996

Diagnostic and prognostic value of cerebral 31P magnetic resonance spectroscopy in neonates with perinatal asphyxia.

The impact of depressed neonatal cerebral oxidative phosphorylation for diagnosing the severity of perinatal asphyxia was estimated by correlating the concentrations of phosphocreatine (PCr) and ATP as determined by magnetic resonance spectroscopy with the degree of hypoxic-ischemic encephalopathy (HIE) in 23 asphyxiated term neonates. Ten healthy age-matched neonates served as controls. In patients, the mean concentrations +/- SD of PCr and ATP were 0.99 +/- 0.46 mmol/L (1.6 +/- 0.2 mmol/L) and 0.99 +/- 0.35 mmol/L (1.7 +/- 0.2 mmol/L), respectively (normal values in parentheses). [PCr] and [ATP] correlated significantly with the severity of HIE (r = 0.85 and 0.9, respectively, p < 0.001), indicating that the neonatal encephalopathy is the clinical manifestation of a marred brain energy metabolism. Neurodevelopmental outcome was evaluated in 21 children at 3, 9, and 18 mo. Seven infants had multiple impairments, five were moderately handicapped, five had only mild symptoms, and four were normal. There was a significant correlation between the cerebral concentrations of PCr or ATP at birth and outcome (r = 0.8, p < 0.001) and between the degree of neonatal neurologic depression and outcome (r = 0.7). More important, the outcome of neonates with moderate HIE could better be predicted with information from quantitative 31P magnetic resonance spectroscopy than from neurologic examinations. In general, the accuracy of outcome predictability could significantly be increased by adding results from 31P magnetic resonance spectroscopy to the neonatal neurologic score, but not vice versa. No correlation with outcome was found for other perinatal risk factors, including Apgar score.

Asphyxia Neonatorum↗
PubMed1998

Persistent increases in cerebral lactate concentration after birth asphyxia.

In this prospective study proton magnetic resonance spectroscopy (1H MRS) was used to test the hypothesis that lactate can be detected later than 1 mo after birth in the brains of infants who display severe neurodevelopmental impairment 1 y after transient perinatal hypoxia-ischemia. Data were obtained from three groups of infants: 1) eight infants suffering birth asphyxia followed by perinatal encephalopathy and abnormal neurodevelopmental outcome at 1 y of age (defined as major neurologic impairment, Griffiths quotient <85%, and low optimality score); 2) 10 infants with signs of perinatal hypoxia-ischemia but normal neurodevelopmental outcome at 1 y; and 3) six control infants with uneventful perinatal courses and normal neurodevelopment at 1 y. Between one and four examinations (median 1) were performed at median (range) 11 (4-68) wk after birth, and the cerebral concentration ratio of lactate to creatine plus phosphocreatine (Cr) calculated from each spectrum. Lactate was detected later than the 1st mo after birth in seven of eight infants with abnormal neurodevelopmental outcome [maximum detected lactate/Cr was median (range) 0.44 (0.24-0.67)]. No lactate was detected later than the 1st mo after birth in infants with normal neurodevelopmental outcome, nor in five of six control subjects, although a small amount of lactate was detected in one control infant (lactate/Cr=0.04). These results suggest that the pathologic postasphyxial process, indicated by persistent cerebral lactate, may not be confined to the period immediately after injury.

Asphyxia Neonatorum↗
PubMed2001

Early biochemical indicators of hypoxic-ischemic encephalopathy after birth asphyxia.

Hypoxic-ischemic encephalopathy (HIE) after perinatal asphyxia is a condition in which serum concentrations of brain-specific biochemical markers may be elevated. Neuroprotective interventions in asphyxiated newborns require early indicators of brain damage to initiate therapy. We examined brain-specific creatine kinase (CK-BB), protein S-100, and neuron-specific enolase in cord blood and 2, 6, 12, and 24 h after birth in 29 asphyxiated and 20 control infants. At 2 h after birth, median (quartiles) serum CK-BB concentration was 10.0 U/L (6.0-13.0 U/L) in control infants, 16.0 U/L (13.0-23.5 U/L) in infants with no or mild HIE, and 46.5 U/L (21.4-83.0 U/L) in infants with moderate or severe HIE. Serum protein S-100 was 1.6 microg/L (1.4-2.5 microg/L) in control infants, 2.9 microg/L (1.8-4.7 microg/L) in asphyxiated infants with no or mild HIE, and 17.0 microg/L (3.2-34.1 microg/L) in infants with moderate or severe HIE 2 h after birth. No significant difference was detectable in serum neuron-specific enolase between infants with no or mild and moderate or severe HIE 2 and 6 h after birth. A combination of serum protein S-100 (cutoff value, 8.5 microg/L) and CK-BB (cutoff value, 18.8 U/L) 2 h after birth had the highest predictive value (83%) and specificity (95%) of predicting moderate and severe HIE. Cord blood pH (cutoff value, <6.9) and cord blood base deficit (cutoff value, >17 mM) increase the predictive values of protein S-100 and CK-BB. We conclude that elevated serum concentrations of protein S-100 and CK-BB reliably indicate moderate and severe HIE as early as 2 h after birth.

Asphyxia↗
PubMed2003

Deficient brain RNA polymerase and altered nucleolar structure persists until day 8 after perinatal asphyxia of the rat.

RNA polymerases (POL) are integral constituents of the protein synthesis machinery, with POL I and POL III coding for ribosomal RNA and POL II coding for protein. POL I is located in the nucleolus and transcribes class I genes, those that code for large ribosomal RNA. It has been reported that the POL system is seriously affected in perinatal asphyxia (PA) immediately after birth. Because POL I is necessary for protein synthesis and brain protein synthesis was shown to be deranged after hypoxic-ischemic conditions, we aimed to study whether POL derangement persists in a simple, well-documented animal model of graded global PA at the activity, mRNA, protein, and morphologic level until 8 d after the asphyctic insult. Nuclear POL I activity was determined according to a radiochemical method; mRNA steady state and protein levels of RPA4O-an essential subunit of POL I and III-were evaluated by blotting methods; and the POL I subunit polymerase activating factor-53 was evaluated using immunohistochemistry. Silver staining and transmission electron microscopy were used to examine the nucleolus. At the eighth day after PA, nuclear POL I decreased with the length of the asphyctic period, whereas mRNA and protein levels for RPA4O were unchanged. The subunit polymerase activating factor-53, however, was unambiguously reduced in several brain regions. Dramatic changes of nucleolar morphology were observed, the main finding being nucleolar disintegration at the electron microscopy level. We suggest that severe acidosis and/or deficient protein kinase C in the brain during the asphyctic period may be responsible for disintegration of the nucleolus as well as for decreased POL activity persisting until the eighth day after PA. The biologic effect may be that PA causes impaired RNA and protein synthesis, which has been already observed in hypoxic-ischemic states.

Animals↗
PubMed1975

X-linked myotubular myopathy with fatal neonatal asphyxia.

A second family with X-linked myotubular myopathy is described. The clinical picture includes decreased fetal movements; hydramnios, in at least three cases, probably resulting from insufficient swallowing in utero; and asphyxia at birth. In three autopsy cases many myotubes were found in the muscle tissue. In five definite female carriers, muscle biopsy revealed changes, including myotubes in four. This family probably is not related to the eariler described family with X-linked myotubular myopathy, from which it differs in its 100 percent fatal outcome in the neonatal period, as compared with 25 percent in the eariler described family. A most important finding, in both families, is the possibility of recognizing clinically healthy female carriers by muscle biopsy.

Asphyxia↗
PubMedDate not supplied

Cerebral surface pH changes during asphyxia, hypotension, and circulatory arrest in the dog.

A technic is described for the measurement of cerebral surface pH in acute experiments in anesthetized dogs. During asphyxia and circulatory arrest, cerebral surface pH fell promptly and more profoundly than arterial blood or muscle surface pH; during hypovolemic hypotension (30 to 50 torr) cerebral surface pH declined later and less than muscle surface pH. The cerebral surface pH reflects the pH of the cortical interstitial fluid. Since the blood brain barrier is effectively impermeable to lactate, the changes recorded in the cerebral surface pH are a useful index of cortical intracellular metabolism.

Acid-Base Equilibrium↗
PubMedDate not supplied

Transient hypothyroxinemia in neonates with birth asphyxia delivered by emergency cesarean section.

The aim of this study was to evaluate the effects of prenatal asphyxia on perinatal thyroid function by measuring the levels of serum T4, FT4, T3, rT3, TSH and TBG in twenty-seven asphyxiated full-term infants delivered by emergency cesarean section, at birth and on the 5th day of age. All the babies had a one-minute Apgar score of less than 6 and body weight from 3 to 4.6 kg. The control group consisted of 30 healthy neonates which were delivered by elective cesarean section. The mean values of T4 and FT4 observed in the cord blood of the asphyxiated neonates were significantly lower compared to the matched controls, while there were no differences in concentrations of T3, rT3, TSH and TBG. At five days of life, serum concentrations of T4 and FT4 became normal. These results demonstrate the existence of transient hypothyroxinemia at birth in hypoxic babies delivered by emergency cesarean section.

Asphyxia Neonatorum↗
PubMed1998

Selective head cooling in newborn infants after perinatal asphyxia: a safety study.

AIMS: To determine the practicality and safety of head cooling with mild or minimal systemic hypothermia in term neonates with moderate to severe hypoxic-ischemic encephalopathy. METHODS: Study group infants >/=37 weeks' gestation, who had an umbilical artery pH </=7. 09 or Apgars </=6 at 5 minutes, plus evidence of encephalopathy. Infants with major congenital abnormalities were excluded. TRAIL DESIGN: Infants were randomized to either no cooling (controls; rectal temperature = 37.0 +/- 0.2 degreesC, n = 10) or sequentially, either minimal systemic cooling (rectal temperature = 36.3 +/- 0.2 degreesC, n = 6) or mild systemic cooling (rectal temperature = 35.7 +/- 0.2 degreesC, n = 6). Head cooling was accomplished by circulating water at 10 degreesC through a coil of tubing wrapped around the head for up to 72 hours. All infants were warmed by servo-controlled overhead heaters to maintain the allocated rectal temperature. The rectal, fontanelle, and nasopharyngeal temperatures were continuously monitored. RESULTS: From January 1996 to October 1997, 22 term infants were randomized from 2 to 5 hours after birth. All infants showed a metabolic acidosis at delivery, with similar umbilical artery pH in the control group (mean +/- standard deviation, 6.79 +/- 0.25), minimal cooling group (6.98 +/- 0.21), and mild cooling group (6.93 +/- 0.11), and depressed Apgar scores at 5 minutes in the control group (4.5 +/- 2), minimal cooling group, (4.7 +/- 2) and mild cooling group (6.0 +/- 1). In the mild-cooled infants, the nasopharyngeal temperature was 34.5 degreesC during cooling, 1.2 degreesC lower than the rectal temperature. This gradient narrowed to 0.5 degreesC after cooling was stopped. No adverse effects because of cooling were observed. No infants developed cardiac arrhythmias, hypotension, or bradycardia during cooling. Thrombocytopenia occurred in 2 out of 10 controls, 2 out of 6 minimal cooling infants, and 1 out of 6 mild cooling infants. Hypoglycemia (glucose <2.6 mM) was seen on at least one occasion in 2 out of 10 controls, 4 out of 6 minimal cooling infants, and 1 out of 6 mild cooling infants. Acute renal failure occurred in all infants. The metabolic acidosis present in all infants at the time of enrollment into the study progressively resolved despite cooling, even in the mild hypothermia group. CONCLUSIONS: Mild selective head cooling combined with mild systemic hypothermia in term newborn infants after perinatal asphyxia is a safe and convenient method of quickly reducing cerebral temperature with an increased gradient between the surface of the scalp and core temperature. The safety of mild hypothermia with selective head cooling is in contrast with the historical evidence of adverse effects with greater depths of whole-body hypothermia. This safety study and the strong experimental evidence for improved cerebral outcome justify a multicenter trial of selective head cooling for neonatal encephalopathy in term infants.

Asphyxia Neonatorum↗
PubMed2003

Treatment of term infants with head cooling and mild systemic hypothermia (35.0 degrees C and 34.5 degrees C) after perinatal asphyxia.

OBJECTIVE: To assess the safety of selective head cooling in birth-asphyxiated term newborn infants while maintaining the rectal temperature at 35.0 degrees C or 34.5 degrees C. METHODS: Twenty-six term infants with Apgar <or=6 at 5 minutes or cord/first arterial pH <7.1, plus evidence of encephalopathy, were studied. After parental consent had been obtained, 13 infants received selective head cooling with the rectal temperature maintained at 35.0 degrees C in 6 infants and at 34.5 degrees C in 7 infants. The remaining 13 infants were normothermic. Cooling was achieved by circulating water at 10 degrees C through a cap placed around the head. Rectal, fontanelle, and nasopharyngeal temperatures were monitored. RESULTS: One cooled infant died 2 days after rewarming, and 3 control infants died. Seizures occurred in 9 (69%)of 13 cooled infants and 5 (38%) of 13 control infants. Respiratory support within the first 72 hours of life was required in 10 of 13 infants in both the cooled and control groups. Three cooled infants and 1 control infant received nitric oxide for persistent pulmonary hypertension. During the same interval, 6 of the cooled infants and 4 of the control infants had episodes in which their blood pressure fell to <40 mm Hg; in 2 infants in each group, the lowest blood pressure was below 35 mm Hg. No requirement for volume expansion or increased inotropic support was seen in any infant during stepwise rewarming. All of the cooled infants demonstrated a fall in heart rate during cooling, but the rate was <80/min in only 2 cases and no infant had a rate <70/min. No infant demonstrated an abnormal rhythm or was clinically compromised by the change in heart rate. One infant cooled to a rectal temperature of 34.5 degrees C had a prolonged QT interval of 570 ms associated with a heart rate of 85/min on electrocardiogram aged 34 hours. This returned to normal after rewarming. Platelet counts below 150 x 10(9)/L, hypoglycemia below 2.6 mmol/L, and highest creatinine were not statistically different between cooled and control infants. Positive precooling blood cultures were found in 1 cooled and 1 control infant. The mean cap water input temperature used during cooling was 10 +/- 1 degrees C. During active cooling, the mean difference between rectal and nasopharyngeal temperature was 1.4 degrees C in the infants who were not receiving respiratory support, but this gradient could not be measured in those who were receiving respiratory support that involved delivery of warmed gases to the nasopharynx. CONCLUSIONS: This study suggests that selective head cooling combined with mild systemic hypothermia of 34.4 degrees C or 35.0 degrees C is a stable, well-tolerated method of reducing cerebral temperature in term newborn infants after perinatal asphyxia.

Anticonvulsants↗
PubMed1999

A resuscitated case from asphyxia by large bronchial cast.

A 62-year-old woman with bronchiectasis suffered from asphyxia due to a large bronchial cast that obstructed the bronchial tree. Immediate bronchoscopic suction of a bronchial cast of 17 cm in length through the intubated tube relieved the patients without any complications. Large bronchial casts appear to be rare in this century but it should be considered in patients with acute exacerbation of excessive sputa not only in patients with asthma or allergy but also in patients with respiratory tract infection.

Airway Obstruction↗
PubMed1997

Long term changes in NADPH-diaphorase reactivity in striatal and cortical neurons following experimental perinatal asphyxia: neuroprotective effects of hypothermia.

Nitric oxide (NO) is known to be involved in the neuropathological mechanisms triggered by excitatory aminoacids. NO(+) neurons in the brain may be detected histochemically by nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemical technique, as the latter readily labels NO synthase in the central nervous system (CNS). NADPH-d stained striatal and cortical sections were studied in 6-month-old male Sprague-Dawley rats exposed to perinatal asphyxia (PA) at 37 degrees C, as well as in animals subjected to PA plus hypothermia treatment at 15 degrees C. Quantitative image analysis was performed to compare the staining pattern in the various groups. NADPH-d(+) neurons in striatum and cortex from subsevere and severe asphyctic animals showed a significant increase in soma size and in dendritic processes versus controls and hypothermia-treated rats. These findings indicate that chronic NO changes are involved in postischemic striatal and cortical alterations induced by PA that may be prevented by hypothermia.

Animals↗
PubMed2005

Expression of intestinal trefoil factor, proliferating cell nuclear antigen and histological changes in intestine of rats after intrauterine asphyxia.

AIM: To study the expressions of intestinal trefoil factor (ITF) and proliferating cell nuclear antigen (PCNA) and histologic changes in intestine, to investigate the relationship between ITF and intestinal damage and repair after intrauterine hypoxia so as to understand the mechanism of intestinal injury and to find a new way to prevent and treat gastrointestinal diseases. METHODS: Wistar rats, pregnant for 21 d, were used to establish animal models of intrauterine asphyxia by clamping one side of vessels supplying blood to uterus for 20 min, another side was regarded as sham operation group. Intestinal tissues were taken away at 0, 24, 48 and 72 h after birth and stored in different styles. ITF mRNA was detected by RT-PCR. PCNA expression was measured by immunohistochemistry. Intestinal tissues were studied histologically by HE staining in order to observe the areas and degree of injury and to value the intestinal mucosa injury index (IMDI). RESULTS: ITF mRNA appeared in full-term rats and increased with age. After ischemia, ITF mRNA was decreased to the minimum (0.59+/-0.032) 24 h after birth, then began to increase higher after 72 h than it was in the control group (P<0.01). PCNA positive staining located in goblet cell nuclei. The PCNA level had a remarkable decline (53.29+/-1.97) 48 h after ischemia. Structure changes were obvious in 48-h group, IMDI (3.40+/-0.16) was significantly increased. Correlation analyses showed that IMDI had a negative correlation with ITF mRNA and PCNA (r = -0.543, P<0.05; r = -0.794, P<0.01, respectively). CONCLUSION: Intrauterine ischemia can result in an early decrease of ITF mRNA expression. ITF and PCNA may play an important role in the damage and repair of intestinal mucosa.

Animals↗
PubMed1998

[Immunohistochemical studies on neuronal changes in brain stem nucleus of forensic autopsied cases. I. Various cases of asphyxia and respiratory disorder].

Several nuclei in brain stem are well known to play an important role in supporting human life. However, the connection between neural changes of brain stem and the cause of death is not yet fully understood. To investigate the correlation of brain stem damage with various cause of respiratory disorders, neural changes of the arcuate nucleus (ARC), the hypoglossal nucleus (HN) and the inferior olivary nucleus (IO) were examined using immunohistochemical technique. Based on the cause of death, the forensic autopsy cases were divided into 5 groups as follows. Group I: hanging, ligature strangulation and manual strangulation, Group II: smothering and choking, Group III: drowning, Group IV: respiratory failure, control group: heat stroke and sun stroke. Brain was fixed with phosphate-buffer formalin, and the brain stem was horizontally dissected at the level of apex, then embedded in paraffin. The sections were stained with the antibodies against microtubule-associated protein 2 (MAP2), muscalinic acetylcholine receptor (mAChR), c-fos gene product (c-Fos) and 72 kD heat-shock protein (HSP70). Three nuclei showed no obvious morphological changes in all examined groups. However, in case of asphyxia (Group I to III), neurons in HN were positively stained with both HSP70 and c-Fos antibodies. This may indicate that the occlusion of upper airway results in the neuronal damage of HN without their morphological changes. Positive staining of HSP70 and c-Fos in IO was more frequently observed in Group III than other 4 groups. Since IO is involved in maintaining body balance which is often disturbed by drowning, it seems possible that neuronal damage in IO observed in drowning may be related to the disturbance of body balance. These observations indicate that immunohistochemical study on the damage to neurons in brain stem nuclei can provide useful information for determining the cause of death.

Arcuate Nucleus of Hypothalamus↗
PubMed1999

[Anion gap in perinatal asphyxia].

The aim of this study was to assess the usefulness of the anion gap (AG) for the diagnosis of Perinatal Asphyxia (PA), as well ass to evaluate the relation of AG with umbilical artery cord pH and the outcome of the newborn. We studied 62 infants in whom umbilical artery blood gases were obtained within the first 15 minutes of life. Serum sodium, chloride and potassium were simultaneously measured. AG was calculated according to the following formula: (Na + K) - (Cl + HCO3). Patients were divided in two groups depending on their pH values. Infants with a pH of 7.10 or less, were assigned to the PA group (n = 22); infants with a cord pH higher than this value, were taken as a control group. Additionally, the total group of patients was divided in survivors and non-survivors. Statistical analysis was done with mean comparation tests. Pearson's correlation index, and the sensibility, specificity and predictive values, positive and negative were calculated for a diagnosis test. Both groups were similar in gestational age, birthweight and serum electrolytes. There was significative difference in the Apgar score at one (4 vs 5.5 for PA and control group respectively) and five minutes (6 vs 7.5 respectively), as well as in the pH (6.89 +/- 0.20 vs 7.25 +/- 0.06) and the anion gap (23.4 +/- 8.1 for PA group vs 13.9 +/- 3.1 in control group). 20 mEq/L was considered as the cut-off point for AG normality. The sensibility of the test for diagnosis PA was 0.81, specificity 0.52, positive predictive value 0.48 and negative predictive value 0.84. From 37 infant newborns with a higher value than 20 mEq/L, were 11 nonsurvivors, than from 25 with a lowest measurement was 4 nonsurvivors, without statistically difference between these groups. From the total of 62 patients, were 47 survivors and 15 nonsurvivors, without difference between them in their AG, Apgar score, gestational age or serum ions. We did find statistically significant differences regarding birthweight (p < 0.05), pH (p < 0.05), and bicarbonate (p < 0.001), all these values were higher in the survivors infants. No significant correlation was found between AG and pH, however was positive correlation between AG and HCO3 (r = 0.33, p < 0.01), sodium (r = 0.22, p < 0.01) and chloride (r = 0.33, p < 0.001).

Acid-Base Equilibrium↗