Decrease In Arterial Blood pH Research Articles

Changes of Acid-Base Variables in Dairy Cows with Chronically Implanted Fetal and Maternal Catheters during Late Gestation and Calving.

Simple SummaryA fetal catheterization is an efficient tool allowing longitudinal in vivo studies on hormonal and metabolic changes, including fetal blood gases and acid-base changes. These surgical techniques made it possible to take blood samples daily under aseptic conditions to determine arterial and/or venous blood samples for acid-base variables (like pH, blood gas tensions: partial pressure of carbon dioxide and partial pressure of oxygen, oxygen saturation, bicarbonate concentration, total carbon dioxide, and base excess). All these examinations may contribute to a better understanding of the physiological changes that occur during calving, which may help reach a significant reduction in losses caused by perinatal mortality, which is still high today.The objective of the present study was to evaluate the changes in maternal and fetal arterial acid-base variables withdrawn from catheterized dams and fetuses during the last days before and during calving. The average gestation length in nine cows with chronically catheterized fetuses was 285 ± 10 (SD) days. The arterial acid-base variables of a catheterized dam and fetus were very stable during late gestation. Four newborn calves showed small differences between prenatal and postnatal pH values (−0.035). At the same time, pCO2 values started to increase significantly (p = 0.02), indicating a shift towards physiological respiratory acidosis during calving. The partial pressure of oxygen and oxygen saturation values showed some non-significant improvements immediately after birth, while the other acid-base parameters did not differ. The remaining five newborn calves showed a significant decrease in arterial blood pH (p < 0.01) and BE (p = 0.01), while pCO2 tended to be higher (p = 0.06), indicating a shift towards physiological respiratory and metabolic acidosis, while the other acid-base parameters hardly differed. It is essential to mention that physiological (n = 2) and mild metabolic acidosis (n = 2) developed gradually in four newborn calves during the second stage of calving, lasting about ≤ 2 h. In contrast, in the remaining newborn calf the physiological metabolic acidosis developed during the last 3 min of birth because immediately before birth, the BE value was 0.4 mmol/L. After birth, it was −5.4 mmol/L. The results indicate that the acid-base variables may start to move gradually in the direction of expressed respiratory and metabolic acidosis only after appearing the amniotic sac and fetal feet in the vulva during the second stage of labor; therefore, it is essential to complete obstetrical assistance in time.

Effects of dexmedetomidine combined with commonly administered opioids on clinical variables in dogs.

OBJECTIVE To evaluate cardiopulmonary, sedative, and antinociceptive effects of dexmedetomidine combined with commonly administered opioids in dogs. ANIMALS 8 healthy Beagles. PROCEDURES Dogs were sedated by IM administration of each of 7 treatments. Treatments comprised dexmedetomidine (0.01 mg/kg; Dex) and the same dose of dexmedetomidine plus butorphanol (0.15 mg/kg; Dex-But), meperidine (5 mg/kg; Dex-Mep), methadone (0.5 mg/kg; Dex-Meth), morphine (0.5 mg/kg; Dex-Mor), nalbuphine (0.5 mg/kg; Dex-Nal), or tramadol (5 mg/kg; Dex-Tram). Cardiorespiratory and arterial blood gas variables and sedative and antinociceptive scores were measured before drug injection (time 0; baseline) and at 15-minute intervals for 120 minutes. RESULTS Heart rate was reduced at all time points after injection of Dex-But, Dex-Mep, Dex-Meth, and Dex-Mor treatments. There was a significant reduction of mean arterial blood pressure for Dex-But, Dex-Mep, and Dex-Mor treatments at all time points, compared with baseline. There was a significant decrease in respiratory rate, compared with the baseline value, for Dex, Dex-But, Dex-Meth, and Dex-Tram treatments from 15 to 120 minutes. A significant decrease in arterial blood pH was detected from baseline to 120 minutes for all treatments, with differences among Dex, Dex-Mep, and Dex-Mor. Reduction in Pao2 was greater for the Dex-Mep treatment than for the other treatments. The highest sedation scores were detected for Dex-Mep and Dex-Meth treatments. Antinociceptive effects were superior for Dex-But, Dex-Meth, Dex-Mor, and Dex-Nal treatments. CONCLUSIONS AND CLINICAL RELEVANCE Drug combinations caused similar cardiorespiratory changes, with greater sedative effects for Dex-Mep and Dex-Meth and superior antinociceptive effects for Dex-But, Dex-Meth, Dex-Mor, and Dex-Nal.

Identification of Three Exercise-induced Mortality Risk Factors in Patients with COPD

The survival rate of chronic obstructive pulmonary disease (COPD) patients with severely reduced exercise capacity is extremely low. We recently identified three life-threatening pathophysiological conditions during cardiopulmonary exercise testing (CPET): (1) exercise-induced hypoxemia, (2) sympathetic overactivity, and (3) progressive respiratory acidosis at low-intensity exercise. The present prospective observation study aimed to determine whether these parameters constitute risk factors of mortality in moderate-to-very severe COPD. Ninety-six COPD patients were followed-up, monthly, for >3 years. Subsequently, spirometry and CPET were performed to examine parameters of exercise-induced hypoxemia ([PaO2 slope, mmHg/L · min−1] = Decrease in PaO2/ΔV˙ O2 (Difference in ΔV˙ O2 between at rest and at peak exercise)), progression of acidosis ([ΔpH/ΔV˙ O2,/L · min−1] = Decrease in pH/ΔV˙ O2), and sympathetic overactivity ([Δnorepinephrine (NE)/ΔV˙ O2, ng/mL/L · min−1] = Increase in NE/ΔV˙ O2). Univariate analysis revealed a significant association between the three conditions with increased mortality. Kaplan–Meier analysis showed that the quartile combining the steepest PaO2 slope (≤–55 mmHg/ΔV˙ O2 [L/min]), steepest decrease in arterial blood pH (≤ –1.72/ΔV˙ O2 [L/min]), and most rapid increase in plasma NE level (≥ 5.2 ng/VO2 [L/min]) during incremental exercise was associated with higher all-cause mortality. These conditions showed cumulative effects on COPD patients’ survival. Multivariate analyses revealed that these three life-threatening factors are also independent predictors of mortality based on age, heart rate and PaO2 at rest, body mass index, and forced expiratory volume in 1 s. Thus, these new exercise-induced mortality risk factors may lead to more efficient pulmonary rehabilitation programs for COPD patients based on patient-specific exercise-induced pathophysiological profiles.

Risk factors for liver abscess formation in patients with blunt hepatic injury after non-operative management.

To identify risk factors for liver abscess formation in patients with blunt hepatic injury who underwent non-operative management (NOM). From January 2004 to October 2008, retrospective data were collected from a single level I trauma center. Clinical data, hospital course, and outcome were all extracted from patient medical records for further analysis. A total of 358 patients were enrolled for analysis. There were 13 patients with liver abscess after blunt hepatic injury. Patients with abscess had a significant increase in glutamic oxaloacetic transaminase (GOT, p=0.006) and glutamic pyruvic transaminase (GPT, p<0.0001), and a decrease in arterial blood pH (p=0.023) compared to patients without abscess in the univariate analyses. In addition, high-grade hepatic injury and transarterial embolization (TAE, p<0.001) were also risk factors for liver abscess formation. Five factors (GOT, GPT, pH level in the arterial blood sample, TAE, and high-grade hepatic injury) were included in the multivariate analysis. TAE, high-grade hepatic injury, and GPT level were statistically significant. The odds ratios of TAE and high-grade hepatic injury were 15.41 and 16.08, respectively. A receiver operating characteristic (ROC) analysis was used for GPT, and it suggested cutoff values of 372.5 U/L. A prediction model based on the ROC analysis had 100% sensitivity and 86.7% specificity to predict liver abscess formation in patients with two of the three independent risk factors. TAE, high-grade hepatic injury, and a high GPT level are independent risk factors for liver abscess formation.

A randomized controlled study evaluating the effects of the temperature of insufflated CO2 on core body temperature and blood gases (an experimental study)

Heated carbon dioxide (CO2) was used for pneumoperitoneum (Pp) to prevent hypothermia. This study aimed to investigate the relationship between the temperature of the insufflated CO2 and blood gases together with the core body temperature (CBT). A prospective controlled study was performed with 24 pigs weighing approximately 20 kg randomized into four groups of 6 pigs each. A pneumoperitoneum at 12 mmHg of pressure was applied for 60 min with the pig under general anesthesia. The CO2)temperature was 22 degrees C in group 1, 37 degrees C in group 2, and 7 degrees C in group 3. In the "sham" group, pneumoperitoneum was not applied. Arterial blood pH and partial pressure of CO2 (PaCO2) were analyzed before insufflation, every 15 min during the pneumoperitoneum, and 15 min after the desufflation. The CBT was recorded before the insufflation, every 20 min during pneumoperitoneum, and 20 min after the desufflation. Blood gas analyses and CBT records for the "sham" group were performed at the same intervals. Arterial blood pH gradually decreased during pneumoperitoneum. At the 60th minute of pneumoperitoneum, a minimum decrease in arterial blood pH (0.04; p = 0.027) and a minimum increase in PaCO2 (3.67; p = 0.027) were recorded in group 3, whereas a maximum decrease in arterial blood pH (0.18; p = 0.027) and a maximum increase in PaCO2 (17.17; p = 0.027) were recorded in group 2. There was a significant negative correlation between PaCO2 and arterial blood pH in all the groups (r = -0.993; p < 0.01). The mean values of CBT decreases were statistically significant in all the groups: group 1 (p = 0.023), group 2 (p = 0.026), group 3 (p = 0.026), and "sham" group (p = 0.024). The changes in PaCO2 were directly proportional and the changes in pH contrarily proportional to the temperature of the insufflated CO2. Significant differences in CBT decreases were found between the groups receiving heated gas and room temperature gas and the groups receiving heated gas and gas below room temperature.

Acid-base analysis of individuals following two weight loss diets

To examine the effects of low-carbohydrate, ketogenic (LCKD) and low-fat (LFD) diets on acid-base status. Prospective analysis of volunteers from two clinical trials. Subset of 39 volunteers from a randomized trial comparing the effects of an LCKD with an LFD, and a single-arm trial of an LCKD. Outpatient research clinic. LCKD (initially <20 g of carbohydrate daily) or LFD (<30% of energy from fat, 500-1000 kcal energy reduction) instruction. Arterial blood gas analysis, serum chemistries (electrolytes, urea nitrogen/creatinine, glucose, ketone bodies, lactate), anion gap, and urine ketone bodies measured at weeks 0, 2, 8, and 24. Participants had a mean (+/-standard deviation) age of 43.5+/-9.3 years; 28 (72%) were female, 29 (74%) were Caucasian. Using linear mixed-model analysis to examine blood test changes from baseline to 24 weeks, the LFD group experienced a decrease in arterial blood pH from a mean of 7.43 at week 0 to 7.40 at week 24 (P=0.03), and the LCKD group experienced a decrease from 7.42 at week 0 to 7.40 at week 24 (P=0.01). The lowest pH measurements observed were 7.34 in the LFD group and 7.37 in the LCKD group. Although serum bicarbonate appeared to decrease from baseline at weeks 2 and 8 in the LCKD group, the change at 24 weeks was not statistically significant in either diet group, and only four of 131 (two of 92 from the LCKD group) measurements were less than 22 mmol/l. The proportion of participants with elevated urine and serum ketone body levels rose in the LCKD group only, was highest at week 2, and decreased over the subsequent time points. In individuals following an LCKD or an LFD, blood pH decreased mildly and the LCKD group experienced a small, transient decrease in serum bicarbonate in conjunction with mild ketosis. This suggests that an LCKD induced a mild compensated metabolic acidosis, but no individual showed evidence of significant metabolic derangement.

The effects of endothelin-1 on the cardiorespiratory physiology of the freshwater trout (Oncorhynchus mykiss) and the marine dogfish (Squalus acanthias).

The aim of the present study was to evaluate the effects of endothelin-l-elicited cardiovascular events on respiratory gas transfer in the freshwater rainbow trout (Oncorhynchus mykiss) and the marine dogfish (Squalus acanthias). In both species, endothelin-1 (666 pmol kg(-1)) caused a rapid (within 4 min) reduction (ca. 30-50 mmHg) in arterial blood partial pressure of O2. The effects of endothelin-1 on arterial blood partial pressure of CO2 were not synchronised with the changes in O2 partial pressure and the responses were markedly different in trout and dogfish. In trout, arterial CO2 partial pressure was increased transiently by approximately 1.0 mmHg but the onset of the response was delayed and occurred 12 min after endothelin-1 injection. In contrast, CO2 partial pressure remained more-or-less constant in dogfish after injection of endothelin-1 and was increased only slightly (approximately 0.1 mmHg) after 60 min. Pre-treatment of trout with bovine carbonic anhydrase (5 mg ml(-1)) eliminated the increase in CO2 partial pressure that was normally observed after endothelin-1 injection. In both species, endothelin-1 injection caused a decrease in arterial blood pH that mirrored the changes in CO2 partial pressure. Endothelin-1 injection was associated with transient (trout) or persistent (dogfish) hyperventilation as indicated by pronounced increases in breathing frequency and amplitude. In trout, arterial blood pressure remained constant or was decreased slightly and was accompanied by a transient increase in systemic resistance, and a temporary reduction in cardiac output. The decrease in cardiac output was caused solely by a reduction in cardiac frequency; cardiac stroke volume was unaffected. In dogfish, arterial blood pressure was lowered by approximately 10 mmHg at 6-10 min after endothelin-1 injection but then was rapidly restored to pre-injection levels. The decrease in arterial blood pressure reflected an increase in branchial vascular resistance (as determined using in situ perfused gill preparations) that was accompanied by simultaneous decreases in systemic resistance and cardiac output. Cardiac frequency and stroke volume were reduced by endothelin-1 injection and thus both variables contributed to the changes in cardiac output. We conclude that the net consequences of endothelin-1 on arterial blood gases result from the opposing effects of reduced gill functional surface area (caused by vasoconstriction) and an increase in blood residence time within the gill (caused by decreased cardiac output.

Stimulation of pulmonary C fibres by lactic acid in rats: contributions of H+ and lactate ions.

1. The contributions of H+ and lactate ions to the stimulation of single pulmonary C fibres by lactic acid were examined in anaesthetized and artificially ventilated rats. 2. Lactic acid injected into the right atrium caused a transient decrease in arterial blood pH (pHa) and a short but intense burst of afferent activities in pulmonary C fibres, whereas sodium lactate had no effect. The fibre activity usually reached a peak within 1-1.5 s, with an onset latency of < 1 s, and returned to the baseline in 5 s. 3. The injection of hydrochloric acid at the same pH as that of lactic acid did not significantly decrease pHa, nor did it stimulate any C fibres studied. 4. Formic acid has a pKa value (the negative logarithm of the dissociation constant) almost identical to that of lactic acid; thus, its injection decreased pHa to the same degree as did the injection of lactic acid. However, the response of C fibres to lactic acid was 134% stronger than that to formic acid. 5. We conclude that H+ is primarily responsible for the activation of pulmonary C fibres by lactic acid, probably through a direct effect of H+ on these afferent endings. The lactate ion, by itself, does not activate C fibres, but it seems to potentiate the stimulatory effect of H+ on these afferents.

Effects of growth hormone on plasma ionic regulation, respiration and extracellular acid-base status in trout (Oncorhynchus mykiss) transferred to seawater

The effects of trout recombinant growth hormone (rtGH) treatment (0.25 μg g(-1) by intraperitoneal implant) on plasma ionic regulation, extracellular acid-base status and respiration were investigated in freshwater rainbow trout and during a 4-day period after direct transfer into seawater (35 g 1(-1)).In freshwater, rtGH treatment resulted in a significant increase in gill (Na(+), K(+)) ATPase activity and in standard metabolism (MO2). The latter would mainly result from a higher rate of protein synthesis. Direct transfer from freshwater to seawater induced a decrease in arterial blood pH, far more pronounced in controls than in treated fish. This effect could be regarded in both groups mainly as a metabolic acidosis resulting from extracellular ion composition changes (i.e., an increase higher in chloride than in sodium, more marked in controls than in treated fish). As the rise in PaCO2, in spite of an increase in ventilatory activity, is more significant in controls than in treated fish, it can be assumed that rtGH treatment lightened the decrease in the gas diffusing capacity of gills induced by transfer to seawater. The initial increase in MO2 in both controls and treated fish could be the consequence of an increase in energetic cost of ventilation and osmoregulation. Then, in treated fish, the persistent high level of M may indicate a stimulation of intermediary metabolism by rtGH. In addition, the absence in treated fish of an increase in plasma lactate concentration, as observed in controls, would indicate that rtGH attenuated the decrease in O2 affinity of haemoglobin foreseeable from the metabolic acidosis.

CHANGES IN EPINEPHRINE (E) AND MEAN ARTERIAL BLOOD PRESSURE (MABP) DURING HYPERCARBIA (HC): EFFECTS ON BRAIN BLOOD FLOW (BBF) IN THE NEWBORN PIGLET

We have previously shown that HC results in spontaneous elevations of MABP and pressure passive increases in brain blood flow (BBF) in the newborn piglet. We further analyzed the mechanism of this phenomena by correlating these changes with acid base and plasma E data in 20 awake newborn piglets where HC (PaCO2:50-60 mmHg) was induced by breathing 15% CO2. During HC, E, MABP, and BBF increased significantly (p<0.05). The increase in MABP was directly related to E (r=.71 p<0.001). However, both E and MABP also demonstrated a significant correlation with the decrease in arterial blood pH (pH vs E:r=-.91, p<0.001; pH vs MABP:r=-.84 p<0.001) and the increase in base deficit (BD) (BD vs E:r=0.83, p<0.001), BD vs MABP:r=0.84 p<0.001). PaCO2 was not related to the E or MABP increase. The increase in total BBF (TBBF) and regional BBF were directly related to the elevations of MABP (TBBF:r=0.58 p<0.01 cerebrum r=0.57 p<0.01, cerebellum:r=0.67 p<0.01, boundary zone r=0.62 p<0.01 and periventricular area r=.76 p<0.001). We conclude that HC induced hypertension and brain hyperperfusion is partly due to catecholamine (epineprine) release which in turn is mediated through concurrent metabolic acidosis.

Effects of exercise stress on acid-base balance and respiratory function in blood of the teleost Tinca tinca

We measured the effects of severe, short-term exercise stress on the acid-base balance, the O 2 transporting properties and the cofactors for O 2 binding in the blood of tench, Tinca tinca. Short-term severe exercise resulted in a drastic decrease in arterial blood pH which is attributed to a mixed respiratory and metabolic acidosis. Concomitantly arterial P o 2 rose in apparent compensation for the detrimental effects of the acidosis on O 2 transport by the blood.

Sodium and chloride balance in the african catfish Clarias mossambicus

1. 1. Ionic regulation and respiration was studied in the African cat fish Clarias mossambicus. 2. 2. In freshwater Na + and Cl − total effluxes were about 0.3 mM/kg/hr for each ion, values similar to those reported for other freshwater fish. Approximately half the ionic efflux originated from the gills, around 30% from the urine and the remainder possibly from the skin. 3. 3. When taken out of water and placed in moist surroundings ionic losses decreased to less than half the former rate and were divided equally between urine and possibly skin. 4. 4. Emersed catfish showed a marked acidosis (significant decrease in arterial blood pH from pH 7.66 to 7.52), probably arising from inability to expel metabolic CO 2. 5. 5. In water Clarias had a total nitrogen output of 0.3 mM N/kg/hr, predominantly ammonia with 13% urea. Returned to water after 4 in air the N output increased to 1.14 mM N/kg/hr containing 36% urea.

Physiologic effects of transfusing red blood cells with high or low affinity for oxygen to passively hyperventilated, anemic baboons: systemic and cerebral oxygen extraction.

Anemic, passively hyperventilated baboons were given preserved red blood cells either with increased or with slightly reduced affinity for oxygen to restore the red cell volume. In the high affinity group there was a 50% increase in cerebral blood flow immediately after the transfusion, but there was no significant change in the low affinity group. The cardiac output decreased slightly in the low affinity group, and increased slightly but insignificantly in the high affinity group. Two hours after transfusion the cerebral blood flow had returned to normal in the high affinity group. In both groups there was a decrease in arterial blood pH and an increase in Po2 in blood from the pulmonary artery and the jugular vein after transfusion. A 40% restoration of the 2,3 DPG level occurred within 4 hours of the transfusion of red cells with high affinity for oxygen, and this rapid increase was associated with increases in blood pH and inorganic phosphorus levels. Preserved red cells with high affinity for oxygen and low 2, 3 DPG levels significantly increased the cerebral circulation during the 2-hour posttransfusion period. These findings lend support to the recommendation that preserved red cells with normal or elevated 2,3 DPG levels be administered to patients in hemorrhagic or septic shock, and to patients subjected to extracorporeal circulation during cardiac surgery in order to lessen the demand for increased blood flow and to ensure adequate tissue oxygenation during the postoperative period.

Cardiovascular and hematological parameters affected by feeding various polychlorinated biphenyls to the single comb white leghorn cockerel.

The effect of dietary PCBs (50–200 ppm) on some cardiovascular and hematological parameters in the SCWL cockerel was investigated. Heart rate was significantly reduced by PCB 1242 and 1254 at ≥100 ppm and was not altered by PCB 1221 or 1260 at 150 ppm. A significant decrease in arterial blood pH was observed with PCB 1254 at 150 ppm. Mean blood pressure was unaffected by any treatment used. Hemoglobin concentration, HCT, and total erythrocyte count were found to be significantly decreased by PCBs 1242 and 1254 at ≥50 ppm. These same parameters were not affected by PCB 1221 or 1260 at any level used. It was concluded that the anemia observed was due solely to a decrease in total erythrocyte concentration. The possibility that these changes may be due to a decrease in erythropoiesis is discussed. Pericardial fluid volume was increased with PCBs 1242 and 1254; however, there was no correlation between the magnitude of the bradycardia and the amount of pericardial fluid.

Quinidine intoxication: An experimental study of the effect of molar sodium lactate and potassium chloride

1. 1. Thirty-six dogs which weighed 7 to 13 kilograms were studied for the changes in plasma potassium, sodium, arterial blood pH, electrocardiogram, and arterial blood pressure after intravenous administration of quinidine. The effects of molar sodium lactate and potassium chloride given prior to or after the administration of quinidine were determined. 2. 2. There was a definite decrease in the concentration of plasma potassium and in arterial blood pH after the intravenous administration of quinidine. The mean decrease in plasma potassium was 0.6 and 0.9 mEq. per liter for moderate and severe quinidine intoxication, respectively. The mean decrease in arterial blood pH ranged from 0.04 to 0.09. No significant change in plasma sodium was noted. 3. 3. When quinidine was given initially and followed by molar sodium lactate, there was a further decrease in plasma potassium (mean decrease of 0.4 mEq. per liter), a moderate increase in blood pressure and pulse rate, narrowing of the P-R interval and QRS duration, and appearance of a prominent U wave. 4. 4. When given prophylactically, molar sodium lactate failed to prevent the hypotensive effect of quinidine, and had no significant beneficial effect on severe quinidine intoxication. 5. 5. When quinidine was followed by potassium chloride, 2 out of 5 dogs developed a significant increase in pulse rate and blood pressure. Similar doses of potassium chloride given prior to the administration of quinidine did not enhance the effect of quinidine. 6. 6. The possible mechanisms of action of molar sodium lactate are discussed. 7. 7. Whether molar sodium lactate has any significant value in the treatment of quinidine intoxication remains to be determined.