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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drug-induced acid-base disorders may be classified into four categories with respect to the mechanism. 1. Metabolic acidosis is induced by a large acid loads incurred from exogenous sources (e.g. NH4Cl, or toxin ingestion) or endogenous acid production (e.g. generation of ketoacids or lactic acids by alcohol or phenformin) or base loss (e.g. abuse of laxatives). 2. Metabolic alkalosis results from exogenous bicarbonate loads (e.g. milk-alkali syndrome) or effective extracellular fluid contraction, potassium depletion plus hyperaldosteronism (e.g. vomiting, diuretics, or licorice). 3. Renal tubular acidosis is induced by the drugs which mainly impair proximal and/or distal tubules (e.g. vitamin D, NSAID, acetazolamide or amphotericin B). 4. Respiratory acidosis or alkalosis results from drug-induced respiratory center depression or neuromuscular impairment (e.g. anesthetic, sedative overdosage or curare) or hyperventilation (salicylates, paraldehyde, epinephrine, or nicotine).
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PMID:[Drug-induced acid-base disorders]. 143 17

Our experience of the administration of xylazine and ketamine for an induction of halothane inhalation anaesthesia in dogs is described in this paper. After this procedure had been evaluated in 10 test dogs, the xylazine-ketamine induction was used for different surgical interventions in 160 patients. After joint i.m. atropine (0.05 mg/kg) and xylazine (1.5-2 mg/kg) pre-medication general anaesthesia of the dogs was induced by an i.v. administration of 1% ketamine (2 mg/kg). After intubation and anaesthetizer connection halothane vapours had to be applied for 2 to 8 minutes at a 2.5% to 3.5% concentration to induce the tolerance stage of anaesthesia. Then the anaesthesia level was maintained by an application of halothane vapours at a 0.5 to 1.5% concentration (Tab. I). In addition to an evaluation of the anaesthesia proper, breathing-rate, inspiratory and expiratory volumes, internal body temperature were recorded, ECG was made and venous blood samples were taken to evaluate acid-base balance changes. The processing of the obtained data (Figs. 1 to 5, Tab. II) revealed a transient breathing attenuation after the xylazine-ketamine induction and partly compensated respiratory acidosis. On the basis of our results this tested method can replace the traditional thiopental induction associated with the risks of cardiopulmonary depression, or even blood circulation stoppage.
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PMID:[Use of xylazine and ketamine in the induction of halothane anesthesia in dogs]. 164 55

We compared extracellular and intracellular acid-base state in turtles (Chrysemys picta bellii) subjected to anoxic submergence to turtles made anoxic by N2-breathing. Measurements made on control animals and on animals after 1, 2, 4, or 6 h of anoxia included blood pH, PO2, PCO2, and lactate as well as liver, heart, skeletal muscle, and brain pHi (using DMO equilibration), lactate, and glycogen concentrations. We hypothesized that the anaerobic metabolic rate of submerged turtles would be depressed by the more severe extra- and intracellular acidosis, and that this would be indicated by reduced lactate accumulation and glycogen depletion. Submerged turtles became extremely acidemic due to a combined metabolic and respiratory acidosis and had significantly lower arterial pH than N2-breathing animals (6.98 and 7.34, respectively, after 6 h). In spite of this disparity in pHa, 6 h pHi values for liver, heart, and brain were similar. Likewise, our data on glycogen depletion and lactate accumulation at h 6 in these tissues suggest no dramatic differences in anaerobic metabolic rate. While skeletal muscle pHi was somewhat lower at h 6 in the submerged group (6.73 vs 6.91 for N2-breathers), we observed no differences in either glycogen depletion or lactate accumulation in this tissue between our two treatments. Thus, at h 6, in spite of a 0.37 pH unit difference in pHa and a nearly 70 mm Hg difference in arterial and presumably cytosolic PCO2, pHi and tissue lactate and glycogen concentrations were similar. These results can be explained if the in vivo intracellular buffer values (beta) of turtle tissues are very high. We conclude that extracellular acid-base state is not necessarily reflected intracellularly in vivo in turtles and care must be taken in extrapolating from one compartment to another when attempting to make inferences about metabolic depression or acid-base regulation in this species.
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PMID:Extracellular and intracellular acid-base effects of submergence anoxia and nitrogen breathing in turtles. 206 19

We studied the effect of aminophylline on twitch tension (TT) and intracellular pH (pHi) in isolated rat diaphragm strips that were fatigued, hypercapnic, or hypoxic. Superfused muscles were directly stimulated at 0.5 Hz. The pHi was measured from distribution volumes of dimethyl-oxazolidinedione. Fatigue was induced by intermittent tetanic stimulation. Hypercapnia and hypoxia were produced by altering superfusate carbon dioxide tension (PCO2) or oxygen tension (PO2). Aminophylline (1.0 mmol.l-1) reversed the twitch decay seen during fatigue or hypercapnic acidosis, and caused partial recovery of twitch depression during hypoxia. Muscle fatigue was not due to an intracellular acidosis. Both hypercapnia and hypoxia lowered pHi. Aminophylline did not alter pHi in unstimulated muscles, but caused a significant fall in pHi in stimulated muscles that were fatigued or hypoxic. High dose aminophylline improved twitch tension in diaphragm strips that were fatigued, acidotic, or hypoxic. Twitch potentiation was not due to an intracellular alkalosis. Aminophylline lowered pHi in stimulated muscle, and thus, theoretically, could sometimes be harmful in the treatment of muscle fatigue.
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PMID:The effect of aminophylline on function and intracellular pH of the rat diaphragm. 228 69

This study investigated developmental changes in the effect of acidosis on intracellular pH (pHi) and [Ca]i in the isolated heart and isolated myocyte preparations. The whole heart or myocytes of newborn (5-7 days old) and adult rabbits were loaded with the fluorescent pH indicator 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) or calcium indicator fura-2. Left ventricular pressure in the isolated heart preparation and the magnitude of cell contraction in the single-cell preparation were monitored. The heart and single cell were illuminated with excitation lights (340 and 380 nm, respectively, for fura-2 and 438 and 490 nm for BCECF). The intensity of fluorescence from the ventricular surface or from the cell was detected. [Ca]i was estimated from the following ratio: fluorescence at 505 nm during excitation at 340 nm/fluorescence at 505 nm during excitation at 380 nm. pHi was estimated from the following ratio: fluorescence at 530 nm during excitation at 490 nm/fluorescence at 530 nm during excitation at 438 nm. In the newborn, depression of contractile function during respiratory acidosis or metabolic acidosis was less than in the adult. Diastolic and systolic [Ca]i increased during respiratory acidosis in both the newborn and adult, and the net changes in [Ca]i were similar in the two age groups. During respiratory or metabolic acidosis, pHi decreased, but the decrease in the newborn was significantly less than in the adult. These data suggest that the greater resistance of the newborn myocardium to acidosis is due to the smaller change of pHi in this age group and not due to the difference in [Ca]i alteration.
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PMID:Effect of acidosis on intracellular pH and calcium concentration in the newborn and adult rabbit myocardium. 236 86

It is generally believed that metabolic acidosis prevails during cardiac arrest. However, recent experimental and clinical studies have demonstrated that respiratory acidosis in mixed venous blood and respiratory alkalosis in arterial blood with only minor increases in lactic acid characterize the early acid-base changes that follow cardiac arrest and cardiopulmonary resuscitation (CPR). While continued CO2 production with critical reduction in systemic perfusion explains the accumulation of CO2 in the venous side, the reduction of pulmonary blood flow with maintenance of constant minute ventilation explains the decreases in expired CO2 and therefore arterial PCO2. In the heart, marked increases in CO2 tension and lactic acid are associated with dramatic decreases in myocardial pH with consequent depression of contractile function. Administration of sodium bicarbonate, however, neither increases resuscitability nor improves long term outcome. Moreover, adverse effects stemming from increases in plasma osmolality, increases in hemoglobin-O2 affinity, induction of alkalemia and generation of CO2 are potentially deleterious for myocardial and cerebral function. Consequently, the American Heart Association has recently discouraged the routine administration of bicarbonate during the initial 10 minutes of CPR in which interventions with proven efficacy such as artificial ventilation, precordial compression, electric defibrillation and epinephrine administration take place. Alternative experimental buffer therapy with agents that consume CO2 have also failed to alter the outcome of cardiac arrest.
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PMID:[Cardiopulmonary resuscitation: acid-base alterations and alkalizing therapy]. 256 3

Analgesic effects were evaluated in patients who received sublingual administration of buprenorphine (0.2mg ampule for injection) as programmed every 8 hours for 3 days following upper abdominal surgery. Patients who received periodic sublingual buprenorphine obtained satisfactory postoperative analgesia and also required less analgesics than those who never received periodic administration of analgesics. Approximately one half of patients who received periodic sublingual buprenorphine required no additional analgesics. Arterial blood-gas analysis showed a significant increase in carbon dioxide tension after sublingual buprenorphine. One patient revealed marked respiratory acidosis after sublingual buprenorphine. These results suggest that periodic sublingual buprenorphine makes up for slow onset in sublingual administration and that it is also effective, convenient, and safe for pain relief after upper abdominal surgery. We, however, should pay attention to the respiratory depression caused by sublingual buprenorphine.
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PMID:[Periodic sublingual buprenorphine for pain relief after upper abdominal surgery]. 272 12

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.
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PMID:Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise. 274 55

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion. 302 33

Effects of respiratory and metabolic acidosis (pH approximately 6.8) on myocardial function were studied in the newborn and adult rabbits. Mechanical function was studied in the isolated arterially perfused heart preparation. Acidosis was induced either by increase of the perfusate PCO2 or by decrease of the bicarbonate content. During respiratory acidosis, developed tension (DT) decreased to 43 +/- 3% of control (n = 18) in the adult and this depression was significantly greater than in the newborn (DT = 92 +/- 4%, n = 6). Depression of DT by respiratory acidosis was observed even at high extracellular Ca. During metabolic acidosis, mechanical function decreased gradually and DT at 30 min into acidosis in the adult was 78 +/- 3% of control (n = 6). This depression of DT in the adult was significantly greater than in the newborn (DT at 30 min = 96 +/- 1% of control, n = 6). Statistical analysis using paired t test showed that respiratory acidosis, but not metabolic acidosis, caused significant negative inotropism in the newborn. Myofibrils were isolated and the ATPase was measured at 10(-8) to 10(-4) M Ca and at pH of 7.1 (control), 6.5, and 6.0. Reducing pH depressed the ATPase activity similarly in the newborn and adult. Intracellular buffer capacity was determined by titrating muscle homogenate with HCI. Although the initial pH was not different, addition of HCl to the homogenate caused less decrease in pH in the newborn. These data indicate that contractile function in the newborn heart is more resistant to acidosis and this may be due partly to the greater intracellular buffer capacity.
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PMID:Effect of acidosis on contractile function in the newborn rabbit heart. 315 69


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