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PubMed1980

The role of intracellular buffers in acid-base disturbances: mathematical modelling.

Shifts of Na+, K+, Cl- and HCO3- between the cells and extracellular fluid of nephrectomized mammals in acute response to hypercapnia and to HCl or KCl infusion are simulated in steady state models involving just intracellular buffering and a simply defined interdependence of ionic gradients. Such models integrate diverse kinds of data and suggest new interpretations. In respiratory acidosis K+, HCO3- and water leave some cells and move both to where chemical buffering is least (ECF and other cells) and to cells that regulate pH particularly well by active transport. Buffering by erythrocytes is important, but the effects of distinguishing erythrocytes from other cells in a model is mainly just to emphasize Cl- movements. Effects of departures from the mammalian norm of body composition are explored.

Acid-Base Equilibrium↗
PubMed1982

Acid-base regulation in response to environmental hypercapnia in two aquatic salamanders, Siren lacertina and Amphiuma means.

The partial pressure of CO2 (PCO2) in certain areas of the aquatic habitat of the salamanders Siren lacertina and Amphiuma means frequently rises to values of up to 60 mm Hg. This ambient hypercapnia occurs due to hindrance of gas exchange between water and air caused by dense water-surface vegetation. In order to investigate the acid-base regulation in response to the respiratory acidosis, which wound be expected to result from the high CO2 conductance of the amphibian skin, specimens of both species were subjected to water PCO2 of 47 mm Hg while having free access to normocapnic air in a closed water recirculation system. Arterial PCO2 rose considerably from 12 to 35 mm Hg in Siren and from 17 to 36 mm Hg in Amphiuma. The resultant fall in plasma pH remained uncompensated, whereas intracellular pH of white muscle and heart muscle of Siren were little affected owing to elevated intracellular bicarbonate concentrations. The bicarbonate accumulated in the intracellular compartments was in part produced by intracellular and extracellular nonbicarbonate buffering, and in part gained from the environment in exchange for Cl- ions. Elevated water bicarbonate concentration or bicarbonate infusion into Siren had no effect on the acid-base regulation. These data suggest that the availability of bicarbonate is not a limiting factor for extracellular compensation of increased PCO2, but that the threshold of the bicarbonate-regulating structures is simply not readjusted in hypercapnia. This type of regulation may have evolved as a result of the specific environmental conditions of these animals and may be considered as an energetically efficient way of maintaining a constant milieu for the pH-sensitive intracellular structures.

Acid-Base Equilibrium↗
PubMed1984

The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. I. Extra- and intracellular acid-base status.

The extracellular acid-base status of the freshwater rainbow trout (Salmo gairdneri) was continuously monitored during 24 h normoxia (PIO2 = 120-150 torr; control), 72 h hyperoxia (PIO2 = 500-600 torr) and 24 h return to normoxia. Hyperoxia induced a marked respiratory acidosis (delta pHe = -0.23 unit) due to a 3-fold elevation in arterial CO2 tension which was completely compensated over 72 h by a comparable rise in plasma bicarbonate, reflecting effective removal of acidic equivalents from the ECF. Upon return to normoxia, arterial CO2 tension rapidly returned to normal against a background of high plasma bicarbonate, provoking a metabolic alkalosis which was largely compensated by 24 h. This effective restoration of acidic equivalents in the ECF occurred more rapidly than the original removal. Intracellular acid-base status was measured during normoxia and after 72 h hyperoxia using the steady state distribution of 14C-DMO. The rate of 14C-DMO excretion was 0.479 +/- 0.048 (% DMO lost per hour) during normoxia, and significantly decreased with hyperoxia. A considerable overestimate of mean whole body pHi would have resulted had this not been taken into account. Whole body and white expaxial muscle were similar with a pHe - pHi gradient of ca. 0.5 during normoxia, and underwent identical changes during hyperoxia. Intracellular pH was completely compensated by 72 h hyperoxia as intracellular bicarbonate increased 4-fold. The overall net removal of acidic equivalents from the ICFV was approximately one half that from the ECFV , but pHe regulation did not occur at the expense of pHi regulation. The ultimate restoration of both pHe and pHi during hyperoxia must have occurred via kidney or gills.

Acid-Base Equilibrium↗
PubMed1984

The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. II. The role of the kidney.

Plasma ionic status and renal excretion of acidic equivalents and electrolytes were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control); 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. Plasma [Cl-] progressively declined in approximate equivalence to the rise in [HCO-3] which compensated the respiratory acidosis of hyperoxia, while [Na+] increased only slightly. [Ca2+] and [K+] rose, [phosphate] declined, and [NH+4] was unchanged. During normoxic recovery, the [Na+], [Cl-] and [HCO-3] changes were reversed, [K+] and [Ca2+] showed further elevations, and [NH+4] increased sharply . Renal acid output increased greatly during hyperoxia with elevations in both NH+4 and titratable components, though the latter predominated due to a marked elevation of phosphate excretion. Renal efflux rates of other electrolytes were generally homeostatic for ECF composition, with increased Na+, K+, and Ca2+ effluxes, and decreased Cl- efflux. Clearance calculations indicated that net tubular reabsorption increased for Cl-, fell for Na+ and K+, and changed over to marked net secretion for phosphate, while net ammonia secretion increased. Most trends were reversed upon return to normoxia. The critical role of phosphate in urinary electrolyte balance and acid-base regulation is emphasized. The net renal excretion of acidic equivalents accounted for only 7-10% of the total compensation observed for the whole animal during hyperoxia. The kidney contributed primarily in conserving ECF HCO-3 and secondarily in balancing branchial exchanges.

Acid-Base Equilibrium↗
PubMed1984

The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. III. Branchial exchanges.

Fluxes of both acidic equivalents (JH+net) and electrolytes across the gills were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control), 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. A highly negative JH+net (i.e., excretion) was responsible for over 90% of the compensation of respiratory acidosis induced by hyperoxia in the whole animal. Similarly, a highly positive JH+net (i.e., uptake) accounted for virtually all the compensation of metabolic alkalosis induced by normoxic recovery. Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was associated with large net losses of Na+ and net gains of Cl-, effects reflected in ECF composition. Unidirectional flux analyses with radiotracers (22Na, 36Cl) demonstrated that these net flux alterations resulted from rapid and complex changes in both influx and efflux components such that the difference between JNa+net and JCl-net was stoichiometrically equivalent to JH+net. The results support the concept that Na+ vs acidic equivalent (H+, NH+4) and Cl- vs basic equivalent (HCO-3, OH-) exchanges at the gill are dynamically adjusted in order to correct internal acid-base disturbances.

Acid-Base Equilibrium↗
PubMedDate not supplied

Oxygen consumption and acid-base balance during shallow hypothermia in the pigeon.

In pigeons, during shallow nocturnal hypothermia induced by food deprivation, body temperature falls to values between 35 degrees C and 38 degrees C. Body temperature, oxygen consumption, and arterial blood pH and PCO2 were recorded during the entrance into such nocturnal hypothermic periods. In vivo pH was kept constant, while in vivo PCO2 increased slightly during hypothermia. This caused the temperature-corrected value of pH (pH*, measured at 40 degrees C) to fall by -0.014 units/degrees C, and the total CO2-content to rise by 3.2 mM, an increase of 16%. These changes in the acid-base balance represent, in effect, a respiratory acidosis that closely parallels the normal buffer line for pigeons. Q10 values, relating oxygen uptake to body temperature, were higher than 4.0 at the very beginning of the entrance into hypothermia, indicating that the metabolic rate was actively inhibited. However, the present results do not indicate any relationship between the acidosis and the inhibition of the metabolic rate.

Acid-Base Equilibrium↗
PubMed1988

The effects of short-term hypertensive left ventricular hypertrophy on intracellular pH and intracellular electrolytes in rats.

Experiments were performed to assess the effect of left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either: (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to an acute respiratory acidosis (by varying the concentration of inspired PCO2). In association with left ventricular hypertrophy (secondary to hypertension), left ventricular pHi became significantly alkaline in all experimental hypertensive groups compared with control values; pHi control (in response to an acidosis) was also significantly improved. There was no change in resting levels of pHi or pHi control in right ventricular or skeletal muscle tissue in any hypertensive group. There was no change in resting levels of pHi or pHi control in left ventricular, right ventricular or skeletal muscle tissue from sham-operated animals. This suggests that these changes are the result of hypertrophy per se, rather than due to a generalised mechanism secondary to hypertension and operating on all tissues. There was no change in intracellular electrolyte concentration or content in association with hypertension in any tissue or group studied.

Acid-Base Equilibrium↗
PubMed1988

The effects of long-standing hypertensive left ventricular hypertrophy on intracellular pH and intracellular electrolytes in rats.

Experiments were performed to assess the effect of long-standing (4-8 weeks) left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. In this study the hypertension (and therefore the hypertrophy) was of long (4-8 weeks) duration. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to a respiratory acidosis (by varying the concentration of inspired PCO2). As described previously [Oldershaw PJ, Cameron IR, Int J Cardiol 1988;18:131-141], in the earlier stages of left ventricular hypertrophy (1-4 weeks duration) left ventricular pHi was significantly alkaline at normal levels of extracellular pH. At this late stage, with the exception of animals with aortic constriction, pHi had returned to control values. There was no change in resting levels of pHi in right ventricular or skeletal muscle tissue in any hypertensive group. The improved control of pHi in left ventricular tissue observed with hypertrophy of short duration (1-4 weeks [Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131-141]) persisted in all experimental groups at this stage (4-8 weeks) after the onset of development of left ventricular hypertrophy. There was no change in pHi control in right ventricular or skeletal muscle tissue. Neither was there any change in intracellular electrolyte concentrations or content in association with hypertension in any tissue or group studied.

Acid-Base Equilibrium↗
PubMed1995

The hemodynamic and arterial blood gas response to asphyxiation: a canine model of pulseless electrical activity.

OBJECTIVE: Asphyxiation is a time-honored animal model for producing pulseless electrical activity cardiac arrest. To date, there has not been a detailed description of the hemodynamic and arterial blood gas response to asphyxiation in a large number of animals. Our objective was to describe a single laboratory's experience with a standardized canine model of asphyxial pulseless electrical activity arrest. METHOD: Design--Data from 4 separate research protocols using a standardized asphyxial model were retrospectively reviewed. Setting--Resuscitation research laboratory. Participants--169 mixed-breed dogs. Interventions--Each animal was anesthetized and instrumented for hemodynamic monitoring. The endotracheal tube was clamped and hemodynamic data was monitored. Following loss of aortic fluctuations by thoracic aortic catheter, animals remained in pulseless electrical activity for up to 20 min. Hemodynamic data was measured continuously and arterial blood gases were sampled intermittently. RESULTS: Following endotracheal tube clamping, there was a characteristic increase in heart rate and systolic blood pressure. The heart rate peaked at 2-3 min following clamping, while the systolic blood pressure peaked at 7 min. Both heart rate and systolic blood pressure then steadily decreased until loss of aortic fluctuations. Loss of aortic fluctuations occurred 11.4 +/- 2.4 min following clamping. Following loss of aortic fluctuations, the heart rate steadily decreased. Arterial blood gases during asphyxiation and pulseless electrical activity arrest showed profound hypoxemia with hypercarbia (pH 7.03 +/- 0.07; Pco2 93 +/- 19; Po2 12 +/- 7 at loss of aortic fluctuation). CONCLUSIONS: In this canine asphyxial model of pulseless electrical activity, a characteristic hemodynamic pattern of mild tachycardia-hypertension-bradycardia-hypotension was produced. Arterial blood gases reflect a profound hypoxemia and respiratory acidosis.

Animals↗
PubMed1986

Cutaneous and renal responses to intravascular infusions of HCl and NH4Cl in the bullfrog (Rana catesbiana).

This study examined the ability of bullfrogs to correct a non-respiratory acidosis by renal and cutaneous mechanisms. Acidosis was induced by intravascular infusions of HCl (3 mmole/kg) or NH4Cl (4 mmole/kg). The acid load was removed primarily by increased renal excretion of NH4+, while urine pH and titratable buffer acid excretion changed little. Acid loading resulted in an increase in cutaneous permeability, shown by large ion losses and elevated water uptake across the skin. It is concluded that infused mineral acids were immediately buffered by the extracellular fluids, moved rapidly into the intracellular fluid compartment, and only later were slowly cleared.

Acid-Base Equilibrium↗
PubMed1992

Differential effects of hypothermia upon blood acid-base state and blood gases in sodium pentobarbital and urethane anaesthetised rats.

1. The effects of two anaesthetics, sodium pentobarbital and urethane, and the effects of anaesthesia-associated hypothermia on acid-base status and blood gases were studied in rats without assisted ventilation. 2. Manipulation of conscious rats produces a progressive increase in arterial lactate associated with slight hyperventilation. 3. Sodium pentobarbital anaesthesia produces mild respiratory acidosis accompanied by increase in lactate arterial values. Urethane anaesthesia leads to partially compensated metabolic acidosis. 4. Hypothermia reduces metabolic acidosis and hypercapnia induced by sodium pentobarbital anaesthesia. No difference between hypothermic and normothermic values was observed in urethane anaesthesia.

Acid-Base Equilibrium↗
PubMed1984

Hypothesis. Biochemical changes at the menopause: possible role of the central nervous system.

Some of the biochemical changes which occur at the menopause can be attributed to an increased rate of loss of bone but others cannot be explained in this way. Data, collected through literature search, are presented which suggest that the rise in plasma phosphate concentration at the menopause is not due primarily to increased breakdown of bone but rather to the following sequence of events: progesterone deficiency----respiratory hypoventilation----mild respiratory acidosis and hypoxia----compensatory metabolic alkalosis----altered carbohydrate metabolism----rise in plasma phosphate concentration. Increases in the concentration of many plasma constituents occur at the menopause, which appear to be due to fluid loss and haemoconcentration. A possible cause of these changes is a reduced secretion of vasopressin by the pituitary gland as a result of oestrogen deficiency. Increases in the fasting urinary excretion of phosphate, sodium and magnesium also occur at the menopause. These changes cannot be attributed to increased bone loss but could be due to the effects of oestrogen deficiency on circadian rhythms in the hypothalamus.

Acid-Base Equilibrium↗
PubMed1990

Interactions between alveolar hypercapnia and epoprostenol on the pulmonary circulation: clinical and pharmacological implications.

Hypoxic vasoconstriction has been the subject of many studies, but little is known about the interaction of hypercapnia and the pulmonary circulation. We performed two haemodynamic studies on each of three patients with pulmonary vascular disease secondary to congenital heart disease. On the first occasion ventilation was inadequate due to technical problems, and the patients were therefore hypercapnic (arterial pCO2 greater than 5.3 kPa). On the second occasion, they were normocapnic. Pulmonary vascular resistance was measured on each occasion while the patients were breathing 100% oxygen (alveolar hyperoxia) and while epoprostenol (prostacyclin) was infused at doses of 5-20 ng/kg/min. Pulmonary vascular resistance was elevated in the presence of hypercapnia and, despite oxygen and epoprostenol, could not be reduced to the levels observed in the normocapnic study. We conclude that hypercapnia causes significant vasoconstriction in infants; and that epoprostenol is a relatively ineffective pulmonary vasodilator in infants who are hypercapnic due to inadequate ventilation. Where possible, respiratory acidosis should be corrected before using oxygen or epoprostenol as a pulmonary vasodilator.

Carbon Dioxide↗
PubMed1989

Accumulation of carbon dioxide during eye surgery.

During cataract surgery, both the surgeon and the anesthesiologist need access to the patient's face. At our institution we achieved a working compromise by using an oxygen insufflating hoop, which allowed the surgeon access to the eye and a sterile field. The patient's airway was kept free by the hoop, and the patient breathed a high inspired oxygen fraction. We measured the partial pressure of carbon dioxide (PCO2) of the gas mixture under the surgeon's drapes because they form a semiclosed breathing system for the patient. Accumulation of CO2 occurred in all patients (mean +/- SD, 6.1 +/- 3.1 mmHg), but an oxygen flow of 10 L/min through the hoop prevented an additional rise of CO2 levels during the operation. Reducing the oxygen flow below 10 L/min led to increased retention of CO2 under the drapes. Paper drapes are permeable to CO2, but plastic drapes are impermeable. We did not measure the arterial partial pressure of CO2, and so we do not know whether CO2 accumulation was accompanied by respiratory acidosis.

Carbon Dioxide↗
PubMed2004

Physiological effects of dietary cadmium acclimation and waterborne cadmium challenge in rainbow trout: respiratory, ionoregulatory, and stress parameters.

A suite of respiratory, acid-base, ionoregulatory, hematological, and stress parameters were examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 45 days and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Blood sampling via an indwelling arterial catheter revealed that dietary Cd had no major effects on blood gases, acid-base balance, and plasma ions (Ca(2+), Mg(2+), K(+), Na(+), and Cl(-)) in trout. The most notable effects were an increase in hematocrit (49%) and hemoglobin (74%), and a decrease in the plasma total ammonia (43%) and glucose (49%) of the dietary Cd-exposed fish relative to the nonexposed controls. Dietary Cd resulted in a 26-fold increase of plasma Cd level over 45 days (approximately 24 ng/mL). The fish exposed to dietary Cd showed acclimation with increased protection against the effects of waterborne Cd on arterial blood P(aCO2) and pH, plasma ions, and stress indices. After waterborne Cd challenge, nonacclimated fish, but not Cd-acclimated fish, exhibited respiratory acidosis. Plasma Ca(2+) levels declined from the prechallenge level, but the effect was more pronounced in nonacclimated fish (44%) than in Cd-acclimated fish (14%) by 72 h. Plasma K(+) was elevated only in the nonacclimated fish. Similarly, waterborne Cd caused an elevation of all four traditional stress parameters (plasma total ammonia, cortisol, glucose, and lactate) only in the nonacclimated fish. Thus, chronic exposure to dietary Cd protects rainbow trout against physiological stress caused by waterborne Cd and both dietary and waterborne Cd should be considered in determining the extent of Cd toxicity to fish.

Acclimatization↗
PubMed2005

Thrombosed arch vessels after cardiac arrest because of pulmonary embolism.

An unusual case of thrombus formation in the arch vessels after cardiac arrest because of pulmonary embolism is reported. A 67-year-old woman developed pulmonary embolism that soon led to cardiac arrest. Although percutaneous cardiopulmonary support was started, the blood pressure of her upper extremity was below 20 mm Hg and blood gas analysis showed marked metabolic and respiratory acidosis. Transesophageal echocardiography revealed thrombus in the right pulmonary artery, thrombus with floppy movement in the aortic arch, and 3 arch branch arteries filled with thrombus with little blood flow around it. After thrombolytic therapy, the thrombi gradually shrunk and perfusion in the upper extremities improved. The patient was successfully weaned from percutaneous cardiopulmonary support and was discharged alive. Thrombus formation can occur in the arch branch arteries after cardiac arrest, causing unusual laboratory data. Transesophageal echocardiography is useful for obtaining real-time information in the cardiovascular system at bedside in such a critically ill patient.

Aged↗
PubMed2004

Management of congenital tracheal stenosis.

OBJECTIVES: Congenital tracheal stenosis is a rare disease. Various methods for treatment exist but there is still much debate as to the appropriate surgical procedure. We present our surgical experiences of patch tracheoplasty and slide tracheoplasty as viable methods for the treatment of congenital tracheal stenosis. METHODS: From 1994 to 2002, 13 patients were diagnosed with congenital tracheal stenosis. Eight patients (7 symptomatic and 1 asymptomatic) had their stenosis corrected, three by means of pericardial patch tracheoplasty, four by slide tracheoplasty, and one by resection and anastomosis. Concomitant operations were performed on six patients to treat congenital cardiovascular disease. Five patients showing no significant symptoms did not undergo tracheal surgery and received only cardiac procedures. A retrospective review of the hospital course, complications, and long-term results was conducted. RESULTS: Among the patch tracheoplasty group, every patient suffered from granulation tissue formation. One patient died of respiratory acidosis and one was hospitalized due to recurrent granulation tissue, which required frequent bronchoscopy. The third patient from this group is free of all symptoms. Among the slide tracheoplasty group, one patient died of anastomosis disruption. The three remaining patients are alive and well. The one patient who received resection and anastomosis is alive without symptoms. CONCLUSIONS: Surgical repair of long-segment congenital tracheal stenosis exhibited high mortality and morbidity rates. Every patient that underwent pericardial patch tracheoplasty suffered from troublesome granulation tissue. As slide tracheoplasty provided relatively good results in the short and mid-term follow-up periods, it seems to be a preferred method for the treatment of long-segment congenital tracheal stenosis.

Female↗
PubMed2005

Positive pressure ventilation in the management of acute and chronic cardiac failure: a systematic review and meta-analysis.

Chronic heart failure (CHF) is a common condition and is associated with excess morbidity and mortality, in spite of the many advances in its treatment. Chronic stable heart failure is also associated with an increased incidence of sleep-related breathing disorders, such as central sleep apnoea (CSA) and Cheyne Stokes respiration (CSR). Continuous positive airways pressure (CPAP) has been shown to alleviate the symptoms of CHF, improve left ventricular function and oxygenation. To a certain extent, CPAP also abolishes sleep-related breathing disorders in patients with chronic heart failure. In patients with acute pulmonary oedema, the use of positive pressure ventilation improves cardiac haemodynamic indices, as well as symptoms and oxygenation, and is associated with a lower need for intubation. However, some studies have cast doubts about its safety and suggest a higher rate of myocardial infarction associated with its use. In our opinion, non-invasive positive pressure ventilation and CPAP offers an adjunctive mode of therapy in patients with acute pulmonary oedema and chronic heart failure, who may not be suitable for intubation and in those not responsive to conventional therapies. Non-invasive ventilation also helps to improve oxygenation in those patients with exhaustion and respiratory acidosis. Many trials are still ongoing and the results of these studies would throw more light on the present role of non-invasive ventilation in the management of CHF.

Acute Disease↗