Plasma Acid-base Status Research Articles

Effects of Broiler Rearing Environment on Transmission of F-Strain Mycoplasma gallisepticum from Commercial Layer Hens to Broiler Chickens: Role of Acid-Base Balance

Two trials were conducted concurrently to determine and compare, blood pH, blood gases, hematocrit and hemoglobin in F-strain Mycoplasma gallisepticum (FMG) inoculated layers and FMG contactinfected broilers. At the termination of the study, FMG-inoculated layers had the highest partial pressure of O and the lowest partial pressure of CO as compared with the other treatment groups. Blood pH values 2 2 were unaffected by FMG inoculation. Hematocrit and blood concentrations of hemoglobin were slightly higher and HCO levels were lowest in FMG contact-infected broilers in comparison to the other treatments groups. 3 Mycoplasma gallisepticum inoculated layers also resulted in a significant increase in blood concentrations of K , a decrease in Na , but no significant effects on blood concentrations of Ca and Cl . There were no + + 2+ differences in plasma glucose, cholesterone, triglyceride and anion gap, but osmolality was significantly reduced in FMG contact-infected broilers. Results indicate that inoculation of layers with FMG vaccine results in changes in plasma acid-base status along with changes in other blood metabolic variables. However, the FMG inoculation did not prevent homeostatic regulation of acid-base balance, as indicated by constant blood pH. The significant increase in pO in FMG inoculated layers is generally associated with an oxygen2 dependent improvement in tissue oxygenation. Elevated arterial partial pressure of oxygen is beneficial to maximize oxygen transport capacity along with high concentrations of hemoglobin and hematocrit to carry oxygen throughout the body. It was concluded that in addition to protecting birds from MG infection, an FMG vaccine may improve the layer chicken’s ability to withstand the harmful effects of stressors on their performance and well-being.

Stress and acid-base balance in chickens

Two trials were conducted to study the effects of continuous infusion of adrenocorticotropic hormone (ACTH) on acid-base balance in broiler chickens. Osmotic pumps delivered 8 IU of ACTH in saline/kg of BW/d for 7 d or the same saline volume as used in ACTH at 1 µL/h for 7 d. Blood samples were taken on d 0 (baseline values) and on d 4, 7, and 14 after onset of the infusions. The ACTH treatment increased the hematocrit, partial pressure of CO2, anion gap, corticosterone, mean corpuscular hemoglobin concentration, the blood concentrations of hemoglobin and HCO3-, and reduced the partial pressure of O2, plasma concentrations of Na+, K+, and Cl-. Blood pH values and plasma concentrations of Ca2+ were unaffected by ACTH treatment. The ACTH infusion also resulted in a significant increase in plasma glucose, cholesterone, high-density lipoprotein, and triglyceride. There were no differences in any of the blood constituents measured from control groups. Results indicate that infusion of ACTH resulted in changes in plasma acid-base status along with changes in other blood metabolic variables. However, the ACTH treatment did not prevent homeostatic regulation of acid-base balance, as indicated by constant blood pH. There was, however, an increased need for O2 to support gluconeogenic energy production; the birds responded by increased erythropoiesis. This adaptive response provided greater numbers of erythrocytes and thus a higher amount of circulating hemoglobin to deliver O2 for metabolism.

Hypokalaemia and paralysis.

It is not uncommon for patients to present to the emergency room with severe weakness and a markedly low plasma potassium concentration. We attempted to identify useful clues to the diagnosis of hypokalaemic periodic paralysis (HPP), because its acute treatment aims are unique. We retrospectively reviewed charts over a 10-year period: HPP was the initial diagnosis in 97 patients. Mean patient age was 29+/-1.1 and the male:female ratio was 77:20. When the final diagnosis was HPP (n=73), the acid-base state was normal, the urine K(+) concentration was low, and the transtubular K(+) concentration gradient (TTKG) was <3. In patients with thyrotoxic periodic paralysis (TPP) (n=39), hypokalaemia was very commonly accompanied by hypophosphataemia (1.9+/-0.1 mg/dl). A clinical diagnosis of sporadic periodic paralysis (SPP) was made if hyperthyroidism and a family history of HPP were both absent (n=29). One subgroup of patients with HPP had a severe degree of hypernatraemia (167+/-5.0 mmol/l, n=3). There were only two patients with familial periodic paralysis (FPP). In 24 patients, the initial diagnosis was HPP, but subsequent studies failed to confirm this diagnosis. Each of these patients had an acid-base disorder, a high rate of renal K(+) excretion in the presence of hypokalaemia, and a TTKG of close to 7. With respect to therapy, much less K(+) was given to patients with HPP, yet 1:3 subsequently had a plasma K(+) concentration that eventually exceeded 5.0 mmol/l. Using plasma acid-base status, phosphate and K(+) excretion parameters allows a presumptive diagnosis of HPP with more confidence in the emergency room.

Calciuric response to an acute acid load in healthy subjects and hypercalciuric calcium stone formers

Excessive animal protein consumption is associated with a greater risk of occurrence of renal calcium stone, presumably because of the attendant endogenous acid production. Indeed, chronic acid load enhances urinary calcium excretion possibly through an increased bone calcium release. Because acute studies are best designed to elucidate the mechanism, renal or extra renal, underlying hypercalciuria in the setting of enhanced acid load, we examined the response of 9 healthy adults (8 males, 1 female, aged 38 +/- 3 years, weight 67 +/- 2 kg) and 34 hypercalciuric recurrent calcium stone formers (31 males, 3 females, aged 44 +/- 2 years, weight 72 +/- 2 kg), without any associated disease, to an oral acid load (NH4Cl 2 mmol/kg body wt). After an overnight fast, each patient and control was studied during one one-hour period before and three two-hour periods after their intake of the acid load. An additional group of four time-control subjects (4 males, aged 33 +/- 2 years, weight 66 +/- 2 kg) was studied as the experimental groups except that they did not receive the acid load. On baseline, the three groups exhibited similar glomerular filtration rates, net acid excretions, and plasma calcium and magnesium concentrations. However, fasting urine calcium and magnesium excretions were higher in hypercalciuric calcium stone formers than in healthy control or time-control subjects. In time-control subjects, plasma acid base status, net acid excretion, filtered loads of calcium and magnesium, and urinary calcium and magnesium excretions remained unchanged all over the study. By contrast, after the oral acute acid load, net acid excretion increased and urinary pH decreased similarly in patient and control groups; glomerular filtration rate did not change, as well as plasma calcium and magnesium concentrations. Nevertheless, urinary calcium and magnesium excretions markedly increased, in both groups, independently of changes in tubular sodium handling and in plasma parathyroid hormone concentration. The increase in urinary calcium and magnesium excretions that occurred in the absence of any change in the filtered load of calcium and magnesium was therefore mediated by a decrease in tubular calcium and magnesium reabsorption, independent of PTH, but dependent on changes in net acid excretion. A positive linear relationship between urinary calcium and magnesium excretions suggested that the target tubular site for acid load was the thick ascending limb of Henle's loop. Finally, a negative linear relationship was demonstrated between the acid load-induced increase in urinary calcium excretion and fasting urinary calcium excretion; indeed, the lowest calciuric responses were observed in patients with the highest fasting urinary calcium excretion. Thus there was no additional effect of the acid load-induced inhibition on intrinsic defect in tubular calcium reabsorption which suggests that the tubular target site for acid load and the site of calcium transport defect in idiopathic hypercalciuria may be the same.

Lidocaine extraction by the in vivo and isolated perfused pig liver

Hepatic lidocaine elimination is increasingly being used to assess hepatic function. Although the isolated liver is extensively used as a model of in vivo function, it is necessary to determine whether this is a suitable model for in vivo lidocaine elimination. Fourteen male pigs (22-25 kg) were divided into two groups. Seven were anesthetized, and catheters and perivascular flow probes placed for transhepatic sampling and hepatic arterial and portal venous flow measurement. Sampling was performed at hourly intervals to determine hepatic function and plasma composition. Hepatic lidocaine elimination was determined during the second hour of a lidocaine infusion (1.41 mg.kg-1.min-1 for 10 min, then 0.165 m.kg-1.min-1), during which time the mean hepatic blood flow rates, plasma acid base status and body temperature were measured so that these could be emulated in the isolated perfused liver experiments. Seven male pigs were then anesthetized and the liver resected and cannulated for isolated liver perfusion. Hepatic arterial and portal venous blood flow and perfusate temperature were set to the mean in vivo values, and hepatic function and perfusate composition assessed at corresponding times. Hepatic lidocaine elimination was determined at a similar hepatic inflow whole blood concentration (+/- 5 micrograms.ml-1) to that in vivo over the second hour of lidocaine administration (40 mg bolus, then 2.8 mg.min-1). Lidocaine extraction ratio in vivo (0.61 +/- 0.04) [mean +/- SEM] and ex vivo (0.63 +/- 0.02) was similar, as was hepatic blood clearance (381 +/- 70 vs 363 +/- 16 ml.min-1) and hepatic blood intrinsic clearance (1132 +/- 280 vs 1069 +/- 109 ml.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of lungs and inactive muscle in acid-base control after maximal exercise.

The pulmonary responses and changes in plasma acid-base status occurring across the inactive forearm muscle were examined after 30 s of intense exercise in six male subjects exercising on an isokinetic cycle ergometer. Arterial and deep forearm venous blood were sampled at rest and during 10 min after exercise; ventilation and pulmonary gas exchange variables were measured breath by breath during exercise and recovery. Immediately after exercise, ventilation and CO2 output increased to 124 +/- 17 1/min and 3.24 +/- 0.195 l/min, respectively. The subsequent decrease in CO2 output was slower than the decrease in O2 intake (half time of 105 +/- 15 and 47 +/- 4 s, respectively); the respiratory exchange ratio was greater than 1.0 throughout the 10 min of recovery. Arterial plasma concentrations of Na+, K+, and Ca2+ increased transiently after exercise. Arterial lactate ion concentration ([La-]) increased to 14-15 meq/l within 1.5 min and remained at this level for the rest of the study. Throughout recovery there was a positive arteriovenous [La-] difference of 4-5 meq/l, associated with an increase in the arteriovenous strong ion difference ([SID]) and by a large increase in the venous Pco2 and [HCO3-]. These findings were interpreted as indicating uptake of La- by the inactive muscle, leading to a fall in the muscle [SID] and increase in plasma [SID], associated with an increase in muscle PCO2. The venoarterial CO2 content difference was 38% greater than could be accounted for by metabolism of La- alone, suggesting liberation of CO2 stored in muscle, possibly as carbamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-base regulation following acute acidosis in seawater-adapted rainbow trout, Salmo gairdneri: a possible role for catecholamines.

A fall in blood pH was induced by intra-arterial infusion of HCl in seawater-adapted rainbow trout (Salmo gairdneri). The acute acidosis resulting from HCl infusion caused a short-lived decrease in plasma bicarbonate concentration ([HCO3-]) and an increase in arterial CO2 tension (PaCO2). Erythrocyte pH and bicarbonate concentrations were not significantly altered by the infusion of acid. Injection of acid did, however, stimulate a branchial net H+ efflux which could be primarily accounted for by a net uptake of bicarbonate equivalent ions from the environmental water. Acid infusion of animals pre-treated with the beta-adrenergic blocking agent, propranolol, induced a similar pattern of change in plasma acid-base status. However, the recovery of plasma pH and restoration of plasma [HCO3-] were slower than in animals infused with acid alone. Red cell pH fell significantly in the face of plasma acidosis in the beta-blocked animals. Erythrocyte [HCO3-] showed a similar pattern of change to that of erythrocyte pH. Branchial net H+ efflux increased to a lesser extent following acid infusion in animals treated with propranolol. We conclude that catecholamines released into the bloodstream during periods of acute acidosis may play an important role in facilitating branchial H+ efflux in seawater-adapted rainbow trout.

Effects of parathyroid hormone and urinary phosphate on collecting duct hydrogen secretion.

Urine-minus-blood PCO2 (U - B PCO2) during alkaline diuresis (urinary pH greater than 7.8) was determined in paired experiments using bicarbonate-loaded rats to assess the effects of parathyroid hormone (PTH) and urinary phosphate concentration [( Pi]u) on collecting duct H+ secretion. U-B PCO2 was higher for any value of urinary bicarbonate concentration ([HCO3]u) in the presence of PTH [intact rats and thyroparathyroidectomized (TPTX) PTH-infused rats] than in its absence (calcium-infused intact rats and TPTX rats). However, when [Pi]u was maintained constant by prior phosphate infusion, PTH administration in TPTX rats failed to elevate U-B PCO2. When PTH was infused in TPTX rats to maintain constant the plasma PTH level, subsequent phosphate infusion increased [Pi]u and elevated U-B PCO2 for any value of [HCO3]u. Moreover, when the data were pooled, there was a positive linear relationship between U-B PCO2 factored for [HCO3]u and [Pi]u (P less than 0.001). In all experiments, other factors that may affect U-B PCO2, such as plasma acid-base status, urinary osmolality, and extracellular fluid volume, did not vary. We conclude that PTH stimulates collecting duct H+ secretion indirectly via the increase in [Pi]u.

Is urea formation regulated primarily by acid-base balance in vivo?

Large quantities of ammonium and bicarbonate are produced each day from the metabolism of dietary protein. It has recently been proposed that urea synthesis is regulated by the need to remove this large load of bicarbonate. The purpose of these experiments was to test whether the primary function of ureagenesis in vivo is to remove ammonium or bicarbonate. The first series of rats were given a constant acid load as hydrochloric acid or ammonium chloride; individual rats received a constant nitrogen load at a time when their plasma acid-base status ranged from normal (pH 7.4, 28 mM HCO3) to severe metabolic acidosis (pH 6.9, 6 mM HCO3). Urea plus ammonium excretions and the blood urea, glutamine, and ammonium concentrations were monitored with time. Within the constraints of non-steady-state conditions, the rate of urea synthesis was constant and the plasma glutamine and ammonium concentrations also remained constant; thus it appears that the rate of urea synthesis was not primarily regulated by the acid-base status of the animal in vivo over a wide range of plasma ammonium concentrations. In quantitative terms, the vast bulk of the ammonium load was converted to urea over 80 min; only a small quantity of ammonium appeared as circulating glutamine or urinary ammonium. Urea synthesis was proportional to the nitrogen load. A second series of rats received sodium bicarbonate; urea synthesis was not augmented by a bicarbonate load. We conclude from these studies that the need to dispose of excess bicarbonate does not primarily determine the rate of ureagenesis in vivo. The data support the classical view that ureagenesis is controlled by the quantity of ammonium to be removed.

Responses of A Stenohaline Freshwater Teleost (Catostomus Commersoni) to Hypersaline Exposure: I. The Dependence of Plasma Ph and Bicarbonate Concentration on Electrolyte Regulation

ABSTRACT The effects of exposure to 0·94% (300mosmoll−1) sodium chloride on plasma electrolyte and acid-base status were examined in the freshwater stenohaline teleost Catostomus commersoni (Lacépède), the white sucker. Four days’ exposure to this maximum sublethal salinity resulted in an increase in plasma concentrations of both sodium and chloride but a decrease in the Na+/Cl− ratio. Since the plasma concentrations of free amino acids and other strong ions - Ca2+, Mg2+ and K+ - remained unchanged, plasma strong ion difference (SID) decreased. Additionally, plasma pH and bicarbonate concentration decreased at constant. The changes in electrolyte and acid-base status that occurred after the 96 h were not appreciably altered after a further 2–3 weeks of saline exposure. The ambient calcium concentration had no influence on these results. Haemolymph non-bicarbonate buffer capacity (β) calculated as Δ[HCO3−]/ ΔpH, increased in saline-exposed fish. Consequently ΔH+, the apparent proton load, was zero despite the apparent change in acid-base status. Although β was directly proportional to the haemoglobin concentration in both control and experimental fish, this could not account for the increase in β since haemoglobin remained at control values. These results can be explained solely by the change in plasma SID and serve to illustrate the dependence of plasma acid-base status on the prevailing electrolyte characteristics, weak acid concentration and .

Acid–base balance, ionic status, and renal function in resting and acid-exposed white suckers (Catostomus commersoni)

Renal function was investigated in the stenohaline Catostomus commersoni held at water pH 7.3 for 5 days. Urine displayed remarkably low levels of Na+, Cl−, K+, Ca2+, and Mg2+ and was very acidic (mean pH 6.5). Renal electrolyte conservation was characterized by almost complete reabsorption of NaCl and to a lesser degree, K+, Ca2+, and Mg2+. Net H+ excretion was + 11.2 μequiv∙kg−1∙h−1, resulting primarily from a high titratable acid content. The physiological consequences of exposure to ambient pH 4.3 for 4 days included disturbances in plasma acid–base status with relatively minor changes in both plasma ion levels and renal output (E). A mixed metabolic and respiratory acidosis developed, which was not compensated for by increased renal H+ excretion. Both plasma NaCl levels and ENa+ decreased but ECl− remained unchanged. EK+ was correlated with plasma hyperkalemia. No changes in plasma levels or excretion of Ca2+ or Mg2+ occurred. These findings provide some physiological evidence supporting the contention that suckers are relatively acid tolerant. It is suggested that the copious amounts of mucus covering their gills may have served a protective role by retarding proton entry and limiting branchial ion loss.

Evidence of active regulation of cerebrospinal fluid acid-base balance.

To test the passive transport hypothesis of cerebrospinal fluid (CSF) [H+] regulation, we altered the relationship between plasma [H+] and the electrical potential difference between CSF and blood (PD) by elevating plasma [K+] during 6-h systemic acid-base disturbances. In five groups of pentobarbital-anesthetized dogs, we increased plasma [K+] from 3.5 to an average of 7.8 meq/l. Hyperkalemia produced an increase in the PD of 6.3 mV by 6 h with normal plasma acid-base status (pHa 7.4), of 8.3 mV with isocapnic metabolic acidosis (pHa 7.2), of 5.3 mV with isocapnic metabolic alkalosis (pHa 7.6), of 9.2 mV with isobicarbonate respiratory acidosis (PaCO2 61 Torr) and of 5.7 mV with isobicarbonate respiratory alkalosis (PaCO2 25 Torr). The change in CSF [H+] at 6 h in each group was the same as that observed in normokalemic animals (Am. J. Physiol. 228: 1134-1154, 1975). This result is not consistent with the passive transport hypothesis. The CSF-blood PD is therefore not an important determinant of CSF [H+] CSF [H+] homeostasis must result from some form of active transport control.

Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus.

1. The regulation of cerebrospinal fluid (c.s.f.) bicarbonate concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. Decreases in plasma bicarbonate concentration caused relatively small changes in the c.s.f. bicarbonate concentration. 3. Alterations in c.s.f. bicarbonate concentration (c.s.f. HCO3-=9 or 28 m-equiv/l.) were countered by changes in the bicarbonate concentration of the fluid produced by the plexus or in the rate of bicarbonate transport which returned c.s.f. bicarbonate towards normal. 4. There was significant regulation of pH in the choroid plexus fluid during hypocapnia and hypercapnia. 5. Alterations of plasma acid-base status did not significantly alter the potential difference across the choroid plexus. However, the potential difference increased when c.s.f. bicarbonate was increased and decreased when c.s.f. bicarbonate was decreased. 6. The data indicate that the bicarbonate concentration in the c.s.f. is actively regulated by the choroid plexus during acid-base disturbances occurring either systemically or in the c.s.f.

Renal adaptation to a high potassium intake. The role of hydrogen ion.

The influence on urinary acidification of prolonged ingestion of a high potassium diet was explored in normal men and dogs. In men, the response to acute ingestion of ammonium chloride was assessed in a paired fashion after 5 days of ingesting a formula diet of normal or high potassium content; whereas in animals chronically ingesting a small amount of hydrochloric acid, the response to an increase in daily potassium intake was assessed. Urine pH was lower in the potassium-loaded state with both these models, and the effect persisted in the dog studies as long as a high potassium intake was continued. The decrease in urine pH could not be accounted for by changes in plasma acid-base status, net acid excretion, rate of urine flow, urine ionic strength, or fixed buffer excretion, i.e., phosphate, creatinine, or organic acids. Studies of men with administration of exogenous aldosterone and studies of adrenalectomized dogs with constant, maintenance steroid replacement indicated that the decrease in urine pH does not result from altered aldosterone secretion.In the human studies the largest decreases in urine pH were associated with a concomitant diminution in both ammonium and net acid excretion, suggesting a primary decrease of ammonia diffusion into the urine. These events during potassium loading, which are the mirror image of changes during potassium depletion, suggest that the relation between potassium, urine acidification, and ammonia metabolism may play an important role in the maintenance of hydrogen ion and possibly potassium homeostasis during alterations in potassium intake.