Acid-base changes in milk and blood of rats in acidosis and alkalosis

1976 ◽  
Vol 231 (1) ◽  
pp. 132-135 ◽  
Author(s):  
R Yagil ◽  
Z Lerner ◽  
Z Etzion ◽  
GM Berlyne

Lactating white rats (Rattus norvegicus) were subjected to metabolic and respiratory acidosis and metabolic alkalosis. Before and during the various treatments, the acid-base status of heart blood and milk was determined. Acute metabolic acidosis lowered the pH of plasma and milk; Pco(2) and bicarbonate concentrations in plasma were lowered, and in milk Pco(2) was raised and the bicarbonate concentration remained unchanged. Respiratory acidosis and acetazolamide caused a drop in blood pH and in blood and milk bicarbonate concentrations; milk pH remained unchanged, but Pco(2) was raised in both plasma and milk. Acute metabolic alkalosis raised the blood pH and milk Pco(2); plasma Pco(2) and bicarbonate concentrations in blood and milk remained unchanged. The data show that greater changes occur in acid-base parameters of blood than milk when animals are exposed to acidifying and alkalinizing stimuli.

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.


1997 ◽  
Vol 273 (5) ◽  
pp. F698-F705
Author(s):  
R. Unwin ◽  
R. Stidwell ◽  
S. Taylor ◽  
G. Capasso

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7–10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux ([Formula: see text]) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([[Formula: see text]]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion ([Formula: see text]) increased threefold, but LOH[Formula: see text]was unchanged. In ARA, blood pH fell to 7.2, and blood [[Formula: see text]] rose from 28 to 34 mM; [Formula: see text] was reduced to <0.1%, but LOH[Formula: see text]was unaltered. In CRA, blood pH fell to 7.2, and blood [[Formula: see text]] increased to >50 mM, whereas[Formula: see text]decreased to <0.1%.[Formula: see text]was reduced by ∼30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH[Formula: see text]increased (by 30%) to normal. These results suggest that LOH[Formula: see text]is affected by the blood-to-tubule lumen [[Formula: see text]] gradient and[Formula: see text] backflux. When the usual perfusing solution at 20 nl/min was made[Formula: see text] free, mean[Formula: see text]was −34.5 ± 4.4 pmol/min compared with 210 ± 28.1 pmol/min plus [Formula: see text]. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 × 10−4 M, to abolish H+-dependent[Formula: see text]) was used,[Formula: see text]was −112.8 ± 5.6 pmol/min. Comparable values for[Formula: see text]at 10 nl/min were −35.9 ± 5.8 and −72.5 ± 8.8 pmol/min, respectively. These data indicate significant backflux of[Formula: see text] along the LOH, which depends on the blood-to-lumen [[Formula: see text]] gradient; in addition to any underlying changes in active acid-base transport mechanisms, [Formula: see text]permeability and backflux are important determinants of LOH[Formula: see text]in vivo.


1979 ◽  
Vol 82 (1) ◽  
pp. 345-355
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS

Cutaneous CO2 excretion is reduced as the skin dries during dehydration but an increase in breath frequency acts to regulate the arterial blood Pcoco2 and thus pHα. Moreover, the toad does not urinate and water is reabsorbed from the bladder to replace that lost by evaporation at the skin and lung surfaces. The animal does, however, produce a very acid bladder urine to conserve circulating levels of plasma [HCO3-] and this together with an increased ventilation effectively maintains the blood acid-base status for up to 48 h of dehydration in air. Water loss and acid production are presumably also reduced by the animal's behaviour; animals remain still, in a crouched position or in a pile if left in groups. Dehydrated toads are less able than hydrated toads to regulate blood pH during hypercapnia: they hyperventilate and mobilize body bicarbonate stores in much the same fashion as hydrated animals but due to the restrictions on cutaneous CO2 excretion and renal output, there is comparatively little reduction in the PCOCO2 difference between arterial blood and inspired gas thereby resulting in a more severe respiratory acidosis. These factors further contribute to the persistent acidosis which continues even when the animals are returned to air.


1987 ◽  
Vol 128 (1) ◽  
pp. 235-253 ◽  
Author(s):  
S. I. Perry ◽  
M. G. Vermette

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels of this hormone to those measured during periods of acute extracellular acidosis (approximately 5 X 10(−8) mol l-1). Concomitant effects on selected blood respiratory acid-base and ionic variables were evaluated. Infusion of epinephrine caused a transient respiratory acidosis as a result of hypoventilation and/or inhibition of red blood cell (RBC) bicarbonate dehydration. The acidosis was regulated by gradual accumulation of plasma bicarbonate. Even though whole blood pH (pHe) was depressed by 0.16 units, RBC pH (pHi) remained constant, thereby causing the transmembrane pH gradient (pHe-pHi) to decrease. A similar effect of epinephrine on RBC pH was observed in vitro, although the response required a higher concentration of epinephrine (2.0 X 10(−7) mol l-1). We speculate that the release of epinephrine during periods of depressed blood pH is important for preventing excessive shifts in RBC pH and for initiating a series of responses leading to plasma HCO3- accumulation and eventual restoration of blood acid-base status.


1982 ◽  
Vol 243 (2) ◽  
pp. F188-F196
Author(s):  
D. R. Roy ◽  
K. L. Blouch ◽  
R. L. Jamison

Effects of acute-base disturbances on fractional delivery of potassium to the juxtamedullary end-descending limb were examined by micropuncture in the rat to test the hypothesis that potassium is reabsorbed from the collecting duct and is secreted in juxtamedullary pars recta or descending limb in the renal medulla. In metabolic acidosis, fractional potassium delivery was only slightly reduced compared with control values and was a function of potassium excretion, as the hypothesis predicts. Fractional potassium delivery was sharply reduced both in respiratory acidosis and metabolic alkalosis and was no longer a function of potassium excretion. Although seemingly inconsistent with the recycling hypothesis, the latter finding may be reconciled by the following observations. In respiratory acidosis, vasa recta blood flow nearly doubled, which would lead to vascular washout of interstitial potassium. In metabolic alkalosis, flow rate in the pars recta or descending limb was reduced by 28%, which would limit transepithelial potassium addition. The results indicate complex effects of acid-base disturbances on fractional potassium delivery to the end-descending limb, which can be unified by postulated changes in transepithelial potassium concentration differences across the juxtamedullary pars recta or descending limb. An unexpected observation emerged--fractional delivery of water to the end-descending limb declined as a function of plasma bicarbonate concentration when all groups were combined.


2021 ◽  
Vol 9 (2) ◽  
pp. 588-596
Author(s):  
Hayder Aledan ◽  
Jawad Rasheed ◽  
Zahraa Jasim ◽  
Manal Abdul Razak

The available treatments of metabolic alkalosis should be given in the hospital and may be associated with serious adverse events. We aimed to use rice broth for treatment of metabolic alkalosis. Patients with metabolic alkalosis were received oral rice broth solution; serum electrolytes and acid-base parameters were measured before and after the treatment. The majority of patients were older and in the ICU. After treatment with rice broth solution, there was statistical significant decreased in blood PH and serum [HCO3-] from a mean of 7.45 ± 0.03 to 7.4 ± 0.009 and 34.5 ± 4.4 to 24.9 ± 1.1 mmol/l respectively and statistical significant increase in serum [Na+], serum [Cl-], serum [K+], serum [Ca+2], serum [PO4-2] and serum [Mg+2] from a mean of 132.5 ± 3.7 to 136.5 ± 1.9 mmol/l, 93.2 ± 5.4 to 101.9 ± 2.7 mmol/l, 3.1 ± 0.3 to 3.6 ± 0.2 mmol/l, 0.99 ± 0.1 to 1 ± 0.1mmol/l, 3.4 ± 0.5 to 3.6 ± 0.4 mg/dl and 1.88 ± 0.2 to 2.28 ± 0.17 mg/dl respectively. Rice broth is an effective oral treatment of metabolic alkalosis.


1986 ◽  
Vol 250 (5) ◽  
pp. G588-G593 ◽  
Author(s):  
J. D. Wagner ◽  
P. Kurtin ◽  
A. N. Charney

We previously reported that changes in ileal net Na absorption correlated with arterial pH, changes in net HCO3 secretion correlated with the plasma HCO3 concentration, and changes in net Cl absorption correlated with arterial CO2 partial pressure (PCO2) during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediated these effects, we measured pHi and calculated [HCO3]i in the distal ileal mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4,-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis, and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, mucosal pHi was not altered, but there were strong correlations between mucosal [HCO3]i and both arterial PCO2 (r = 0.97) and [HCO3] (r = 0.61). When we considered the rates of ileal electrolyte transport that characterized these acid-base disorders [A. N. Charney and L.P. Haskell, Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G230-G235, 1983], we found strong correlations between mucosal [HCO3]i and both net Cl absorption (r = 0.88) and net HCO3 secretion (r = 0.82). These findings suggest that the systemic acid-base disorders do not affect ileal mucosal pHi but do alter mucosal [HCO3]i as a consequence of altered arterial PCO2 and [HCO3]. The effects of these disorders on ileal net Cl absorption and HCO3 secretion may be mediated by changes in [HCO3]i. Arterial pH does not appear to alter ileal Na absorption through changes in the mucosal acid-base milieu.


1992 ◽  
Vol 173 (1) ◽  
pp. 181-203 ◽  
Author(s):  
B. James-Curtis ◽  
C. M. Wood

The relative roles of the kidney and urinary bladder in ion, fluid and acid-base regulation were examined in freshwater rainbow trout chronically infused with either 140 mmol l-1 NaCl or 140 mmol l-1 NaHCO3 (3 ml kg-1 h-1) for 32 h. NaCl had a negligible effect on blood ionic and acid-base status, whereas NaHCO3 induced a metabolic alkalosis characterized by a rise in arterial pH and [HCO3-] and an equimolar fall in [Cl-]. Urine was collected via either an internal catheter, which bypassed bladder function, or an external urinary catheter, which collected naturally voided urine. As a percentage of the infusion rate, glomerular filtration rate increased by about 135 %, but urine flow rate (UFR) by only 80 %, reflecting increased tubular reabsorption of H2O. During NaCl infusion, virtually all of the extra Na+ and Cl- filtered was reabsorbed by the kidney tubules, resulting in an increased UFR with largely unchanged composition. During NaHCO3 infusion, tubular Na+ and Cl- reabsorption again kept pace with filtration. HCO3- reabsorption also increased, but did not keep pace with filtration; an increased flow of HCO3--rich urine resulted, which excreted about 10 % of the infused base load. At rest, fish fitted with external catheters voided in discrete bursts of about 0.85 ml kg-1 at 25 min intervals. During infusion, burst frequency increased by about 40 % and burst volume by about 20 %. Reabsorption by the bladder reduced UFR by 25 %, the excretion of Na+ and Cl- by 50 %, of K+ by 44 % and of urea by 25 %. These differences persisted on a relative basis during NaCl and NaHCO3 infusion despite the decreased residence time. However, HCO3- was neither secreted nor reabsorbed by the bladder. We conclude that the freshwater kidney functions to remove as much NaCl as possible from the urine, regardless of the NaCl load, and this role is supplemented by bladder function. The bladder plays no role in acid-base regulation during metabolic alkalosis.


1988 ◽  
Vol 136 (1) ◽  
pp. 351-361
Author(s):  
LEONA MATTSOFF ◽  
MIKKO NIKINMAA

We studied the effects of acute external acidification on the acid-base status and plasma and red cell ion concentrations of lampreys. Mortality was observed within 24 h at pH5 and especially at pH4. The main reason for the high sensitivity of lampreys to acid water appears to be the large drop in blood pH: 0.6 and 0.8 units after 24 h at pH5 and pH4, respectively. The drop of plasma pH is much larger than in teleost fishes exposed to similar pH values. The difference in the plasma pH response between lampreys and teleosts probably results from the low buffering capacity of lamprey blood, since red cells cannot participate in buffering extracellular acid loads. Acidification also caused a decrease in both Na+ and C− concentrations and an elevation in K+ concentration of plasma. The drop in plasma Na+ concentration occurred faster than the drop in plasma Cl− concentration which, in turn, coincided with the decrease in total CO2 concentration of the blood.


1999 ◽  
Vol 202 (3) ◽  
pp. 267-278 ◽  
Author(s):  
B. Bagatto ◽  
R.P. Henry

The dynamics of bimodal respiration, diving behaviour and blood acid-base status in the softshell turtle Trachemys scripta and the pond slider Apalone ferox were investigated at rest and under conditions of stress induced by exercise and forced submergence. During periods of forced submergence, only A. ferox doubled its aquatic gas exchange rate. Both A. ferox and T. scripta increased their aerial gas exchange profoundly following exercise and forced submergence, a pattern indicative of increased anaerobic respiration. Emersion duration increased significantly in A. ferox following forced submergence, and mean apnoeic time decreased significantly in A. ferox following exercise, indicating that a larger proportion of time at the surface was spent ventilating. Also, A. ferox maintained a one-breath breathing bout regardless of treatment. Submergence produced a respiratory acidosis in the plasma of approximately 0.2 pH units in magnitude in T. scripta and a mixed respiratory/metabolic acidosis of 0.4 pH units in A. ferox. Exercise induced an acidosis of 0.2 pH units of primarily metabolic origin in both species. Intra-erythrocyte pH was also reduced in both species in response to submergence and exercise. Both intracellular and extracellular acidoses were more severe and longer lasting in A. ferox after each treatment. Plasma [HCO3-] decreased by 25 % in both species following exercise, but only in A. ferox following submergence. Plasma lactate concentrations increased by equal amounts in each species following exercise; however, they returned to resting concentrations sooner in T. scripta than in A. ferox. A. ferox had significantly higher lactate levels than T. scripta following forced submergence as well as a slower recovery time. A. ferox, which is normally a good bimodal gas exchanger at rest, utilizes aerial respiration to a greater extent when under respiratory and/or metabolic stress. T. scripta, although almost entirely dependent on aerial respiration, is physiologically better able to deal with the respiratory and metabolic stresses associated with both forced submergence and exercise.


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