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PubMed1975

Cyclic-AMP and pancreatic bicarbonate secretion in response to secretin in dogs.

In anesthetized dogs given secretin intravenously in doses doubling every 60 min and ranging from 0.5 to 8 units per kg body weight per hr, cyclic-AMP levels in pancreatic tissue rose continuously, whereas DNA concentrations were slightly decreased. Bicarbonate concentrations and bicarbonate outputs, cyclic-AMP tissue concentrations and bicarbonate outputs, as well as cyclic-AMP tissue concentrations and juice outputs, were significantly correlated. In conscious pancreatic fistula dogs, there was also a significant correlation between cyclic-AMP and bicarbonate concentrations and outputs in the pancreatic juice after stimulation by exogenous secretin. Accordingly, enhanced release of endogenous secretin achieved by intraduodenal acidification led to a dose-dependent increase in bicarbonate and cyclic-AMP outputs in both conscious and anesthetized dogs. Phosphodiesterase inhibitors (aminophylline, caffeine, and papaverine) given alone to the conscious dogs did not initiate pancreatic bicarbonate secretion, but they potentiated bicarbonate responses to exogenous secretin. These data suggest that cyclic-AMP plays a part in secretin-stimulated pancreatic secretion.

Aminophylline↗
PubMed2001

Bicarbonate secretion in the murine gallbladder--lessons for the treatment of cystic fibrosis.

The epithelium lining the gallbladder of mammalian species has absorptive and secretory functions. An important function is the secretion of a bicarbonate rich fluid that helps neutralise stomach acid and provides an appropriate environment for intestinal enzymes. In cystic fibrosis (CF) this secretory function is lost. This study concerns the bicarbonate secreting activity of murine gallbladders in vitro using wild type and CF mice and four main questions are considered as follows: a) Does the murine gallbladder secrete bicarbonate electrogenically and is this prevented in CF? b) Can the secretory activity in CF gallbladders be restored by gene therapy or pharmacologically? c) How is the cystic fibrosis transmembrane conductance regulator (CFTR) involved in bicarbonate secretion? d) Does the data offer prospects for the treatment of CF?. Work from both the author's laboratory and the literature will be reviewed. Consideration of the currently available data indicates that the wild type murine gallbladder does secrete bicarbonate electrogenically and that this is absent in CF mice. Further it has been demonstrated that bicarbonate secretory activity can be restored by both gene therapy and by the use of drugs. The role of CFTR in bicarbonate secretion remains equivocal. Much evidence suggests that CFTR can act as a channel for HCO(3)(-) ions as well as Cl(-) ions, while others propose a parallel arrangement of CFTR with a Cl(-)/HCO(3)(-) exchanger is necessary. The matter is further complicated by the regulatory role of CFTR on other transporting activities. Opportunities for possible application to man are discussed.

Animals↗
PubMed1976

Defective bicarbonate secretion in response to duodenal acidification in patients with chronic gastric or duodenal ulceration.

Histamine infusion studies were performed in 54 healthy persons, in 58 patients with duodenal ulcers and in 29 patients with gastric ulcers. The acid load entering the duodenum was estimated by measuring the loss of an intragastric marker, phenol red. The volume of duodenal juice that had refluxed into the stomach and which was aspirated with the gastric juice was estimated by the sodium content of the aspirate. The bicarbonate concentration of the refluxed duodenal juice was calculated from the relationship between neutralisation and total electrolyte concentration, since the reaction of one bicarbonate ion removes two ions from the resultant mixture. The mean bicarbonate concentration of the refluxed duodenal juice in the control group was 116,4 (+/- 9) mEq/1, and the individual bicarbonate concentrations showed the expected dependence on the magnitude of the intraduodenal acid load. The mean bicarbonate concentration in patients with duodenal ulcers was 84,6 (+/- 9) mEq/1, which was significantly lower than in healthy persons. In patients with duodenal ulcers and in those with gastric ulcers, the reflux bicarbonate concentrations were independent of acid load. These results confirm previous reports of an impaired pancreatic bicarbonate secretion in response to duodenal acid load in patients with duodenal ulcers, and indicate a similar response in patients with gastric ulcers.

Bicarbonates↗
PubMed2004

Effect of bicarbonate on neonatal serum ionized magnesium in vitro.

Sodium bicarbonate is used to treat metabolic acidosis, or to induce metabolic alkalosis in sick neonates. The aim of this study was to quantify the decrease in serum concentration of ionized magnesium ([Mg2+]) when sodium bicarbonate is added to neonatal serum in vitro. Sodium bicarbonate was added to 30 cord serum samples of term infants to reach incremental concentrations of 0 to 2.0 mEq/L and [Mg2+] was measured. Serum [Mg2+] decreased significantly with the addition of sodium bicarbonate. At incremental sodium bicarbonate concentrations of 1.0 to 2.0 mEq/L, which is within the range of the desired aim in the treatment of metabolic acidosis, the magnitude of the decrease in serum [Mg2+] was approximately 0.084 to 0.158 mmol/L (18% to 34%) from the average baseline value. The addition of sodium bicarbonate causes a significant decrease in [Mg2+]. From this in vitro study we speculate that fast infusion of sodium bicarbonate in human neonates may potentially cause a clinically significant decrease in serum [Mg2+].

Bicarbonates↗
PubMedDate not supplied

Correlation between intradialytic hypotension in patients undergoing routine hemodialysis and use of acetate compared in bicarbonate dialysate.

AIM: To determine the incidence of intradialytic hypertension (IDH) during hemodialysis (HD) in end-stage renal disease (ESRD) patients using acetate dialysate compared to those using bicarbonate dialysate. METHODS: This study was a double-blind cross-over randomized clinical trial. The effect of acetate and bicarbonate dialysate on blood pressure was analyzed in two consecutive HD sessions. The selected subjects were 41 stable ESRD patients scheduled for dialysis 2 times/week/from the HD unit of Dr.Soetom Hospital Surabaya, aged between 21-65 years old, with a hemoglobin level > or = 7 g/dL, serum albumin > or = 3 mg/dL and interdialytic weight gain < 4 Kg, and an average Qb 150-250 ml/minute. The dialysate sodium level was 138 mEq/L/ The study subjects were divided into tow groups: 21 patients in the group who received Acetate on the first session and Bicarbonate on the next (AB) and 20 patients in the group receiving Bicarbonate first (BA). Comparison of IDH during use of each dialysate was analyzed by Chi-Square and Mc Nemar Chi-Square test. RESULTS: No characteristic differences were found in both groups: HD duration (for AB) was 28.83 +/- 13.89 vs. 34.95 +/- 24.80 months (for BA) (p = 0.333); Age (for AB) was 47.61 +/- 9.49 vs. 47.75 +/- 11.80 years (for BA) (p = 0.969); Hemoglobin (Hb) level (for AB) 8.19 +/- 0.84 vs. 7.94 +/- 0.41 mg/dL (for BA) (p = 0.238); serum Albumin (for AB) was 3.79 +/- 0.26 vs. 3.82 +/- 0.30 g/dl (for BA) (p = 0.652). The number of patients with IDH during acetate dialysate with IDH during bicarbonate dialysate was 1 (2.4%). Overall, there were 11 patients with Diabetic Kidney Disease (26.8%). Six out of them (54.5%) had IDH during acetate dialysate and only and 1 patient (9.1%) had IDH during acetate and bicarbonate. CONCLUSION: The incidence of IDH in hemodialysis using acetate is significantly greater than that when bicarbonate is used (p = 0.000).

Acetates↗
PubMed2006

Expression of vascular endothelial growth factor, fibroblast growth factor, and lactate dehydrogenase by human peritoneal mesothelial cells in solutions with lactate or bicarbonate or both.

In patients on long-term continuous ambulatory peritoneal dialysis, the efficiency of dialysis declines because of peritoneal neovascularization and loss of peritoneal mesothelial cells. In this study, we investigated the influence of lactate and bicarbonate in peritoneal dialysis fluid on such changes of the peritoneum. We studied the production of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), which induce peritoneal neovascularization, by human peritoneal mesothelial cells (HPMCs) cultured with lactate or bicarbonate or both. Lactate dehydrogenase (LDH) was also measured to assess cell necrosis. Levels of VEGF, bFGF, and LDH in the culture supernatant showed a significant decrease after incubation of HPMCs with 15 mEq/L lactate plus 25 mEq/L bicarbonate, or with 40 mEq/L bicarbonate, as compared with incubation with 40 mEq/L lactate. Levels of VEGF and bFGF showed a concentration-dependent decrease when the cells were incubated with lactate or bicarbonate; a concentration-dependent increase of LDH was simultaneously observed. These results suggest that dialysis fluid containing 40 mEq/L bicarbonate is superior to fluid containing 40 mEq/L lactate with regard to its influence on the production of VEGF and bFGF although lactate and bicarbonate are both toxic for HPMCs.

Bicarbonates↗
PubMed1991

Effect of pH and bicarbonate on phosphoenolpyruvate carboxykinase and glutaminase mRNA levels in cultured renal epithelial cells.

A gluconeogenic strain of renal epithelial cells (LLC-PK1-F+) was used to characterize the effect of pH and bicarbonate concentration on the levels of phosphoenolpyruvate carboxykinase (PCK) and glutaminase (GA) mRNAs. The levels of both mRNAs are markedly dependent upon medium glucose concentration. The level of PCK mRNA is increased with increasing glucose concentration from 0 to 40 mM, whereas the level of GA mRNA is maximal between 3 and 5 mM glucose. When LLC-PK1-F+ cells are grown with 5 mM glucose and then subjected to an acute decrease in pH (from 7.4 to 6.9) and bicarbonate concentration (from 25 to 10 mM), the level of PCK mRNA exhibits a biphasic response. The PCK mRNA is initially increased 4-fold within 3 h, then decreases slightly and subsequently increases between 10 and 20 h to a level that is 17-fold greater than normal. Only the initial increase parallels the changes observed in vivo. In contrast, after onset of acidosis, the level of GA mRNA initially remains unchanged, is then increased 8-fold between 10 and 16 h, and then decreases slightly. This response closely mimics the results obtained in vivo. A decrease in media pH at constant bicarbonate causes a marked increase in both mRNAs. However, the levels of the two mRNAs are also elevated by decreasing bicarbonate at a constant pH. Thus, both parameters independently affect the level of the two mRNAs. The use of actinomycin D to measure the half-lives of PCK and GA mRNAs at pH 7.4 and 6.9 indicates that stabilization may fully account for the induction of GA mRNA and contributes to the inductive effects of decreased pH and/or bicarbonate on PCK mRNA. Following recovery from acidic conditions, the two mRNAs exhibit a rapid and coordinate decrease (t1/2 approximately 20 min). Dexamethasone had no effect on the level of either mRNA, whereas cAMP increased only PCK mRNA. The latter effect was additive with the increase caused by decreased pH and/or bicarbonate and was reversed by incubating in alkalotic media. Thus, the induction of PCK and GA mRNAs during acidosis is initiated in direct response to a decrease in extracellular pH and/or bicarbonate.

Acidosis↗
PubMed1975

The absence of renal bicarbonate reabsorption maxima during carbonic anhydrase inhibition.

Present studies were performed to examine the effect of carbonic anhydrase inhibition on bicarbonate reabsorption under experimental conditions where extracellular fluid volume expansion was minimized. The data showed no tubular maximum for bicarbonate reabsorption in the normal state or after carbonic anhydrase inhibition. The data support a model which assumes that the bicarbonate reabsorption is accomplished by two processes. One process is independent of protonation from H+ secretion into the tubule and probably involves reabsorption of bicarbonate ion as such. This process has an unlimited capacity for reabsorption of bicarbonate. The contribution of this process increases with an increase in plasma bicarbonate. The second process is dependent on protonation, through the intracellular hydration of carbon dioxide. The relative contribution, through the intracellular hydration of carbon dioxide. The relative contribution of this process is normally about 33% and decreases with increased plasma bicarbonate.

Absorption↗
PubMed1989

Distal tubule bicarbonate reabsorption in NH4Cl acidotic rats.

NH4Cl acidosis--a common experimental model of hyperchloremic metabolic acidosis--elicits complex intrarenal responses whereby the fall in plasma bicarbonate concentration can be restored to normal after the initial acid load. Using the technique of in vivo micropuncture of surface distal tubules of the rat kidney, we attempted to further define controlling mechanisms underlying the enhanced bicarbonate reabsorption in this setting. Specifically, we wished to determine the dependence of distal tubule bicarbonate reabsorption (JtCO2) on sodium transport, water reabsorption, and carbonic anhydrase activity. Surface distal tubules of Sprague-Dawley rats made acidotic by ammonium chloride gavage (arterial blood pH: 7.15 +/- 0.01, [HCO3]: 14.8 +/- 0.5 mM) were perfused in vivo at 8 and 24 nL/min with 4 different isoosmotic, 25 mM bicarbonate solutions: Group 1 was perfused with 60 mM Na, Group 2 with 60 mM choline, Group 3 with 60 mM choline + 3 x 10(-4) M amiloride, and Group 4 with 60 mM Na + 10(-3) M acetazolamide. At 8 nL/min, significant bicarbonate reabsorption occurred with all perfusates. JtCO2 was 65 +/- 4, 59 +/- 5, 58 +/- 6, and 40 +/- 4 pmol.min-1.mm-1, in Groups 1, 2, 3, and 4, respectively. However, JtCO2 in Group 4 was significantly less than that in Groups 1 and 2 (p less than 0.01 and p less than 0.05, respectively). Amiloride added to the low sodium perfusate did not reduce bicarbonate reabsorption. We conclude that bicarbonate reabsorption in distal tubules of acidotic rats is acetazolamide-sensitive and is not significantly sustained by sodium or water movements.

Absorption↗
PubMed1976

Bicarbonate re-absorption in renal stone patients with acidification defects.

A pathological renal response to ammonium chloride loading was found to be common in renal stone formers. In order to elicit further information about the impaired acidification capacity eight patients were investigated by bicarbonate loading. One patient with a mild acidification defect had normal tubular re-absorption of bicarbonate. Five of these eight patients with suspected proximal acidification defect and two patients with impaired distal acidification were found to have a low bicarbonate threshold and an increased, fractionated, bicarbonate excretion at a normal plasma bicarbonate level. Four of the patients with suspected, proximal, acidification defect reached a maximal re-absorption of bicarbonate (Tm) that was low, while three patients did not reach a Tm. These three factors indicate increased bicarbonate wastage from the kidneys. A constantly alkaline urine, such as exists in patients with proximal acidification defect may give rise to an increased risk of the precipitation of renal stones - primarily calcium-phosphate stones.

Acidosis, Renal Tubular↗
PubMed1978

Cornea endothelial bicarbonate fluxes following preservation in solutions of varying composition.

Numerous modifications have been made in MK solution, primarily concerned with alterations in both bicarbonate concentration and PCO2. Variations of the solutions from high bicarbonate to low bicarbonate and either high or low PCO2 were made which resulted in a decreased net bicarbonate flux across the endothelium after a 3-day storage period. Even with drastic changes in the storage solution there was a relatively small change in the net bicarbonate flux. Higher passive fluxes were found at a pH above 8, and a higher net flux with a bicarbonate concentration of 17.5 nM or higher. Variation in PCO2 made little difference to the net endothelial fluxes; when a high PCO2 was used, there was a concurrent elevation of PO2 in the storage solution, but no beneficial effect was found on the endothelial transport system. It was apparent that a good storage solution contained a buffer (bicarbonate was better than phosphate) and 5% dextran and was at a neutral pH (between 7 and 8).

Animals↗
PubMed1986

Effects of acetate and bicarbonate dialysis on cardiac performance, transmural myocardial perfusion and acid-base balance.

The effects of acetate and bicarbonate dialysis on cardiac performance, myocardial oxygen balance and acid-base balance were evaluated in 7 patients with end-stage renal failure. During acetate dialysis cardiac output increased and was significantly higher than during bicarbonate dialysis (p less than 0.05). Systemic vascular resistance was significantly lower during acetate than during bicarbonate dialysis (p less than 0.05). The myocardial oxygen balance estimated from the supply/demand ratio (DPTI/SPTI) was significantly reduced after acetate dialysis and significantly lower than during bicarbonate dialysis (p less than 0.05). After 90 min acetate dialysis DPTI/SPTI dropped to its lowest value as a result of an excess of myocardial oxygen demand (SPTI) over myocardial oxygen supply (DPTI), signifying transient hypoperfusion of the subendocardium which did not occur during bicarbonate dialysis. Acidosis was more adequately corrected with bicarbonate dialysis, and there was no change in pCO2 which was significantly higher than during acetate dialysis (p less than 0.05). During bicarbonate dialysis a stable hemodynamic circulation and well balanced acid-base values were seen. Acetate dialysis leads to improvement in left ventricular performance, but at the expense of myocardial oxygen balance, which falls to marginal safety levels in uremic patients.

Acetates↗
PubMed1983

[Bicarbonate-containing dialysate: a critical study].

Renewed interest in bicarbonate as the dialysate base replacement during hemodialysis has introduced new settings on acetate-dialysate delivery systems commercially available. Numerous technical problems are associated with unstable bicarbonate solutions. Therefore, several precautions must be observed: 1) Bicarbonate dialysis requires two concentrates: one containing the base replacement bicarbonate and the other containing basically calcium and magnesium chlorides, 2) A two-stream proportioning system afforded by an appropriate dialysate delivery machine should be used to mix the bicarbonate and acid concentrates, in order to ensure on-line production of the final dialysate, 3) Additional monitors, such as pH monitor, are required to prevent misuse of concentrates. These new ancillary equipments and the relatively high cost of bicarbonate concentrates could slow down the extension of bicarbonate dialysis which is potentially beneficial for all dialysis patients.

Bicarbonates↗
PubMed1984

Pancreatic bicarbonate response to food-bound hydrogen ion along the gut.

Recent reports suggest most solid food enters the duodenum as small particles. Our studies showed that small particles of liver were capable of binding hydrogen ions (H+), but there was slow equilibration of H+ between particulate and aqueous phases. We wondered whether titratable acid as H+ bound to meat particles could effectively stimulate pancreatic bicarbonate secretion despite slow diffusion. We studied mongrel dogs with chronic pancreatic fistulas; the intestinal lumen was washed free of endogenous pancreatic enzymes. Pancreatic bicarbonate and protein responses were measured during duodenal perfusion with pH 2 or pH 3 gels that delivered 1, 2, or 4 mEq/15 min of titratable acid (endpoint pH 4.5). Gels consisted of acidified, 0.1-0.7-mm particles of beef liver or bovine serum albumin or lactic acid suspended with 2% starch in 0.15 M NaCl. The liver, bovine serum albumin, and lactate had similar titration curves. At pH 2 or pH 3, liver particles were about as effective as bovine serum albumin in stimulating pancreatic bicarbonate secretion. Likewise, pH 3 liver particles were equipotent with pH 3 lactate on pancreatic bicarbonate secretion when both perfusates were allowed access to the whole intestine. However, when confined to the first 45 cm of proximal intestine, much less H+ was dissipated from the liver versus the lactate; and, correspondingly, there was a much greater decrement in pancreatic bicarbonate secretion from whole gut responses with liver versus lactate. We conclude that titratable acid bound to solid food particles is a potent stimulus of pancreatic bicarbonate secretion despite its slow diffusion. Our studies suggest that H+ slowly diffusing from particles excites pancreatic bicarbonate secretion by triggering H+ receptors along more distal intestine.

Animals↗
PubMed1981

[Comparison of acetate and bicarbonate in hemodialytic treatment. Echocardiographic and polycardiographic study of the left ventricle].

During standard haemodialysis, cause of calcium and magnesium insoluble salts formation, the bicarbonate as a buffer has been replaced by the more soluble and stable acetate. But the new and more efficient dialytic systems cause an increase of intradyalitic bicarbonate loss and acetate gain the latter, by a direct calcium binding or by calcium displacement from the active sites, has been believed to be responsible for vasodilatation and myocardial contractility depression. Aim of this study is to verify if the bicarbonate dialysis versus acetate dialysis modifies left ventricular performance, investigated by non invasive tools (systolic time index and echocardiography). This work deals with twelve patients undergoing standard haemodialysis (three times a week) since 28 months on the average. Echocardiographic and systolic time index study was performed before and after the acetate dialysis and before and after the tenth bicarbonate dialysis observing the same interdialytic period. The echo has shown improvement concerning the fractional shortening (P less than 0.025) and the cardiac output (P less than 0.05) and only before the tenth bicarbonate dialysis. Systolic time index data have shown reduction of the ratio PEP/LVET (P less than 0.05) and LVET less negative than after acetate only in the end of the tenth bicarbonate dialysis (P less than 0.05). These results seem point out left ventricular performance improvement in accordance with the decrease of clinical intradialytic (nausea, vomiting, and hypotension) and interdialytic troubles (headache, asthenia and washed-out feeling) probably due to the bicarbonate more effective as a buffer in the acid-base and electrolytic balance.

Acetates↗
PubMedDate not supplied

[Simultaneous study of duodenal and biliopancreatic bicarbonates in rats].

OBJECTIVES: The aim of the present study was to assess the relative contribution of duodenal and biliopancreatic bicarbonate secretion to acid neutralization in the duodenum, in basal conditions, during stimulation by PGE2 and during acid infusion in the duodenum. METHODS: Forty rats were anaesthetized and the duodenum was infused with 0.9% saline. Bicarbonate originating from duodenal mucosa and from biliopancreatic secretion was independently collected and measured. In neutralization studies, HCl was infused in the duodenum, and the amount of residual acid escaping from the duodenum was determined with and without bile and/or pancreatic juice diversion. RESULTS: Basal duodenal and biliopancreatic bicarbonate outputs were respectively 10.0 +/- 0.66 and 2.4 +/- 0.31 mumol/10 min. PGE2 increased duodenal mucosal bicarbonate by about 100%. Eighty-five percent of infused HCl was neutralized by duodenal mucosal bicarbonate. In neutralizing the remaining 15%, pancreatic secretion was slightly predominant, 46% for a HCl concentration of 5 mM and 71% for a HCl concentration of 40 mM. CONCLUSIONS: These results shows that in the anaesthetized rat, available bicarbonate in the duodenal lumen and HCl neutralization ability are mainly dependent upon bicarbonate secreted by the duodenal mucosa.

Animals↗
PubMed1995

[Precipitation of pH-adjusted local anesthetics with sodium bicarbonate].

Sodium bicarbonate has been added to various local anesthetics for shortening the onset time. We often noticed the precipitate in the pH-adjusted local anesthetics several minutes after adding the bicarbonate. We confirmed that this drug interaction was caused by large changes in pH. We have analyzed the precipitates by mass spectrometry and infrared absorption spectrum and have revealed it as unionized base forms of local anesthetics. Since these forms tend to be insoluble, we must limit the amount of 7% sodium bicarbonate. This study proposes a guideline for adding 7% sodium bicarbonate to the various local anesthetics. The amount of 7% sodium bicarbonate which can be added to bupivacaine without precipitation is below 0.02 ml. In cases of mepivacaine and lidocaine, allowable amount of 7% sodium bicarbonate is 0.5 ml. It is not known whether this lower dose of 7% sodium bicarbonate compared with the recent reports is effective or not. Further clinical investigation may be necessary.

Anesthetics, Local↗
PubMed1994

Correction of intramyocardial hypercarbic acidosis with sodium bicarbonate.

Although it has been hypothesized that exogenously administered bicarbonate can exacerbate intramyocardial acidosis and compromise contractile function, this phenomenon has not been demonstrated in an intact model in which intramyocardial pH (pH(int)), regional venous pCO2, and regional contractile function have been simultaneously monitored. In 20 anesthetized dogs, we studied the effects of intracoronary infusions of sodium bicarbonate NaHCO3 30 mEg over 15 min, on regional pH(int), (glass electrode) and regional stroke work (SW, sonomicrometry) before and after creating systemic hypercarbic acidosis by hypoventilation. During NaHCO3 administration, regional coronary venous pCO2 increased rapidly during the first minute (eucapnea; 34 +/- 7 to 55 +/- 18 mm Hg; hypercapnea: 70 +/- 15 to 98 +/- 23 mm Hg, P < 0.05 for both increases). Regional venous pH rose from 7.36 +/- .04 to 7.55 +/- .06 (P < 0.05) after the first minute of NaHCO3 infusion during eucapnea and from 7.09 +/- .09 to 7.22 +/- .09 (P < 0.05) during hypercapnea. During the first minute of NaHCO3 infusion, pH(int) declined minimally. However, during the remaining 14 min of each infusion, pH(int) increased significantly (eucapnea: 7.19 +/- 0.10 to 7.43 +/- 0.12; hypercapnea: 6.86 +/- 0.14 to 7.02 +/- 0.15, P < 0.05 for both changes). Regional SW decreased significantly during the first minute of infusion, both during eucapnea (23,400 +/- 7,400 to 18,000 +/- 6,300 ergs/cm2, P < 0.05) and hypercapnea (27,000 +/- 9,100 to 25,000 +/- 10,000 ergs/cm2, P < 0.05). The first minute of contractile dysfunction was followed by recovery and ultimately supranormal contractile function during the remainder of each bicarbonate infusion. To test the hypothesis that transient intracellular acidosis during bicarbonate infusions was underestimated by measurements of pH(int), measurements of intracellular pH using the pH-sensitive dye, BCECF, were performed in isolated guinea pig papillary muscles incubated in vitro. These measurements confirmed the presence of transient intracellular acidosis during bicarbonate infusion. In conclusion, (1) the intracoronary administration of sodium bicarbonate causes a transient depression in myocardial contractile function that is related to transient intracellular acidosis; and (2) despite exacerbating hypercarbia, sodium bicarbonate ultimately neutralizes intracellular acid and augments myocardial contractile function.

Acidosis↗