scholarly journals The spleen is required for 5-HT1A receptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat

2009 ◽  
Vol 296 (5) ◽  
pp. R1392-R1401 ◽  
Author(s):  
Ruslan Tiniakov ◽  
Karie E. Scrogin
Keyword(s):  
Metabolic Acidosis ◽  
Hemorrhagic Shock ◽  
Receptor Agonist ◽  
Blood Gases ◽  
Filling Pressure ◽  
Whole Body ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mean Circulatory Filling Pressure ◽  
Base Balance

The 5-HT1A receptor agonist, 8- OH-DPAT, increases whole body venous tone (mean circulatory filling pressure; MCFP), and attenuates metabolic acidosis in a rat model of unresuscitated hemorrhagic shock. To determine whether improved acid-base balance was associated with sympathetic activation and venous constriction, MCFP, sympathetic activity (SA), and blood gases were compared in hemorrhaged rats following administration of 5-HT1A receptor agonist 8-OH-DPAT, the arterial vasoconstrictor arginine vasopressin (AVP), or saline. To further determine whether protection of acid-base balance was dependent on splenic contraction and blood mobilization, central venous pressure (CVP), MCFP, and blood gases were determined during hemorrhage and subsequent 8-OH-DPAT-administration in rats subjected to real or sham splenectomy. Subjects were hemorrhaged to an arterial pressure of 50 mmHg for 25 min and subsequently were treated with 8-OH-DPAT (30 nmol/kg iv), AVP titrated to match the pressor effect of 8-OH-DPAT (∼2 ng/min iv), or infusion of normal saline. 8-OH-DPAT increased MAP, CVP, MCFP, and SA, and decreased lactate accumulation. AVP did not affect CVP or SA, but raised MCFP slightly to a level intermediate between 8-OH-DPAT- and saline-treated rats. Infusion of AVP also produced a modest protection against metabolic acidosis. Splenectomy prevented the rise in CVP, MCFP, and protection against metabolic acidosis produced by 8-OH-DPAT but had no effect on the immediate pressor response to the drug. Together, the data indicate that 8-OH-DPAT produces a pattern of cardiovascular responses consistent with a sympathetic-mediated venoconstriction that is, in part, responsible for the drug's beneficial effect on acid-base balance. Moreover, blood mobilization stimulated by the spleen is required for the beneficial effects of 8-OH-DPAT.

Fluids and electrolytes

2017 ◽  
Author(s):  
Grenville Fox ◽  
Nicholas Hoque ◽  
Timothy Watts
Keyword(s):  
Metabolic Acidosis ◽  
Fluid Balance ◽  
Base Excess ◽  
Blood Gases ◽  
Sodium Balance ◽  
Fluid Loss ◽  
Acid Base Balance ◽  
Acid Base ◽  
Newborn Period ◽  
Base Balance

This chapter provides an overview of the background of fluid balance in the neonate, including the need to compensate for fluid loss (output), and the requirement to provide energy and nutrition. It also covers the management of common issues in fluid, electrolyte, and acid-base balance in the newborn period, including dehydration, sodium balance (hyponatraemia and hypernatraemia), hyperkalaemia, interpretation of blood gases (including pH, base excess, and anion gap), respiratory and metabolic acidosis, and hydrops fetalis.

DIGITALIS TOLERANCE IN YOUNG PUPPIES

PEDIATRICS ◽  
1970 ◽  
Vol 46 (5) ◽  
pp. 730-736
Author(s):  
Katherine H. Halloran ◽  
Steven C. Schimpff ◽  
Jean G. Nicolas ◽  
Norman S. Talner
Keyword(s):  
Blood Gases ◽  
Acid Base Balance ◽  
Acid Base ◽  
Littermate Control ◽  
Premature Ventricular Contractions ◽  
Toxic Dose ◽  
Arterial Blood ◽  
Wide Range ◽  
Base Balance ◽  
The Mean

Tolerance to acetyl strophanthidin, a rapid-acting cardiac aglycone, was determined in 28 anesthetized mongrel puppies, ages 16 to 56 days, and compared to tolerance in 16 littermate puppies in whom acute hypercapnic acidemia was produced. The tolerance was also compared to that of four adult mongrel dogs. The toxic dose was defined as the intravenous amount required to produce four consecutive premature ventricular contractions. A marked variation in the toxic dose was found in the 28 control puppies (range 83 to 353 µg/kg, mean 169 µg/kg) which could not be correlated with age, arterial blood gases or pH, serum potassium or sodium, arterial pressure, or heart rate. The toxic dose was significantly greater in the puppies than in the adult dogs, in whom the mean toxic dose was 64 µg/kg (range 50 to 89 µg/kg). A significant increase in tolerance was also observed in the puppies with hypercapnic acidemia (mean toxic dose 220 µg/kg, range 93 to 375 µg/kg) in comparison to tolerance in the control puppies and despite the wide range of tolerance, each of the puppies with hypercapnic acidemia showed greater tolerance than its littermate control puppy. Assessment of the clinical implications of these findings will require study of the effects of alterations in acid-base balance on the inotropic effect of acetyl strophanthidin in addition to the toxic electrophysiologic effects.

Whole body acid-base modeling revisited

2017 ◽  
Vol 312 (4) ◽  
pp. F647-F653 ◽  
Author(s):  
Troels Ring ◽  
Søren Nielsen
Keyword(s):  
Acid Production ◽  
Negative Charge ◽  
Whole Body ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Conventional Model ◽  
Renal Net Acid Excretion ◽  
Base Balance ◽  
Alkali Absorption

The textbook account of whole body acid-base balance in terms of endogenous acid production, renal net acid excretion, and gastrointestinal alkali absorption, which is the only comprehensive model around, has never been applied in clinical practice or been formally validated. To improve understanding of acid-base modeling, we managed to write up this conventional model as an expression solely on urine chemistry. Renal net acid excretion and endogenous acid production were already formulated in terms of urine chemistry, and we could from the literature also see gastrointestinal alkali absorption in terms of urine excretions. With a few assumptions it was possible to see that this expression of net acid balance was arithmetically identical to minus urine charge, whereby under the development of acidosis, urine was predicted to acquire a net negative charge. The literature already mentions unexplained negative urine charges so we scrutinized a series of seminal papers and confirmed empirically the theoretical prediction that observed urine charge did acquire negative charge as acidosis developed. Hence, we can conclude that the conventional model is problematic since it predicts what is physiologically impossible. Therefore, we need a new model for whole body acid-base balance, which does not have impossible implications. Furthermore, new experimental studies are needed to account for charge imbalance in urine under development of acidosis.

Electrolytes, Blood Gases, and Acid–Base Balance

2017 ◽  
pp. 873-938
Author(s):  
Isabel A. Lea ◽  
Susan J. Borghoff ◽  
Gregory S. Travlos
Keyword(s):  
Blood Gases ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

scholarly journals ASSOCIATION OF ACID-BASE PARAMETERS WITH LACTATE LEVEL IN CRITICALLY ILL PATIENTS WITH METABOLIC ACIDOSIS

2018 ◽  
Vol 24 (2) ◽  
pp. 141
Author(s):  
Donaliazarti Donaliazarti ◽  
Rismawati Yaswir ◽  
Hanifah Maani ◽  
Efrida Efrida
Keyword(s):  
Metabolic Acidosis ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Lactate Level ◽  
Linear Regression Analysis ◽  
P Value ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Parameters ◽  
Base Balance

Metabolic acidosis is prevalent among critically ill patients and the common cause of metabolic acidosis in ICU is lactic acidosis. However, not all ICUs can provide lactate measurement. The traditional method that uses Henderson-Hasselbach equation (completed with BE and AG) and alternative method consisting of Stewart and its modification (BDEgap and SIG), are acid-base balance parameters commonly used by clinicians to determine metabolic acidosis in critically ill patients. The objective of this study was to discover the association between acid-base parameters (BE, AGobserved, AGcalculated, SIG, BDEgap) with lactate level in critically ill patients with metabolic acidosis. This was an analytical study with a cross-sectional design. Eighty-four critically ill patients hospitalized in the ICU department Dr. M. Djamil Padang Hospital were recruited in this study from January to September 2016. Blood gas analysis and lactate measurement were performed by potentiometric and amperometric method while electrolytes and albumin measurement were done by ISE and colorimetric method (BCG). Linear regression analysis was used to evaluate the association between acid-base parameters with lactate level based on p-value less than 0.05. Fourty five (54%) were females and thirty-nine (46%) were males with participant’s ages ranged from 18 to 81 years old. Postoperative was the most reason for ICU admission (88%). Linear regression analysis showed that p-value for BE, AGobserved, AGcalculated, SIG and BDEgap were 119; 0.967; 0.001; 0.001; 0.689, respectively. Acid-base balance parameters which were mostly associated with lactate level in critically ill patients with metabolic acidosis were AGcalculated and SIG. 

Effect of systemic acid-base balance on ileal secretion

1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney
Keyword(s):  
Metabolic Acidosis ◽  
Cholera Toxin ◽  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Secretory Process ◽  
Sprague Dawley ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Change ◽  
Base Balance

We previously reported that systemic pH and HCO3 concentration affect ileal water and electrolyte absorption. To determine whether these effects could influence an ongoing secretory process, we measured transport in ileal loops exposed to either saline or 50-75 micrograms cholera toxin in mechanically ventilated Sprague-Dawley rats anesthetized with pentobarbital sodium. The effects of acute respiratory and metabolic acidosis and alkalosis were then examined. Decreases in systemic pH during respiratory acidosis caused equivalent increases in net water (54 +/- 8 microliters . cm-1 . h-1) and Na absorption (7 +/- 1 mu eq . cm- . h-1) and smaller increases in Cl absorption in cholera toxin compared with saline loops. These increases reversed the net secretion of these ions observed during alkalemia in the cholera toxin loops to net absorption. Metabolic acidosis and alkalosis and respiratory compensation of systemic pH of these metabolic disorders also altered cholera toxin-induced secretion in a direction consistent with the pH change. The increase in net HCO3 secretion caused by cholera toxin was unaffected by the respiratory disorders and did not vary with the HCO3 concentration in the metabolic disorders. These findings suggest that the systemic acid-base disorders that characterize intestinal secretory states may themselves alter intestinal absorptive function and fluid losses.

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