==================================CMR38================================== 38. Effects of acidosis on ATP, Na-K-ATPase, citric acid cycle. 1 UI - 87086791 AU - Rouslin W ; Erickson JL TI - Factors affecting the loss of mitochondrial function in autolyzing cardiac muscle. AB - Rates of loss of mitochondrial respiratory function were monitored during autolyses of canine myocardial samples pretreated so as to affect tissue pH and/or tissue ATP content prevailing during tissue autolysis. When autolyses occurred under conditions of differing tissue pH, but at nearly identical tissue ATP levels, the rate of loss of mitochondrial function was virtually unchanged suggesting that tissue acidosis in the absence of a concomitant tissue ATP differential had little or no effect upon the rate of progression of mitochondrial damage. In a second comparison, autolyses were carried out at constant tissue pH, but where tissue ATP content differed dramatically. Here, the rate of loss of mitochondrial function was increased markedly suggesting that tissue ATP depletion in the absence of a concomitant tissue pH differential had a major effect upon the rate of loss of mitochondrial function. Thus, of the two parameters studied, tissue ATP content alone was far more important than tissue pH alone in determining the rate of cell membrane damage during ischemia. Finally, autolyses were carried out where both tissue pH and ATP content differed. Here, an even more dramatic increase in the rate of progression of mitochondrial damage occurred suggesting the operation of synergism between tissue ATP depletion and acidosis in promoting cell injury in ischemic cardiac muscle. MH - Acidosis/PHYSIOPATHOLOGY ; Adenosine Triphosphate/ANALYSIS ; Animal ; Autolysis/*PHYSIOPATHOLOGY ; Coronary Disease/ PHYSIOPATHOLOGY ; Dogs ; Female ; Hydrogen-Ion Concentration ; Iodoacetates/PHARMACODYNAMICS ; Male ; Mitochondria, Heart/ *PHYSIOLOGY ; Oxygen Consumption ; Support, U.S. Gov't, P.H.S. SO - J Mol Cell Cardiol 1986 Nov;18(11):1187-95 2 UI - 87075828 AU - Jimenez R ; Gonzalez J ; Arizmendi C ; Fuertes J ; Medina JM ; Esteller A TI - Changes in biliary secretion and lactate metabolism induced by diethyl maleate in rabbits. AB - Diethyl maleate is a compound which binds with glutathione by means of a glutathione S-transferase and is excreted into bile leading to a rapid depletion of hepatic glutathione. In the rabbit, the activity of the enzyme is fairly low and we were thus prompted to study the possible effects of diethyl maleate on biliary secretion and metabolic status in this species. The administration of diethyl maleate induced a transient choleresis followed by cholestasis. The choleresis coursed with increases in the biliary output of sodium and unaccounted anions, whereas those of chloride, bicarbonate and bile acids were unaffected. Our data seem to confirm that choleresis is due to the osmotic activity of diethyl maleate compounds excreted into bile, as has been reported in rats and dogs. The cholestasis observed coursed with falls in the outputs of sodium, chloride and bicarbonate though that of bile acids remained constant. Following diethyl maleate administration, a metabolic acidosis appeared with progressive increases of blood lactate concentration. In bile the concentration of this anion closely followed that of plasma. The cholestasis is attributed to a lowered biliary secretion of bicarbonate probably secondary to the metabolic alteration. The hepatic values of cytoplasmatic and mitochondrial NADH/NAD ratios and of adenine nucleotide concentrations suggest that the increase in blood lactate results rather from a fall in its hepatic utilization that from an increase in its production. MH - Acid-Base Equilibrium/DRUG EFFECTS ; Adenosine Triphosphate/ METABOLISM ; Animal ; Bile Acids and Salts/SECRETION ; Bile/DRUG EFFECTS/*METABOLISM ; Carbon Dioxide/BLOOD ; Hydrogen-Ion Concentration ; Lactates/*METABOLISM ; Male ; Maleates/ *PHARMACODYNAMICS ; Osmolar Concentration ; Oxygen/BLOOD ; Rabbits SO - Biochem Pharmacol 1986 Dec 1;35(23):4251-60 3 UI - 87051578 AU - Wikman-Coffelt J ; Sievers R ; Parmley WW ; Jasmin G TI - Cardiomyopathic and healthy acidotic hamster hearts: mitochondrial activity may regulate cardiac performance. AB - A 50% decrease in adenine nucleotides and a 60% decrease in adenosine triphosphate concentration was found in glucose perfused myopathic Syrian hamster heart (240 days old) whereas there was an 18% decrease and 40% decrease respectively in acidotic healthy Syrian hamster heart re-equilibrated with a physiological medium. Correspondingly, there was a 60% decrease in cardiac performance with both models. Developed pressure fell when the phosphorylation potential decreased to less than or equal to 2; however, the heart recovered if mitochondrial activity was activated. If a substrate such as pyruvate or ribose was used with either model cardiac performance returned to near normal, although adenine nucleotide and adenosine triphosphate concentrations were further depressed. With glucose as substrate cardiomyopathic hearts, healthy acidotic hearts, and healthy acidotic hearts re-equilibrated with glucose as substrate had low pyruvate concentrations; limited availability of pyruvate depressed mitochondrial activity. Like the myopathic hearts the re-equilibrated acidotic hearts had high myocardial pyruvate concentrations, above normal ratios of phosphocreatine to creatine, and near normal oxygen consumption, developed pressure, dP/dt, and cyclic adenosine monophosphate concentrations when re-equilibrated with a medium containing pyruvate or ribose as substrate, although adenosine triphosphate and adenine nucleotide concentrations were severely depressed. When adenosine triphosphate values fell from 24 to 2 mumol X g-1 dry weight in the pyruvate or ribose perfused and normal functioning heart the heart stopped beating with no progressive fall in performance before termination of the metabolic processes. MH - Acidosis/METABOLISM ; Adenine Nucleotides/METABOLISM ; Adenosine Triphosphate/METABOLISM ; Animal ; Chromatography, High Pressure Liquid ; Hamsters ; Heart/*PHYSIOPATHOLOGY ; Hydrogen-Ion Concentration ; Mesocricetus ; Mitochondria, Heart/METABOLISM ; Myocardial Diseases/METABOLISM/*PHYSIOPATHOLOGY ; Nuclear Magnetic Resonance/DIAGNOSTIC USE ; Oxygen Consumption ; Support, Non-U.S. Gov't SO - Cardiovasc Res 1986 Jul;20(7):471-81 4 UI - 87046414 AU - Adam WR ; Koretsky AP ; Weiner MW TI - 31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats. AB - Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS) MH - Acidosis/*METABOLISM ; Acidosis, Respiratory/METABOLISM ; Adenosine Triphosphate/METABOLISM ; Animal ; Female ; Hydrogen/ *METABOLISM ; Hydrogen-Ion Concentration ; Intracellular Membranes/*METABOLISM ; Kidney/*METABOLISM ; Nuclear Magnetic Resonance ; Phosphorus/DIAGNOSTIC USE ; Potassium Deficiency/ *METABOLISM ; Rats ; Rats, Inbred Strains ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ; Support, U.S. Gov't, P.H.S. SO - Am J Physiol 1986 Nov;251(5 Pt 2):F904-10 5 UI - 86306509 AU - Milligan CL ; Wood CM TI - Tissue intracellular acid-base status and the fate of lactate after exhaustive exercise in the rainbow trout. AB - Exhaustive 'burst-type' exercise in the rainbow trout resulted in a severe acidosis in the white muscle, with pHi dropping from 7.21 to a low of 6.62, as measured by DMO distribution. An accumulation of lactate and pyruvate, depletions of glycogen, ATP and CP stores, and a fluid shift from the extracellular fluid to the intracellular fluid of white muscle were associated with the acidosis. The proton load was in excess of the lactate load by an amount equivalent to the drop in ATP, suggesting that there was an uncoupling of ATP hydrolysis and glycolysis. Initially, lactate was cleared more quickly than protons from the muscle, a difference that was reflected in the blood. It is suggested that during the early period of recovery (0-4 h), the bulk of the lactate was oxidized in situ, restoring pHi to a point compatible with glyconeogenesis. At that time, lactate and H+ were used as substrates for in situ glyconeogenesis, which was complete by 24 h. During this time, lactate and H+ disappearance could account for about 75% of the glycogen resynthesized. The liver and heart showed an accumulation of lactate, and it is postulated that this occurred as a result of uptake from the blood. Associated with the lactate load in these tissues was a metabolic alkalosis. Except for an apparent acidosis immediately after exercise, the acid-base status of the brain was not appreciably affected. Despite the extracellular acidosis, red cell pHi remained nearly constant. MH - *Acid-Base Equilibrium ; Acidosis/METABOLISM ; Adenosine Triphosphate/METABOLISM ; Animal ; Body Fluids/*METABOLISM ; Carbon Radioisotopes ; *Exertion ; Female ; Glycogen/METABOLISM ; Glycolysis ; Hydrogen-Ion Concentration ; Intracellular Fluid/ *METABOLISM ; Lactates/*METABOLISM ; Male ; Muscles/*METABOLISM ; Phosphocreatine/METABOLISM ; Support, Non-U.S. Gov't ; Tritium ; Trout SO - J Exp Biol 1986 Jul;123:123-44 6 UI - 86255825 AU - Abiko Y ; Ichihara K ; Sakai K ; Sashida H ; Ishibashi T TI - A method for evaluating antianginal drugs in experimental animals: assessment of myocardial ischemia by myocardial pH. AB - This paper describes a method by which antianginal drugs can be evaluated in the dog heart in situ. Myocardial pH was measured continuously by a micro glass pH electrode inserted in the left ventricular endocardial layers of the dog anesthetized with pentobarbital. Occlusion of the left anterior descending coronary artery (LAD) decreased myocardial pH, and release of the LAD restored the pH. The myocardial acidosis induced by ischemia was metabolic in nature and accompanied by a decrease in the levels of adenosine triphosphate and creatine phosphate and an increase in the levels of lactate in the myocardium. Drugs were injected intravenously 30 min after incomplete (partial) occlusion ot the LAD, lasting until 60 min after drug injection. Propranolol, atenolol, and sotalol markedly attenuated the myocardial pH that had been decreased by LAD occlusion. Nitroglycerin, diltiazem, and nicorandil also attenuated the pH, but these drugs were less active in attenuating myocardial acidosis. Dipyridamole, nifedipine, and beta-2 adrenoceptor antagonists were least active in this regard. It is concluded that myocardial pH can be used as an indicator of myocardial regional ischemia and utilized for evaluation of antianginal drugs. MH - Acidosis/METABOLISM ; Adenosine Triphosphate/METABOLISM ; Adrenergic Beta Receptor Blockaders/PHARMACODYNAMICS ; Angina Pectoris/*DRUG THERAPY/ETIOLOGY ; Animal ; Coronary Disease/ COMPLICATIONS/*METABOLISM ; Dogs ; Hydrogen-Ion Concentration ; Lactates/METABOLISM ; Myocardium/*METABOLISM ; Phosphocreatine/ METABOLISM ; Time Factors ; Vasodilator Agents/PHARMACODYNAMICS SO - Methods Find Exp Clin Pharmacol 1986 May;8(5):271-8 7 UI - 86229911 AU - Bogusky RT ; Garwood M ; Matson GB ; Acosta G ; Cowgill LD ; Schleich T TI - Localization of phosphorus metabolites and sodium ions in the rat kidney. AB - Relative amounts of phosphorus-containing metabolites and sodium ions present in different regions of the in vivo rat kidney were obtained using a surface-coil probe and recently developed NMR rotating-frame methods. During altered physiologic states, changes in distribution of metabolites and sodium ions within the kidney were identified in one-dimensional metabolite maps. This technique may have important applications to disorders commonly found in clinical medicine. MH - Acidosis/DIAGNOSIS ; Adenosine Triphosphate/ANALYSIS ; Animal ; Desoxycorticosterone/ADMINISTRATION & DOSAGE ; Kidney/ANATOMY & HISTOLOGY/*ANALYSIS ; Male ; Nuclear Magnetic Resonance/ *DIAGNOSTIC USE ; Phosphates/ANALYSIS ; Phosphorus/*ANALYSIS ; Potassium Deficiency/DIAGNOSIS ; Rats ; Rats, Inbred Strains ; Sodium/*ANALYSIS ; Spectrum Analysis ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Magn Reson Med 1986 Apr;3(2):251-61 8 UI - 86212337 AU - Greene DA TI - Acute and chronic complications of diabetes mellitus in older patients. AB - The chronic complications of diabetes are thought to be caused by an interaction between hyperglycemia or other metabolic consequences of insulin deficiency and other poorly defined independent genetic or environmental factors. Several important biochemical sequelae to hyperglycemia are discussed. Macrovascular disease appears to be primarily age-related in diabetic patients. The clinical course, manifestations, and management of diabetic complications are significantly altered when they appear against a background of the degenerative changes of aging, greatly complicating diagnosis and management. In elderly patients, the acute complications of diabetes--ketoacidosis and hyperosmolar dehydration--often occur in the context of chronic complications that greatly compound their management and increase their morbidity and mortality. MH - Acidosis, Diabetic/ETIOLOGY/METABOLISM ; Adenosine Triphosphatase, Sodium, Potassium/METABOLISM ; Adult ; Aged ; *Aging ; Blood Pressure ; Diabetes Mellitus/*COMPLICATIONS/ METABOLISM ; Diabetic Coma/ETIOLOGY ; Diabetic Nephropathies/ ETIOLOGY/METABOLISM/OCCURRENCE ; Glomerular Filtration Rate ; Glucose/*METABOLISM ; Human ; Hyperglycemia/ETIOLOGY/METABOLISM ; Inositol/METABOLISM ; Insulin/ADMINISTRATION & DOSAGE/DEFICIENCY/ METABOLISM ; Intestinal Absorption ; Middle Age ; Osmolar Concentration ; Prognosis ; Review ; United States SO - Am J Med 1986 May 16;80(5A):39-53 9 UI - 86195685 AU - McCartney N ; Spriet LL ; Heigenhauser GJ ; Kowalchuk JM ; Sutton JR ; Jones NL TI - Muscle power and metabolism in maximal intermittent exercise. AB - Muscle power and the associated metabolic changes in muscle were investigated in eight male human subjects who performed four 30-s bouts of maximal isokinetic cycling at 100 rpm, with 4-min recovery intervals. In the first bout peak power and total work were (mean +/- SE) 1,626 +/- 102 W and 20.83 +/- 1.18 kJ, respectively; muscle glycogen decreased by 18.2 mmol/kg wet wt, lactate increased to 28.9 +/- 2.7 mmol/kg, and there were up to 10-fold increases in glycolytic intermediates. External power and work decreased by 20% in both the second and third exercise periods, but no further change occurred in the fourth bout. Muscle glycogen decreased by an additional 14.8 mmol/kg after the second exercise and thereafter remained constant. Muscle adenosine triphosphate (ATP) was reduced by 40% from resting after each exercise period; creatine phosphate (CP) decreased successively to less than 5% of resting; in the recovery periods ATP and CP increased to 76 and 95% of initial resting levels, respectively. Venous plasma glycerol increased linearly to 485% of resting; free fatty acids did not change. Changes in muscle glycogen, lactate, and glycolytic intermediates suggested rate limitation at phosphofructokinase during the first and second exercise periods, and phosphorylase in the third and fourth exercise periods. Despite minimal glycolytic flux in the third and fourth exercise periods, subjects generated 1,000 W peak power and sustained 400 W for 30 s, 60% of the values recorded in the first exercise period.(ABSTRACT TRUNCATED AT 250 WORDS) MH - Acid-Base Equilibrium ; Adenosine Triphosphate/METABOLISM ; Adult ; Energy Metabolism ; *Exertion ; Glycerin/BLOOD ; Glycogen/ METABOLISM ; Glycolysis ; Human ; Male ; *Muscle Contraction ; Muscles/*METABOLISM ; Oxygen Consumption ; Phosphocreatine/ METABOLISM ; Support, Non-U.S. Gov't ; Triglycerides/METABOLISM SO - J Appl Physiol 1986 Apr;60(4):1164-9 10 UI - 86172870 AU - Vinay P ; Lemieux G ; Gougoux A ; Halperin M TI - Regulation of glutamine metabolism in dog kidney in vivo. AB - In summary, we propose: that renal ammoniagenesis is regulated both by factors dependent and independent of the acid-base status, the net effect of the ammoniagenic process on the proton balance being directly related to the rate of urinary ammonium excretion; that the renal metabolism of glutamine should not be examined independently of the metabolism of other substrate physiologically taken up by the kidney; that different pathways for glutamine metabolism will change during acid-base disorders of organic or nonorganic origin; that, among the main glutamine utilizing pathways, only the GLDH pathway is influenced directly by the acid-base status; the ammoniagenic transamination pathways is regulated by substrate availability in the kidney; that the lowest ammoniagenic flux in the kidney coincides with the rate of alanine production since alanine appears to derive directly from glutamine. When this pathway is stimulated without concomitant acidosis, most of the ammonia produced is not excreted in urine but released in the renal venous blood: thus, no significant effect on the acid-base balance is produced; that glutamine is metabolized by proximal kidney tubules of acidotic dogs probably through net oxidation; that the quantitative analysis of the metabolic consequence of this process indicates that the rate of ATP turnover at this site may effectively place an upper limit to the rate of glutamine oxidation, and ammonia production by the kidney, and that this limit is nearly reached in chronically acidotic animals. MH - Acid-Base Equilibrium ; Acidosis/METABOLISM ; Adenosine Triphosphate/METABOLISM ; Alanine/BIOSYNTHESIS ; Ammonia/ METABOLISM ; Animal ; Aspartic Acid/BIOSYNTHESIS ; Bicarbonates/ METABOLISM ; Dogs ; Glutamine/*METABOLISM ; Kidney/*METABOLISM ; Kidney Cortex/METABOLISM ; Lactates/METABOLISM ; Phosphoenolpyruvate Carboxykinases/METABOLISM ; Review ; Support, Non-U.S. Gov't SO - Kidney Int 1986 Jan;29(1):68-79 11 UI - 86164420 AU - Fischer JC ; Ruitenbeek W ; Gabre:els FJ ; Janssen AJ ; Renier WO ; Sengers RC ; Stadhouders AM ; ter Laak HJ ; Trijbels JM ; Veerkamp JH TI - A mitochondrial encephalomyopathy: the first case with an established defect at the level of coenzyme Q. AB - A patient is presented who had therapy-resistant epileptic seizures from the 7th day of life. Examination at the age of 17 months revealed a mentally retarded boy with epileptic seizures, generalised myoclonic contractions, and abnormal ocular movements. A cerebral CT scan showed central and cortical atrophy. Lactate levels in serum, cerebrospinal fluid and urine were elevated, the pyruvate level was raised in serum. A quadriceps muscle biopsy revealed aspecific morphologic signs of a myopathy. Biochemical analysis showed decreased substrate oxidation rates in the mitochondria associated with low rates of ATP production. Total and free carnitine levels were decreased. Investigation of the respiratory chain revealed a defect in the proximal part of respiratory chain involving the region of coenzyme Q. Based on clinical and chemical data it is likely that the patient is suffering from a multi-system disorder. MH - Acidosis/COMPLICATIONS ; Adenosine Triphosphate/METABOLISM ; Brain Diseases/*ENZYMOLOGY ; Case Report ; Epilepsy/COMPLICATIONS ; Human ; Infant ; Lactates/METABOLISM ; Male ; Mental Retardation/COMPLICATIONS ; Mitochondria, Muscle/*ULTRASTRUCTURE ; Muscle Spasticity/COMPLICATIONS/*ENZYMOLOGY ; Myoclonus/ COMPLICATIONS ; Nystagmus/COMPLICATIONS ; NAD/METABOLISM ; Oxidation-Reduction ; Pyruvates/METABOLISM ; Support, Non-U.S. Gov't ; Ubiquinone/*METABOLISM SO - Eur J Pediatr 1986 Feb;144(5):441-4 12 UI - 86156286 AU - Rouslin W ; Erickson JL ; Solaro RJ TI - Effects of oligomycin and acidosis on rates of ATP depletion in ischemic heart muscle. AB - The perfusion of canine cardiac muscle with 10 microM oligomycin produced a nearly 90% slowing of the net rate of tissue ATP depletion from 0.200 to 0.025 mumol X min-1 X g wet wt-1 of tissue during a subsequent myocardial autolytic interval during which tissue pH was held constant. Moreover, lowering the tissue pH during the autolytic process by 0.6 unit from approximately 6.8 to approximately 6.2 produced a nearly 60% slowing of the net rate of tissue ATP depletion from 0.200 to 0.087 mumol X min-1 X g wet wt-1. The pH dependence of the net rate of tissue ATP depletion (by an oligomycin-sensitive process) was that predicted from the mitochondrial ATPase pH-inhibition profiles reported earlier (J. Biol. Chem. 258: 9657-9661, 1983). When taken together with our observation that the mitochondrial ATPase comprises approximately 90% of the total of all of the ATP hydrolyzing activities present in cardiac muscle cells, data reported here suggest that the protonic inhibition of the mitochondrial ATPase plays a major role in regulating the rate of tissue ATP depletion during myocardial ischemia. MH - Acidosis/*METABOLISM ; Adenosine Triphosphatase/METABOLISM ; Adenosine Triphosphate/*METABOLISM ; Animal ; Autolysis/ ENZYMOLOGY/METABOLISM ; Coronary Disease/*METABOLISM ; Dogs ; Female ; Hydrogen-Ion Concentration ; HEPES/PHARMACODYNAMICS ; Male ; Mitochondria, Heart/ENZYMOLOGY ; Myocardium/*METABOLISM ; Myofibrils/ENZYMOLOGY ; Oligomycins/*PHARMACODYNAMICS ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Am J Physiol 1986 Mar;250(3 Pt 2):H503-8 13 UI - 86100796 AU - Fondacaro JD TI - Intestinal ion transport and diarrheal disease. AB - The physiology of intestinal electrolyte transport is currently an area of intense research interest. Also, reports regularly appear that define possible roles of various endocrine, paracrine, and neurohumoral substances in regulating intestinal ion and water flux. A vast body of knowledge has appeared recently that focuses on the action of specific intracellular mediators or second messengers and certain biochemical events that are thought to be involved in this transport process. This area of research has drawn the attention of the clinical investigator as well as the basic scientist because of the implications of these findings to the understanding of secretory disorders of the gastrointestinal tract, in particular diarrheal disease. The purpose of this review is to focus on recent findings reported in three major areas: the physiology of intestinal electrolyte transport and its regulation; the pathophysiology of secretory diarrhea; and current thoughts and practices in the therapeutic approach to the disease. MH - Acid-Base Equilibrium ; Adenosine Cyclic Monophosphate/METABOLISM ; Adenosine Triphosphatase, Sodium, Potassium/METABOLISM ; Adrenergic Alpha Receptor Agonists/THERAPEUTIC USE ; Animal ; Arachidonic Acids/METABOLISM ; Carbachol/PHARMACODYNAMICS ; Chlorides/METABOLISM ; Cholera Toxin/PHARMACODYNAMICS ; Diarrhea/ DRUG THERAPY/*PHYSIOPATHOLOGY ; Electric Stimulation ; Electrolytes/*METABOLISM ; Guanosine Cyclic Monophosphate/ METABOLISM ; Hydroxyeicosatetraenoic Acids/METABOLISM ; *Intestinal Absorption ; Intestine, Small/SECRETION ; Intestines/ *METABOLISM ; Models, Biological ; Narcotics/THERAPEUTIC USE ; Phenothiazines/THERAPEUTIC USE ; Phorbol Esters/PHARMACODYNAMICS ; Phosphorylation ; Protein Kinase C/METABOLISM ; Receptors, Cholinergic/PHYSIOLOGY ; Receptors, Muscarinic/PHYSIOLOGY ; Renin-Angiotensin System ; Review ; Sodium/METABOLISM ; Tetradecanoylphorbol Acetate/PHARMACODYNAMICS SO - Am J Physiol 1986 Jan;250(1 Pt 1):G1-8