The hydrogen-ion concentration of the saliva; the relationship between hydrogen-ion concentration and rate of flow of saliva.
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OBJECTIVE: To determine gastric secretory responses in horses treated with histamine and to determine the dose of histamine needed to elicit maximal gastric secretion. ANIMALS: 6 adult horses with an indwelling gastric cannula. PROCEDURE: Gastric contents were collected in 15-minute periods, and volume, pH, hydrogen ion concentration, hydrogen ion output, sodium concentration, and sodium output were determined. Values were determined without any treatment (baseline), after administration of pyrilamine maleate (1 mg/kg of body weight, i.v., given during a 15-minute period), and during 1-hour infusions of histamine at 3 rates (7.5, 15, and 30 microg/kg/h, i.v.). RESULTS: Volume and hydrogen ion concentration of gastric contents and hydrogen ion output were significantly increased, compared with baseline values, during histamine infusion. Mean hydrogen ion concentration and hydrogen ion output were significantly greater during infusion of histamine at a rate of 15 or 30 microg/kg/h than at a rate of 7.5 microg/kg/h. Sodium concentration was significantly decreased, compared with baseline value, during histamine infusion, but sodium output was unchanged. CONCLUSIONS: Histamine at doses of 15 and 30 microg/kg/h, i.v. stimulated maximal gastric secretion in horses. Histamine appeared to induce only parietal secretion. CLINICAL RELEVANCE: This study provides additional information related to equine gastric physiology, which may benefit further understanding of the pathogenesis of peptic ulcer disease.
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The present investigation studied the effects of hydrogen ion concentration on pulmonary vascular reactivity to the biogenic amines in vitro. Pulmonary arterial segments from cats were dissected free of surrounding tissue and endothelium and isometrically suspended in tissue baths. Cumulative dose-response curves were constructed to norepinephrine, histamine, serotonin, and potassium chloride, and the protocol was designed such that only one agent and hydrogen ion concentration was studied in each vessel segment. Alkalosis ([H+] less than or equal to 28 nmol/l) produced enhanced maximum responses to all of the agents used in this study. Acidosis [( H+] greater than or equal to 52 nmol/l), in contrast, was without effect on the maximum responses to histamine, serotonin, and potassium chloride, but did produce increased maximum responses to norepinephrine. No alterations in the ED50 of the dose-response curves were observed for any of the agents tested. In general, increases in sloped of the dose response curves were correlated with hydrogen ion concentrations that demonstrated increased maximum responses, suggesting that the present observations may have resulted from hydrogen ion-induced changes in amine receptor efficacy. The present data demonstrate that (1) as in the in vivo model, pulmonary vascular amine receptor activity is related to the hydrogen ion concentration; (2) there are two hydrogen ion concentration ranges where adrenergic receptor activity was observed to be enhanced; (3) the effects of acidosis where specific for the adrenergic receptor system, since the reactivity to only norepinephrine was significantly altered by acidosis; and (4) the effects of alkalosis may have resulted from increased overall contractility of the pulmonary vascular smooth muscle cells, since the force developed to all the agents tested was enhanced by alkalosis.
To assess the effect of extracellular hydrogen ion concentration (PH+) on aldosterone secretion, studies in which other known modulators could be controlled were performed on 13 patients undergoing hemodialysis. High (35 mM) or low (14-17 mM) dialysate bicarbonate concentrations were utilized on separate days to either decrease or increase PH+, while plasma potassium concentrations (PK) were held at constant levels and changes in plasma renin activity (PRA) were minimized by avoiding changes in body weight. Changes in PH+ were associated with concordant changes in plasma aldosterone concentration (Pa) in both high- and low-bicarbonate studies. When these changes in Pa in high- and low-bicarbonate studies were analyzed together as a function of corresponding changes in PH+, a significant correlation could be demonstrated (r = 0.659, P less than 0.001). There was no correlation between changes in Pa and changes in PK, plasma sodium, plasma adrenocorticotropic hormone (ACTH), or PRA. Using the same methods to control PH+ and other variables during hemodialysis, the effects of altered PH+ on ACTH-stimulated aldosterone and cortisol secretion were evaluated in studies on six patients who received incremental infusions of ACTH after pretreatment with dexamethasone. In these studies, there was no demonstrable effect of PH+ on Pa or plasma cortisol concentration. We conclude that physiological changes in PH+ have a weak modulating effect on basal aldosterone secretion that may not be evident in the presence of other acutely applied stimuli.
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There appears to be a tendency to convert pH values into "hydrogen ion concentrations" using the antilog of negative pH values. The present communication describes the thermodynamic basis of pH to explain that the above procedure is erroneous and that pH values should be treated as primary variables. Acidity expressed by the hydrogen ion concentrations measured by titrations (base excess or base deficit) has no bearing with the "hydrogen ion concentrations" derived by the antilog of negative pH.
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The effect of variation of blood hydrogen ion concentration on arterial and mixed venous PO2, ideal alveolar-arterial O2 pressure difference (PAiO2--PaO2), venous admixture (Qs/Qt), arterio-alveolar CO2 pressure difference (a--A)DCO2, physiological dead space to tidal volume ratio (VD/VT), cardiac output (Qt) and mean pulmonary arterial pressure (PAP) has been studied. Arterial and mixed venous PO2 increased and (PAiO2--PaO2) decreased with increasing blood hydrogen ion concentration. No change in Qs/Qt, (a--A)DCO2, VD/VT, Qt and PAP was observed. The effect of hydrogen ion concentration on arterial and mixed venous PO2 and on (PAiO2--PaO2) is mainly due to a shift of the blood oxyhemoglobin dissociation curve (ODC), i.e. due to the Bohr effect. The upper part of the ODC is more flat in alkalosis (shift to the left) than in acidosis (shift to the right). Therefore the same end-capillary to arterial O2 content difference results in a greater (PAiO2--PaO2) in alkalosis than in acidosis. Any factor influencing the slope of the upper part of the ODC is expected to affect the arterial PO2 and the (PAiO2--PaO2) by this mechanism. Similarly any factor shifting the steep part of the ODC is expected to affect the PO2 of the mixed venous blood.
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The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.
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Rapid spectrophotometric method of lysosome stability determination depending on hydrogen ion concentration is described. The time of analysis is decreased by 5-6 h in comparison with enzymic method. The process of lysosome degradation was linear at pH 6. The incubation mixture acidity dependence curve of lysosome lysis extend was complex. The lysosome lysis rate rapidly increased at pH much less than 6 less than pH. Lysosome incubation at 0-4 degrees C during 24 h decreased its sensitivity to incubation mixture acidity within the whole investigated pH range. Isolated lysosome acid resistance may be used as an index of its stability and lability in vivo and in vitro by various physicochemical factors. Percentage of initial absorbtion (A520) and initial lysosome lysis rate (delta A520/min) may be index of such effect.
The shapes of the distributions of gastric pH and hydrogen ion concentration [H+] were determined for each of 68 groups of patients scheduled for elective surgery under general anesthesia. The 68 groups comprised a total of 1,326 patients who had served as subjects in 13 of the authors' previously published studies. In general, the results showed that neither pH nor H+ was normally distributed; most of the pH distributions (47 of 68 = 69%) and most of the H+ distributions (53 of 68 = 78%) showed significant departure from the normal distribution. Moreover, the shapes of the distributions varied, depending upon the conditions under which gastric acidity was assessed. Groups receiving no medication for gastric acidity had positively skewed pH distributions (nonsymmetrical distribution with tail pointing to right and majority of cases in lower range), and groups receiving medications for the reduction of acidity had negatively skewed pH distributions (nonsymmetrical with tail pointing to left and majority of cases in upper range). The medications produced an inverse relationship between mean pH and skewness such that the skewness of the groups decreased from positive to negative as mean pH increased. For H+, all groups had positively skewed distributions, but the distributions were more positively skewed for groups receiving medications for gastric acidity. Again, the medication conditions produced an inverse relationship between mean acidity and skewness such that the groups became more positively skewed as the mean H+ decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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The hydrogen ion (H+) concentration and pCO2 were measured in the synovial fluid (SF) from the knee joints of 130 patients with arthritis by an acid-base analyser (ABL2 Acid-Base Laboratory), using a simple technique which prevented contact with air. H+ concentration was significantly higher in SF from 60 RA patients (mean 64.4 n mol/l; range 38-142 n mol/l) compared with patients with OA (mean 44 n mol/l; range 29-56 n mol/l), and 40 with other arthritides (mean 52 n mol/l). The H+ concentration in the SF showed a significant association with other variables of local inflammation-platelet, total leucocyte and polymorph counts, 5-nucleotidase, acid phosphatase and IgA levels in the SF and the clinical knee score, but not with the volume of the effusion. A similar relationship between these variables of inflammatory activity and SF pCO2 was also established. A higher SF H+ concentration was also found in systemically active disease, but no difference in SF pH between seropositive and seronegative patients. Whilst the pH of SF approximated to that of the blood in OA, it was significantly lower in the SF in RA. SF pH is a useful marker of local inflammatory activity, and its measurement is simple, reliable and rapid. It is relevant because changes in pH influence many of the processes involved in inflammation and the pH difference between SF and blood influences the transfer of drugs into the joint.
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