Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
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PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
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PMID:The apparent buffer value of cerebrospinal fluid in acute hypercapnia. 82 71

The pathogenesis of gastroduodenal ulcer associated with chronic pulmonary obstructive disease is complicated, as is the pathogenesis of these two disease entities separately. It is evident that a multifactorial dependence is involved which has not yet been resolved completely. Hence, there is no "magna cause morbi" but rather a multiform and dynamically variable chain of causes, consequences and conditions, some of which may be of genetic dependence. In the possible complex of causes leading to the genesis of gastroduodenal ulcer associated with chronic pulmonary obstructive disease, the author investigated the effect of isolated hypercapnia on the acidity of gastric juice and mucous membrane in 18 healthy normacid subjects. The results of this study that in healthy subjects isolated hypercapnia leads to a statistically significant increase in acidity of gastric juice and mucous membrane.
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PMID:The effect of inhalation hypercapnia in healthy subjects on the acidity of gastric juice. 101 81

The effects of methionine enkephalin (ME) and substance P (SP) were tested on the chemosensory discharge of the cat carotid body-nerve preparation in vitro. ME superfused in concentrations of 10(-8) to 10(-5) M depressed the sensory discharge, an effect followed by receptor excitation (rebound). Bolus applications of ME (30 ng to 3.0 microgram) induced variable effects (excitation or depression) on the discharge, excitation being more pronounced with the smaller doses. Superfusions with SP (10(-8) to 10(-5) M) either excited or depressed the discharge, excitation being more pronounced with higher SP concentrations (i.e. 10(-6) M). Bolus applications of SP (43 ng to 0.5 micrograms) also excited or depressed the sensory discharge. These variations may be dose-dependent. Superfused ME (10(-6) M) significantly depressed the chemoreceptor response to hypoxia (100% N2) and hypercapnia (6% CO2, pH 7.43). The responses to NaCN and acidity (pH 6.0) were marginally depressed. Superfused SP (10(-6) M) clearly depressed the responses to hypoxia, those to hypercapnia and NaCN were marginally affected but the effects of acidity were not altered. When the peptides were tested against the receptor responses to exogenously applied putative neurotransmitters (ACh, dopamine--DA), it was found that ME tended to depress both the ACh and DA actions whereas SP (10(-6) M) tended to increase their effects. Superfusions with naloxone (10(-6) M) increased the basal chemosensory discharge and this enkephalin blocker partially relieved the depressant effect of ME on the ACh-induced response. It is concluded that carotid body chemoreceptors have excitatory and inhibitory reactive sites to both ME and SP although their precise location is still unknown.
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PMID:Effects of methionine-enkephalin and substance P on the chemosensory discharge of the cat carotid body. 241 43

Intracellular recordings were made from glomus cells in the excised, intact or sliced (150-200 microns) carotid body. Carotid nerve discharge was also recorded from intact preparations. Slices were prepared for visual (Nomarski) control of microelectrode impalement. Resting potential (Em), input resistance (Ro) and voltage noise (Erms) were measured in control conditions and in response to several stimulants (interruption of flow, hypoxic and histotoxic [NaCN]anoxia, hypercapnia, asphyxia and acidity) and depressants (alkalinity, cooling) of the carotid nerve sensory discharge. Different glomus cells responded differently to the same stimulus but significant trends were found. The more common responses to zero flow and anoxia (hypoxic and histotoxic) were depolarization (64%) and decreases in Erms (63%) and Ro (71%). When extracellular pH was varied from 8.5 to 5.0, the preponderant responses were cell depolarization, and increases in noise and input resistance as pH decreased. Consequently, cell depolarization induced by zero flow and anoxia tended to be accompanied by reduced Ro, whereas that induced by acidity generally showed increased Ro. Changes in voltage noise usually followed variations in Ro. When nerve discharge frequency was plotted against delta Em or delta Erms there were positive correlations during acid stimulation. However, these correlations were complex (parabolic) during flow interruption and anoxia: an increase in discharge occurred in response to cell depolarization and to hyperpolarization. These results suggest that hypoxia and hypercapnic or acidic stimuli act on glomus cells by different mechanisms. This finding is consistent with evidence obtained by recording carotid nerve discharges in intact animals.
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PMID:Changes in glomus cell membrane properties in response to stimulants and depressants of carotid nerve discharge. 270 87

Arthrosis was induced in the rabbit knee, making it unstable by ligament resection. Acidity and hypercapnia were found in the synovial fluid of the arthrotic knees, whereas oxygen partial pressure was normal. In arthrotic subchondral bone the intraosseous pressure and oxygen partial pressure were increased; intraosseous phlebography showed venous congestion. Histologic specimens showed increased subchondral bone formation, loss of cartilage and total depletion of glycosaminoglycans. The synovial membrane was hyperplastic and fibrosis was found in the underlying tissue. We suggest that changes in environmental haemodynamics and metabolism, although secondary in nature, may play an important role in the arthrotic process.
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PMID:Hemodynamics and metabolism in arthrosis. Studies in the rabbit knee. 308 33

The purpose of the present study was to evaluate the environmental changes in synovial fluid and subchondral bone during synovitis in rabbits in which the knee joint on one side was subjected to a procedure causing instability; a traumatic synovitis rapidly developed. Three weeks following the procedure, partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2) and hydrogen ion concentration (pH) were measured in vivo in the juxta-articular bone and in the synovial fluid of both the normal and the affected sides. Mass spectrometry was used for simultaneous registration of PO2 and PCO2, while a monocrystalline antimony pH electrode was used for simultaneous measurement of pH in vivo. Hypoxia, hypercapnia and relative acidity were found in synovial fluid and subchondral bone of knees with synovitis. The metabolic environment of synovial fluid and subchondral bone was considerably changed at the 3-week stage of experimental osteoarthritis and this was probably secondary to regional venous congestion.
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PMID:Synovitis causes hypoxia and acidity in synovial fluid and subchondral bone. 310 76

Acetazolamide (Diamox) induced carbonic anhydrase inhibition is an efficient means of eliminating surplus water and bicarbonate in the overhydrated and alkalotic patient. Previous studies have demonstrated an unexpected and unexplained increase in arterial and venous oxygenation during acute carbonic anhydrase inhibition. In the present investigation we assessed the effect of acetazolamide 15 mg kg-1 on pulmonary gas exchange in 10 critically ill, mechanically ventilated patients. Median arterial oxygen tension increased by 0.9 kPa and central venous oxygen tension and content by 16-18% and 6-8% respectively. The improved oxygenation could, however, not be attributed to an improved pulmonary oxygen exchange as both pulmonary venous admixture (Qs Qt-1) and physiological dead space ventilation (VD VT-1) increased. The increase in arterial oxygen tension can be explained by a rightward shift of the oxyhemoglobin dissociation curve due to the increased acidity of the blood during carbonic anhydrase inhibition (Bohr effect). Acetazolamide does not depress oxygen consumption, so the increase in central venous oxygen content probably reflects an improved cardiac performance. This could conceivably be mediated via sympathetic activation in response to acetazolamide induced carbon dioxide retention.
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PMID:Respiratory function and carbonic anhydrase inhibition. 311 60

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4

The tumor interstitial pH and its modification play a significant role in cancer treatment. Current in vivo pH measurement techniques are invasive and/or provide poor spatial resolution. Therefore, there are no data on perivascular interstitial pH gradients in normal or tumor tissue. We have optically measured interstitial pH gradients with high resolution in normal and tumor (VX2 carcinoma) tissue in vivo by combining a fluorescence ratio imaging microscopy technique and the rabbit ear chamber preparation. The strengths of our approach include the ability to follow pH in the same location for several weeks and to relate these measurements to local blood flow and vascular architecture. Our results show: (a) tumor interstitial pH (6.75 units; N = 6 animals, n = 324 measurements) is significantly (P < 0.001) less than normal interstitial pH (7.23; N = 5, n = 274). This increased acidity in the tumor interstitium is in agreement with the previously reported data on this tumor; (b) with respect to pH spatial gradients in normal tissue, the interstitial pH decreased by approximately 0.32 pH units over a distance of 50 microns away from the blood vessel, while in tumor tissue, interstitial pH decreased by approximately 0.13 units over the same distance. Although the pH gradient near the vessel wall was steeper in normal tissue compared to tumor, the proton concentration gradient in normal tissue was less than that in the tumor. The approximate increase in proton concentration from 0-50 microns from the vessel was 4.5 x 10(-8)M in normal versus 5.7 x 10(-8)M in tumor tissue; (c) a simple one-dimensional diffusion-reaction model suggested that tumor tissue was producing protons at a rat 65-100% greater than normal tissue; (d) feasibility studies of temporal dynamics resulting from hyperglycemia (6 g/kg) or hypercapnia (10% CO2) led to significant (P < 0.05) interstitial pH reductions. During hyperglycemia, pH dropped by more than 0.2 pH units in about 90 min in tumor tissue but remained constant in normal tissue. Hypercapnia dramatically reduced pH by approximately 0.3 pH units in tumor tissue. Our limited studies on hyperglycemia and hypercapnia are in agreement with the previously published studies and demonstrate the capability of fluorescence ratio imaging microscopy to measure spatial as well as temporal changes in interstitial pH. Fluorescence ratio imaging microscopy should permit noninvasive evaluation of new pH-modifying agents and offer unique mechanistic information about tumor pathophysiology in tissue preparations where the surface of the tissue can be observed.
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PMID:Noninvasive measurement of interstitial pH profiles in normal and neoplastic tissue using fluorescence ratio imaging microscopy. 792 15


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