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PubMed1976

[Comparative evaluation of the effectiveness of diuretics].

The study was conducted in 118 patients with cardiac and pulmonary lesions, aged 18 to 75 years. Among the diuretics the leading role belongs to Uregyt, and Lasix, as judged by their natriuretic and diuretic action, then follow Nuvorit, Hypothiaside and Brinaldix. Renese (polythiaside) produces the same diuretic effect as Nuvorit and Hypothiaside. Renese, Hypothiaside, Lasix and Uregyt enhance kaliuresis and often reduce potassium blood plasma concentrations, while Nuvorit and Brinaldix increase kaliuresis least of all, and often increase the potassium blood plasma level. Within two days of discontinuing Thriamterene nearly all body potassium that was retained under the effect of this drug is excreted. Nuvorit, Hypothiaside, Renese, Brinaldix, Lasix, Uregyt cause similar changes in the acid-base balance (respiratory and metabolic alkalosis), and produce no effect upon the acid-base balance rather seldom. Lasix and Uregyt cause metabolic alkalosis more often than other diuretics. Apart from that, Hypothiaside also causes respiratory acidosis in 1/4 of the patients.

Adolescent↗
PubMed1994

Effects of altered arterial carbon dioxide tension on quantitative electroencephalography in halothane-anesthetized dogs.

Quantitative electroencephalography was assessed in 6 dogs anesthetized with 1.8% end-tidal halothane, under conditions of eucapnia, hypocapnia, and hypercapnia. Ventilation was controlled in each condition. Heart rate, arterial blood pressure, core body temperature, arterial pH, blood gas tensions, end-tidal CO2 tension, and end-tidal halothane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG. Quantitative electroencephalographic data were stored on an optical disk for analysis at a later date. Values for absolute power of the EEG were determined for delta, theta, alpha, and beta frequencies. Hypocapnia was achieved by hyperventilation. Hypercapnia was achieved by titration of 5% CO2 to the inspired gas mixture. Hypercapnia was associated with an increase in the absolute power of the delta band. Hypocapnia caused an increase in the absolute power of delta, theta, and alpha frequencies. Quantitative electroencephalographic data appear to be altered by abnormalities in arterial carbon dioxide tension. Respiratory acidosis or alkalosis in halothane-anesthetized dogs may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.

Animals↗
PubMed1993

Daniel's story: congenital central hypoventilation syndrome.

Central hypoventilation syndrome (CHS) is a disorder characterized by little or no ventilatory or arousal sensitivity to hypercapnia and variable reactivity to hypoxemia, with little or no hypoxic arousal responsiveness. CHS may be congenital or acquired and can be idiopathic or secondary to a known central nervous system abnormality. Infants often present with life-threatening apnea during quiet sleep and develop severe respiratory acidosis because of the inadequate response to hypercapnia and hypoxia. Long-term treatment usually involves use of mechanical ventilation during sleep.

Diagnosis, Differential↗
PubMedDate not supplied

Effect of venous hypercarbia and hyperventilation on myocardial contractility in canine haemorrhagic shock.

To study the effect of venous hypercarbia on myocardial contractility, haemorrhagic shock was produced in six healthy mongrel dogs by ex-sanguination of 15 ml of blood/kg body weight every 20 minutes till a loss of 45 ml/kg was achieved. After recording haemodynamic and respiratory parameters, the dogs were hyperventilated by positive pressure ventilation for 30 minutes and haemodynamic and blood gas parameters reassessed. During haemorrhagic shock, mean cardiac output decreased from 4.23 l min to 0.98 l min (p < 0.01), stroke index from 2.25 to 0.35 ml/kg (p < 0.05) and left ventricular stroke work index from 3.72 to 0.19 g. m/kg. The mean mixed venous pCO2 increased from 35 mmHg to 56.7 mmHg (p < 0.05). During hypoventilation, mixed venous pCO2 decreased to 40 mmHg (p < 0.05) and without any volume replacement, mean cardiac output increased 2.5 l min (P < 0.05), stroke index to 1.13 ml/kg (p < 0.05) and left ventricular stroke work index, and index of myocardial contractility, increased to 0.78 g.m/kg (p < 0.05). Thus, although hypovolaemia is the major cause of low cardiac output in haemorrhagic shock, this study shows that venous hypercarbia (which probably indicates tissue respiratory acidosis) further worsens circulatory failure by decreasing myocardial contractility. Hyperventilation improves cardiac functions and increases output by relieving tissue hypercarbia in spite of persistent hypovolaemia.

Animals↗
PubMed1994

Inhibition of the fetal stress response improves cardiac output and gas exchange after fetal cardiac bypass.

Cardiac bypass in late-gestation fetal lambs causes severe placental vasoconstriction, which leads to fetal death from hypoxemia and respiratory acidosis. This response can be blocked by the administration of indomethacin; however, a fatal metabolic acidosis then gradually develops in the fetus. Because the fetus is known to mount an intensive catecholamine response to stress, and because the fetal myocardium is particularly sensitive to increased afterload, we hypothesized that elevated afterload as a result of fetal stress contributes to diminished cardiac output after bypass. Twenty fetal lambs at 80% gestation underwent 30 minutes of normothermic cardiac bypass at flow rates of 200 to 500 ml/kg per minute. All ewes received general anesthesia with ketamine. In 10 fetuses general anesthesia was specifically designed not to inhibit the release of stress-related catechols (ketamine); the remaining 10 fetuses received a "high" (cisterna magna) total spinal anesthetic with tetracaine, to block the fetal stress response. In each anesthetic group, 5 of the 10 lambs received indomethacin. During operation, normal hemodynamics were preserved in the spinal anesthetic group. Cardiac output, placental blood flow, and arterial carbon dioxide tension were all improved relative to results in the ketamine group. When spinal anesthesia and indomethacin are both given, hemodynamics also approach normal after bypass, and gas exchange is further improved. These data suggest that the inhibition of the stress response by spinal anesthesia improves the hemodynamic status of the fetus during operation and, in combination with indomethacin, allows maintenance of near-normal placental function after fetal cardiac bypass. Similar responses may also be possible in human fetuses with use of a high-dose narcotic technique.

Anesthesia, Spinal↗
PubMed1994

Determination of fetal acidemia at birth from a remote umbilical arterial blood gas analysis.

OBJECTIVE: Sampling of the umbilical artery for determination of acid-base status is performed within 60 minutes of birth, but is not feasible in all hospitals on a 24-hour basis. A desirable alternative would be to perform the arterial cord blood gas analysis hours after the sample was obtained at delivery with reliable identification of whether the newborn was acidotic. STUDY DESIGN: After 19 deliveries multiple umbilical arterial blood samples were withdrawn into five preheparinized syringes, and these were analyzed at 0.5, 15, 30, 45, and 60 hours after delivery. On the basis of observed changes in pH and base deficit over 60 hours, two separate regression equations were generated. These two equations permit calculation of the original pH and base deficit if the following are known: (1) the time interval from delivery to blood gas analysis and (2) the values of the remote pH and remote base deficit. The regression models were validated among 23 subsequent deliveries to assess how accurately they identified newborn acid-base status at birth. RESULTS: The original pH and base deficit can be calculated with two separate equations from linear regression models if two variables are known: the results of the remote umbilical arterial blood gas analysis and time intervals from delivery to analysis. Of 23 newborns during the validation phase of the study, 16 were not acidotic, one had respiratory acidosis, and six had metabolic acidosis. The second umbilical arterial blood gas analysis was performed at a mean (+/- SD) interval of 53.8 +/- 41.5 hours (range 7.5 to 138 hours). The remote gas analysis inaccurately identified 68.7% (11/16) of nonacidotic newborns as being acidotic at birth. However, insertion of these data into these equations produced results with none of the newborns predicted to have normal acid-base when they were acidotic at birth or predicted to be acidotic when the cord pH was normal. CONCLUSIONS: Use of these mathematic models allows the clinician to perform an umbilical arterial blood pH analysis < or = 60 hours after delivery yet with accurate estimation of true acid-base status at birth.

Acidosis↗
PubMed1993

[Anesthesia before and after curare].

Before the advent of curare, muscular relaxation essential for upper abdominal and intrathoracic surgery adequate operating conditions, could only be provided by deep ether or cyclopropane anaesthesia. The required depth of anaesthesia frequently caused severe cardiovascular depression, metabolic and respiratory acidosis and alteration of kidney and liver function. Ether, and especially cyclopropane sensitized the heart to the development of arrhythmias and the danger of explosion was never far away. For fear of anaesthetic mortality essential, life saving operations were often abandoned in poor risk patients. The administration of anaesthesia was more an art, mastered by relatively few, than a science that could be taught to many. It is a tribute to the early masters of anaesthesiology that they were able to carry their patients through the dangers associated with the provision of anaesthesia for major surgical procedures, with relatively low morbidity and mortality. The introduction of curare into anaesthetic practice, by Griffith and Johnson, in 1942, caused profound changes in the efficacy and safety of anaesthesiology. It made possible the development of true balanced anaesthesia, and the elimination of the explosive inhalation anaesthetics and the profound metabolic disturbances associated with their use. The concept of "inoperability," due to severe pathology or extremes of age became obsolete. It would be hard to envisage how open heart, organ transplant and radical brain and cranio-facial surgery could have developed without muscle relaxants.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesiology↗
PubMedDate not supplied

The apparent buffer value of cerebrospinal fluid in acute hypercapnia.

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.

Acetazolamide↗
PubMed1993

[A case of central alveolar hypoventilation syndrome associated with cerebral infarction].

Central alveolar hypoventilation syndrome (CAH), or Ondine's curse, is a very rare disease characterized by dysfunction of respiratory center in the brain stem. Here, we report a case of CAH associated with cerebral infarction. A 59-year-old man developed right facial sensory deficit at age 56. Then, the facial sensory deficit spread to the left side and dysarthria and dysphagia also developed. Since age 58, he often developed respiratory failure and consciousness disturbance. Arterial blood gas analysis revealed alveolar hypoventilation and respiratory acidosis. Disorders of peripheral organs such as lung, airway, thorax and neuromuscular diseases were ruled out. Brain MRI showed cerebral infarction in the brain stem. We diagnosed him as CAH associated with brain stem infarction.

Blood Gas Analysis↗
PubMed1993

[A case of status asthmaticus complicated by with pneumoperitoneum during mechanical ventilation therapy].

A 46-year-old woman was admitted to our hospital for a severe asthma attack. On admission, systemic cyanosis was observed, and her consciousness state was drowsy. Arterial blood gas showed severe respiratory acidosis, hypoxia, and hypercapnea, with pH, PaO2, and PaCO2 of 7.163, 29.9 torr and 81.3 torr, respectively. Immediately, mechanical ventilation was commerced but on the third hospital day pneumomediastinum and subcutaneous emphysema appeared, and on the sixth day pneumoperitoneum also appeared. The chest CT scan on the sixth day showed free air around bilateral internal mammary vessels. This indicated that air moved from the mediastinum into the peritoneal cavity through an anterior route, via the sternocostal triangle formed by the xiphoid origins of the diaphragm medially and the costal origins laterally.

Female↗
PubMed1993

Effects of prolonged CO2 inhalation on shivering thermogenesis during cold-water immersion.

We investigated the effect of prolonged hypercapnia on human thermoregulation during immersion of seven male subjects in a 15 degrees C water bath until their esophageal temperature dropped to 35 degrees C or until 1 h had elapsed. In the control trial, subjects inspired room air, whereas in the other trial the inhaled gas mixture was a 4% CO2:20% O2:76% N2 gas mixture. Oxygen uptake (VO2, liter.min-1), inspired minute ventilation (VI, liter.min-1), esophageal temperature (Tes, degree C), mean unweighted skin temperature (Tsk, degree C), mean heat flux (Q, W.m-2), and electromyographic (EMG, mV) activity of the trapezius muscle were recorded. VO2 and integrated EMG (IEMG) activity were used as the primary indicators of shivering thermogenesis. There was a tendency for elevated VO2, albeit not significant, in the CO2 trial compared to the air trial. We observed no significant differences in the IEMG between the air and CO2 trials. These results suggest that prolonged inhalation of a gas mixture containing 4% CO2 does not have a significant inhibitory effect on shivering thermogenesis and does not enhance the cooling rate of the body core. The absence of any shivering attenuation is most likely due to the small blood PCO2 increase incurred by inhalation of 4% CO2, compensation of hypercapnic-induced respiratory acidosis, and a strong thermal drive from core and peripheral regions. It is unlikely that elevated PICO2 levels contribute significantly to the etiology of hypothermia in divers.

Adult↗
PubMed1977

Evaluation of xylazine and ketamine hydrochloride for anesthesia in horses.

The cardiopulmonary effects resulting from the combination of xylazine and ketamine hydrochloride were evaluated in the adult horse. Xylazine (1.1 mg mg/kg) administered intravenously prior to or simultaneously with ketamine hydrochloride (2.2 mg/kg; intravenous) provided excellent analgesia and light anesthesia in all horses. Cardiac output, arterial blood pressure, pulmonary arterial pressure, central venous pressure, and pulmonary arterial wedge pressure remained within normal limits for the adult horse. Evidence of respiratory acidosis developed with time during the anesthetic period. Induction and recovery from anesthesia appeared smooth and excitement-free. In the horse, larger dosages of ketamine hydrochloride (6.6 mg/kg) following sedation with xylazine (1.1 mg/kg; intravenous) were accompanied by muscular tremor and rigidity, mydriasis, oculogyric movements, sweating, hypertension, tachycardia, and increased rectal temperature during recovery from anesthesia. Providing there is good sedation from xylazine, the combination of xylazine and ketamine hydrochloride as a short-term intravenous anesthetic technique in the horse appears safe and acceptable providing reasonably stable cardiopulmonary function. If the sedative properties of xylazine are not apparent or if excessive dosages of ketamine hydrochloride are used, the drug combination results in serious side effects precluding its use for anesthesia in the horse.

Analgesia↗
PubMedDate not supplied

[Acid-base equilibrium and nitrogen metabolism in rats in a state of artificial hibernation].

Experiments on rats have shown an important role of hypercapnia in the development of condition of artificial hibernation in combination with influence of hypothermia, hypoxia and hypercapnia. It is proved that the joint action of hypothermia, hypoxia and hypercapnia has induced development of respiratory acidosis and hibernation in animals, while removal of the hypercapnia effect has induced development of acute metabolic acidosis and death of animals. It has been found that animals in the state of artificial hibernation have considerable changes in concentrations of main electrolytes (Na+, K+, Ca+, Mg2+, phosphates, Cl-) and metabolites (NH3, glutamine, urea) in blood as well as in activity of enzymes (glutamaldehydrogenase, glutaminase, arginase) in tissues of the liver and kidneys.

Acid-Base Equilibrium↗
PubMed1996

Intestinal pseudo-obstruction (Ogilvie's syndrome) in theophylline overdose.

Intestinal pseudo-obstruction (Ogilvie's syndrome) has previously been reported in 2 patients with theophylline toxicity treated with activated charcoal (AC), mechanical ventilation and opioid induced sedation. We report a case of Ogilvie's syndrome in a theophylline toxic patient treated with AC. A 45-y-old male with severe chronic obstructive pulmonary disease presented with vomiting and multifocal atrial tachycardia after an intentional theophylline overdose. His initial potassium concentration was 2.7 mEq/L and his theophylline was 191 mg/L (1060 mumol/L). The patient was hemodialyzed and given a total of 1,000 g of AC without cathartics during the first hospital day. He also received iv potassium replacement. On the second hospital day he required mechanical ventilation for respiratory acidosis. Clindamycin was given for purulent sputum and fever. Haloperidol was given to treat agitation. No other anticholinergic agents or opioids were given. The patient's potassium rose to 6.5 mEq/L and he was given kayexalate. During the third hospital day the patient developed abdominal distention, tenderness and leukocytosis. Abdominal radiographs revealed a distended cecum. In the operating room the cecum was found dilated to 16 cm with no distal obstruction. A cecostomy tube drained AC and pill fragments. A 6 cm charcoal bezoar was found in the stomach. The patient recovered uneventfully.

Administration, Oral↗
PubMed1996

Immunocytochemistry of renal H-ATPase.

In this review we present immunolocalization studies using a monoclonal antibody raised against the 31-kD subunit of bovine H-ATPase, and indirect immunofluorescent staining. In the proximal tubules there is intense H-ATPase staining in the brush borders of S1 and S2, and linear subvillar invagination staining in S1, S2, and S3 segments. In the thick ascending limb of the loop of Henle there is a mild to moderate degree apical cytoplasmic vesicular staining in both medullary and cortical segments. In distal convoluted tubule the H-ATPase staining is more sharply delineated along the luminal plasma membrane. In the connecting tubule, the connecting tubule cells show mild to moderate staining of the luminal membrane and apical cytoplasmic vesicular staining, and the intercalated cells demonstrated prominent H-ATPase staining which is polarized to either apical or basolateral pole or distributed diffusely throughout the cell. In the cortical collecting duct the principal cells show minimal or no staining while the intercalated cells show very bright H-ATPase sustaining with six discernible subtypes based on polarization of the pump to apical or basolateral poles, and the degree of polarization (well polarized or poorly polarized). In the medullary collecting duct the principal cells show no staining and the intercalated cells show H-ATPase staining only in the apical pole. We also describe adaptive responses to different physiologic conditions, e.g. chronic acid or alkali loads (with or without colchicine), chronic respiratory acidosis, chronic desoxycorticosterone administration, remnant kidney, and chronic potassium depletion diet. Moreover, we demonstrated the immunocytochemical localization of the H-ATPase pump in the rabbit kidney as compared to the rat kidney.

Animals↗
PubMed1996

[The mechanism of controlling regional cerebral blood flow in patients with localization-related epilepsy].

INTRODUCTION: Hypoperfusion around the seizure foci has been reported in interictal CBF studies of partial epilepsy. Hypoperfusion may reflect some interictal pathophysiology characteristic of epilepsy, but the mechanism remains to be elucidated. In order to elucidate the controlling system of rCBF in patients with CPS (complex partial seizure), we measured by positron emission tomography rCBF and CO2 vasoreactivity performing a hyperventilatory task, and made comparisons between the affected and contralateral sides of the temporal lobes in CPS patients and the temporal lobe of normal volunteers. We also measured PaCO2, pH, PaO2 and respiratory rate at rest to elucidate the CBF maintaining system. SUBJECTS: 15 volunteers and 12 medically controlled patients with CPS were examined. The affected side of the brain of the patients was determined by dominance of EEG paroxysm. METHOD: For measuring rCBF, the Shimadzu HEADTOME-IV system (8mm FWHM) and H2(15)O (740-1480 [MBq]/scan) bolus injection method were employed. First a rest scan, then a hyperventilatory task scan was performed, at 20 min. intervals between each scan. During the rest scans, the subjects were required to close their eyes, which were covered through the transmission scan and all the other scans. They were monitered with EEG to insure that they were not asleep. Room lights were dimmed, room sounds were kept to a minimum and noises were damped with earplugs. During the hyperventilatory tasks, the subjects were asked to inspire deeply at a rate of 15/min. for 4.5 min. from 3 min. before the scan up to the end of the 1.5 min. scan, and monitored with a respiratory band around the abdomen. Arterial blood gas pressures (PaCO2, pH and PaO2) were also measured with a blood gas analyzer (Radio Meter ABL 330) at the beginning and at the end of the scans. [HCO3-] was calculated on the formula of Henderson-Hasselbalch. Vascular response to PaCO2 change: VrCO2 was defined as follows: VrCO2 = 100 x (CBFh-CBFr)/CBFr/(PaCO2h-PaCO2r) the subscripts h: hyperventilatory r: resting conditions. RESULTS: Blood gasses, rCBF and corrected-rCBF at rest: In the patients, PaCO2 (mmHg) = 46.11 +/- 2.32, pH = 7.374 +/- 0.020, [HCO3-] (mEq/ml) = 25.98 +/- 1.15, CBF (ml/100g/min) = 45.51 +/- 9.33, corrected-CBF (ml/100g/min) = 40.06 +/- 7.27. In the volunteers, PaCO2 = 40. 67 +/- 2.37, pH = 7.400 +/- 0.021, [HCO3-] = 24.36 +/- 1.66, CBF = 48.76 +/- 8.54, corrected-CBF = 48.02 +/- 9.04. PaCO2 and [HCO3-] in the patients were significantly higher than those in the volunteers. pH and corrected-CBF were significantly lower than those in the volunteers. CBF showed no difference. VrCO2 in the temporal lobe: In the affected side of the patients, VrCO2 = 1.976 +/- 0.54. In the contralateral side of the patients, VrCO2 = 2.145 +/- 0.667. In the temporal lobe of the volunteers, VrCO2 = 2.557 +/- 0.898. In both sides of the temporal lobe of the patients, VrCO2 was significantly lower than those in the volunteers. COMMENTS: The effect of anticonvulsant drugs and the suppressive mechanism around the foci are supposed to reduce CBF of CPS patients. We suppose another mechanism, which is vasoconstriction. A significant difference was noted in CO2-vasoreactivity in the temporal lobe between patients and volunteers. Also no difference was noted in rCBF in the temporal lobe between the volunteers and the patients, when the arteries were maximally constricted with the HIV-task. These two results suggest that vasoconstrictive mechanism may be among the factors for the hypoperfusion seen in the temporal lobe of the patients. In patients, PaCO2, [H+], [HCO3-] were significantly higher compared with the volunteers, which suggests the mechanism of respiratory acidosis. Owing to this hypercapnia, global CBF in the patients is maintained in compensation for the hyperfusion and vasoconstriction seen around the foci. CO2 acts as an anticonvulsant and also reduces glucose metabolites which accumulate around the foci.

Adult↗
PubMed1996

[Continuous ambulatory monitoring in quality control of home therapy of congenital central hypoventilation syndrome (CCHS)].

4 children with congenital central hypoventilation syndrome (CCHS) now aged 6 to 9 years were studied for 1 to 8 years. In all patients CO2-response is missing, hypoxic drive is maintained. All patients required mechanical ventilation after birth. 1 patient is supported by controlled oxygen therapy during sleep since 9 months of age. 2 patients are IPPV-ventilated during sleep. 1 patient is pressure control ventilated with an oro-nasal mask since 6 years of age. All children showed phases of hypo- and hyperventilation (max. pCO2 107 mm Hg) depending on vigilance with respiratory acidosis in awake state and during sleep. These findings required ambulatory monitoring of home-therapy by a professional guard and continuous recording of pCO2 and pulseoximetry. These longtime data (max. pCO2 72 mm Hg) show that ambulatory monitoring and control of therapy is able to avoid extreme variation of blood gases and to stabilize acid-base regulation during sleeptime in patients with CCHS.

Carbon Dioxide↗
PubMed1997

Immunocytochemical localization of the vacuolar H(+)-ATPase pump in the kidney.

In this article we review immunocytochemical localization studies using a monoclonal antibody raised against the 31 kD subunit of bovine H(+)-ATPase, and indirect immunofluorescent staining. In the proximal tubules there is intense H(+)-ATPase staining along the brush borders of S1 and S2, and linear subvillar invagination staining in S1, S2, and S3 segments. In the thick ascending limb of the loop of Henle there is a mild to moderate degree apical cytoplasmic vesicular staining. In distal convoluted tubule there is mild to moderate degree of H(+)-ATPase staining which is sharply delineated along the luminal plasma membrane. In the connecting tubule, the connecting tubule cells show mild to moderate luminal membrane and apical cytoplasmic vesicular staining, and the intercalated cells demonstrate prominent H(+)-ATPase staining which is polarized to either apical or basolateral pole or distributed diffusely throughout the cell. In the cortical collecting duct the principal cells show minimal or no staining while the intercalated cells show very bright H(+)-ATPase staining with 6 identifiable morphologic subtypes based on polarization of the pump to apical or basolateral poles, and the degree of polarization (well polarized or poorly polarized). In the medullary collecting duct the principal cells show no staining and the intercalated cells show prominent H(+)-ATPase staining only in the apical pole. We also describe adaptive responses to different physiologic manipulations e.g., chronic oral acid loads, chronic respiratory acidosis, remnant kidney model, chronic desoxycorticosterone (DOCA) administration, and chronic potassium depletion diet. Moreover, we compare the immunocytochemical localization of the H(+)-ATPase pump of rabbit and kidneys.

Animals↗