PCO2 measurements in surface proximal tubules and peritubular capillaries of the rat kidney

1982 ◽  
Vol 242 (1) ◽  
pp. F78-F85 ◽  
Author(s):  
F. J. Gennari ◽  
C. R. Caflisch ◽  
C. Johns ◽  
D. A. Maddox ◽  
J. J. Cohen
Keyword(s):  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Respiratory Alkalosis ◽  
Proximal Tubules ◽  
Surface Structures ◽  
Peritubular Capillary ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Peritubular Capillaries ◽  
The Difference

PCO2 was measured in surface proximal tubules and peritubular capillaries in the rat under normal acid-base conditions and in three settings with decreased HCO3(-) reabsorption: benzolamide administration, respiratory alkalosis, and metabolic acidosis. Under normal conditions, PCO2 in the early proximal tubule (EP) was 10.5 mmHg higher than PaCO2 (P less than 0.001) and 3-4 mmHg higher than late proximal (LP) and peritubular capillary (PC) PCO2 (P less than 0.001). PCO2 in LP and PC was 7 mmHg higher than PaCO2 (P less than 0.001). Benzolamide (3 mg/kg) had no effect on the difference between PC and arterial PCO2 or between EP and PC PCO2. Increasing benzolamide to 8 mg/kg increased PCO2 in the surface structures relative to arterial PCO2 by 3-5 mmHg (P less than 0.01). Metabolic acidosis did not alter the relationships between cortical and arterial PCO2. By contrast, respiratory alkalosis decreased cortical PCO2 relative to PaCO2 by over 50%. Nonetheless, EP PCO2 was still higher than LP or PC PCO2 (P less than 0.01). Thus, reducing HCO3(-) reabsorption does not obliterate the difference between EP and LP or PC PCO2 nor does it invariably reduce PCO2 in the surface structures of the kidney relative to arterial PCO2.

Micropuncture Study of Pressures in Proximal Tubules and Peritubular Capillaries of the Rat Kidney and Their Relation to Ureteral and Renal Venous Pressures

1956 ◽  
Vol 185 (2) ◽  
pp. 430-439 ◽  
Author(s):  
Carl W. Gottschalk ◽  
Margaret Mylle
Keyword(s):  
Rat Kidney ◽  
Venous Pressure ◽  
Proximal Tubules ◽  
Peritubular Capillary ◽  
Pressure Elevation ◽  
Intratubular Pressure ◽  
Peritubular Capillaries ◽  
Micropuncture Study ◽  
Capillary Pressures ◽  
Hypertonic Dextrose

Methods are described for direct measurement of the hydrostatic pressure in the surface tubules and capillaries of the rat kidney. In fifty-six anesthetized rats intratubular pressure averaged 13.5 ± 2.4 mm Hg. Subsequent microdissection showed that all of the 112 puncture sites so localized were in the first two-thirds of the proximal convoluted tubule. Under all conditions studied, intratubular pressure and the pressure in the peritubular capillaries were approximately the same. Intravenous injection of hypertonic dextrose solution generally produced a brief rise in intratubular and peritubular capillary pressures, which returned to their preinjection levels while the diuresis so produced continued, although at less than the maximal rate. Obstruction of the ureter of kidneys undergoing diuresis resulted in a prompt rise in intratubular pressure, which agreed closely with the simultaneously determined ureteral pressure. Elevation of the ureteral pressure with a pressure bottle had no effect on intratubular or peritubular capillary pressures until it exceeded the pre-existing intratubular and peritubular capillary pressures, and then all rose together up to a maximum intratubular pressure above which elevation of ureteral pressure resulted in no further rise in intratubular or peritubular capillary pressure. Elevation of applied ureteral pressure in kidneys with collapsed tubules and in dead animals did not increase the intratubular pressure, demonstrating that the rise in intratubular pressure produced in this manner in functioning kidneys was not simply a direct back transmission of pressure. Elevation of renal venous pressure by compression of the renal vein also had no effect on intratubular and peritubular capillary pressures until their pre-existing values were exceeded, and then all three pressures rose together.

Cerebral acid-base and gas metabolism in brain injury

1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping
Keyword(s):  
Metabolic Acidosis ◽  
Brain Injury ◽  
Brain Damage ◽  
Close Correlation ◽  
Respiratory Alkalosis ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Gas Metabolism ◽  
Permanent Brain Damage

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

Renal cortical interstitium and fluid absorption by peritubular capillaries

1994 ◽  
Vol 266 (2) ◽  
pp. F175-F184 ◽  
Author(s):  
K. Aukland ◽  
R. T. Bogusky ◽  
E. M. Renkin
Keyword(s):  
Rat Kidney ◽  
Colloid Osmotic Pressure ◽  
Capillary Wall ◽  
Peritubular Capillary ◽  
Fluid Reabsorption ◽  
Fluid Uptake ◽  
Peritubular Capillaries ◽  
Capillary Fluid ◽  
Renal Cortical Interstitium ◽  
Relative Retardation

Every minute, the cortical peritubular capillaries in a 1-g rat kidney take up more than 0.5 ml tubular reabsorbate. Studies of renal lymph and measurements of pressure in capillaries (Pc) and interstitium (Pi) indicate that normally the protein colloid osmotic pressure of peritubular capillary plasma (COPp) provides the necessary absorptive force, keeping Pi at 2-4 mmHg, i.e., 8-10 mmHg lower than Pc. At reduced COPp, continued delivery of fluid from the tubules automatically raises Pi to maintain capillary fluid uptake. The transient Pi response to sudden exposure of the kidney to subatmospheric pressure shows that such adjustment of forces may take place in only 5 s. Most remarkable, adjustment of forces may take place in only 5 s. Most remarkable, reabsorption continues during protein-free perfusion of the isolated rat kidney, apparently effected by a Pi exceeding Pc. A relative retardation of interstitial uptake of ferritin from plasma in this case suggests fluid reabsorption through both small and large pores in the capillary wall. Collapse of the capillaries is presumably prevented by tight tethering to the capillary wall, giving the narrow interstitium a very low compliance.

Chronic metabolic acidosis upregulates rat kidney Na-HCO 3 − cotransporters NBCn1 and NBC3 but not NBC1

2002 ◽  
Vol 282 (2) ◽  
pp. F341-F351 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Christiaan Fulton ◽  
Weidong Wang ◽  
Ira Kurtz ◽  
Jørgen Frøkiær ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Free Access ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
Acid Base ◽  
Chronic Metabolic Acidosis ◽  
Daily Water Intake ◽  
Base Balance ◽  
Access To Water

Several members of the Na-HCO[Formula: see text] cotransporter (NBC) family have recently been identified functionally and partly characterized, including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in the regulation of renal acid-base balance. However, it is unknown whether the expressions of these NBCs are regulated in response to changes in acid-base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these NBCs in kidneys using two conventional protocols. In protocol 1, rats were treated with NH4Cl in their drinking water (12 ± 1 mmol · rat−1 · day−1) for 2 wk with free access to water ( n = 8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87 and 224 ± 35%, respectively, of control levels ( P < 0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). In protocol 2, rats were given NH4Cl in their food (10 ± 1 mmol · rat−1 · day−1) for 7 days, with a fixed daily water intake ( n = 6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262 ± 42%) and NBC3 (160 ± 31%) were significantly increased compared with controls ( n = 6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols, immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na+-dependent HCO[Formula: see text] uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in intercalated cells, whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in the reabsorption of NH[Formula: see text] in the mTAL and increased NBC3 in reabsorbing HCO[Formula: see text].

Teaching acid/base physiology in the laboratory

2010 ◽  
Vol 34 (4) ◽  
pp. 233-238 ◽  
Author(s):  
Ulla G. Friis ◽  
Ronni Plovsing ◽  
Klaus Hansen ◽  
Bent G. Laursen ◽  
Birgitta Wallstedt
Keyword(s):  
Metabolic Acidosis ◽  
Medical Students ◽  
Respiratory Alkalosis ◽  
Theory And Practice ◽  
Single Group ◽  
Acid Base ◽  
Laboratory Exercise ◽  
Base Disorder

Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied.

scholarly journals Acid based disorders in intensive care unit: a hospital-based study

2019 ◽  
Vol 6 (1) ◽  
pp. 62 ◽  
Author(s):  
Babu Rajendran ◽  
Seetha Rami Reddy Mallampati ◽  
Sheju Jonathan Jha J.
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Metabolic Acidosis ◽  
Infectious Diseases ◽  
Respiratory Alkalosis ◽  
Simple Type ◽  
Acid Base ◽  
Icu Patients ◽  
Mixed Acid ◽  
Base Disorder

Background: Acid base disorders are common in the ICU patients and pose a great burden in the management of the underlying condition.Methods: Identifying the type of acid-base disorders in ICU patients using arterial blood gas analysis This was a retrospective case-controlled comparative study. 46 patients in intensive care unit of a reputed institution and comparing the type of acid-base disorder amongst infectious (10) and non-infectious (36) diseases.Results: Of the study population, 70% had mixed acid base disorders and 30% had simple type of acid base disorders. It was found that sepsis is associated with mixed type of acid-base disorders with most common being metabolic acidosis with respiratory alkalosis. Non-infectious diseases were mostly associated with metabolic alkalosis with respiratory acidosis. Analysis of individual acid base disorders revealed metabolic acidosis as the most common disturbance.Conclusions: These results projected the probability of acid bases disorders in various conditions and help in the efficient management. Mixed acid base disorders are the most common disturbances in the intensive care setup which is metabolic acidosis with respiratory alkalosis in infectious diseases and metabolic acidosis is the most common simple type of acid base disorder.

Ventilatory response to chronic metabolic acidosis and alkalosis in the dog

1984 ◽  
Vol 56 (6) ◽  
pp. 1640-1646 ◽  
Author(s):  
N. E. Madias ◽  
W. H. Bossert ◽  
H. J. Adrogue
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Ventilatory Response ◽  
Wide Spectrum ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Plasma Bicarbonate ◽  
Oral Sodium ◽  
Chronic Change

Systematic data are not available with regard to the anticipated appropriate responses of arterial PCO2 to primary alterations in plasma bicarbonate concentration. In the present study, we attempted to rigorously characterize the ventilatory response to chronic metabolic acid-base disturbances of graded severity in the dog. Animals with metabolic acidosis produced by prolonged HCl feeding and metabolic alkalosis of three different modes of generation, i.e., diuretics (ethacrynic acid or chlorothiazide), gastric drainage, and administration of deoxycorticosterone acetate (alone or in conjunction with oral sodium bicarbonate), were examined. The results indicate the existence of a significant and highly predictable ventilatory response to chronic metabolic acid-base disturbances. Moreover, the magnitude of the ventilatory response appears to be uniform throughout a wide spectrum of chronic metabolic acid-base disorders extending from severe metabolic acidosis to severe metabolic alkalosis; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin. Furthermore, the data suggest that the ventilatory response to chronic metabolic alkalosis is independent of the particular mode of generation.

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