PubMed Health⌕ Search

Biomedical subjects

M Raeder

Publications and source records attributed to M Raeder.

At least 19 recordsLinked to original sources
PubMed1992

Determination of active 5-(N,N-hexamethylene)amiloride in pig plasma.

A simple, cheap and specific quantitative method for the determination of the selective Na+/H+ exchange inhibitor, 5-(N,N-hexamethylene)amiloride, in plasma and aqueous solutions has been developed. The method involves extraction with ethyl acetate, thin-layer chromatography and spectrofluorodensitometry. The compound was separated from several unidentified metabolites in plasma. The detection limit was 6 x 10(-7) M. The calculated metabolic extraction by the liver was 29%, and the plasma half-life was 12.8 min. The free, active concentration of 5-(N,N-hexamethylene)amiloride was 19.4% of the total concentration, as determined by equilibrium dialysis.

Amiloride↗
PubMed1989

[Surgical treatment of necrotizing fasciitis].

We present nine patients with necrotizing fasciitis. Two of them had Fourniers gangrene. Predisposing factors included diabetes mellitus, alcohol and drug abuse. Local signs were redness, swelling and pain rapidly followed by fever and deterioration in the patient's general condition. Soft tissue-gas was observed in all patients. It was found either clinically, on roentgenograms or by CT. Bacteria were found in blood cultures and/or necrotic tissues in all patients. The dominating treatment was radical surgical excision and early reexplorations. Antibiotics, intensive care support and early parenteral nutrition were given. Four patients were given hyperbaric oxygen treatment. The overall mortality rate was 11%. Amputation of one lower extremity became necessary in three patients. In these cases 4-8 days had elapsed between the onset and the first surgical excision. We find it important to underline early diagnosis and radical surgical excision in patients with necrotizing fasciitis.

Adult↗
PubMed1983

Mechanism of hepatic bicarbonate secretion and bile acid independent bile secretion.

To examine hepatic bicarbonate transport and bile acid independent bile secretion, bile was sampled via a T-tube inserted into the common bile duct of anaesthetized pigs. Secretin was infused intravenously at a rate of 2.7 C.U./kg body weight h-1 (large dose) or 0.45 C.U./kg body weight h-1 (small dose). Hepatic water and electrolyte secretion were studied during systemic acid-base disturbances while secretin was continuously administered. Systemic acidosis reduced the rate of NaHCO3 secretion which fell in proportion to changes in plasma pH, by 9% and 2% per 0.1 pH unit for the large and small dose of secretin, respectively. Plasma pCO2 and bicarbonate concentration had little influence on NaHCO3 secretion. Consequently, plasma pH appeared to be the main determinant of hepatic NaHCO3 secretion during acid-base changes. Secretion of 1 mol NaHCO3 was accompanied by an isotonic solution containing water and 0.25 mol NaCl. After secretin infusion, 14C-erythritol clearance increased in proportion to bile flow. Bicarbonate secretion is determined by a gradient limited H+-pump at the contraluminal cell. During secretin stimulation bile acid independent bile secretion is osmotically driven by bile NaHCO3 flux.

Acid-Base Equilibrium↗
PubMed1983

Role of sodium, bicarbonate, and plasma osmolality in biliary secretion.

To examine the effect of changes in biliary sodium and bicarbonate secretion on bile formation, experiments were performed on fasted, pentobarbital-anesthetized pigs. During continuous intravenous secretin infusion (2.7 CU X kg body wt-1 X h-1) sodium secretion was altered by increasing or reducing plasma sodium concentration. Bicarbonate secretion was altered by varying arterial plasma pH. At increased biliary sodium secretion, bile formation was depressed, but changes in bicarbonate secretion were accompanied by parallel alterations in bile formation. Bile acid secretion was increased during elevated plasma sodium concentration, whereas reduced plasma sodium concentration depressed bile acid secretion. To distinguish between the effect of changes in plasma osmolality and sodium concentration, bile formation was also studied during intravenous sucrose infusion at normal plasma sodium concentration. About 50% of the effect on bile formation of changing plasma sodium concentration is solely caused by the changes in plasma osmolality. During secretin stimulation bile formation is mainly determined by bicarbonate. Changes in plasma osmolality affect bile secretion through alterations in the net osmotic force across the hepatocellular membrane. Sodium has an impact on the bile-acid-dependent fraction, whereas bicarbonate is the mediator of the bile-acid-independent fraction of bile secretion.

Animals↗
PubMed1982

Abolished relationship between pancreatic HCO-3 secretion and arterial pH during carbonic anhydrase inhibition.

After acetazolamide administration, CO2 hydration in pancreatic cells would be slow and might become a rate-limiting factor to pancreatic HCO-3 secretion. Correspondingly, pancreatic HCO-3 secretion-normally pH dependent-would become slow and pH-independent. However, acetazolamide would not be expected to interfere with the capacity of the secretory mechanism to generate a proton potential gradient between pancreatic cells and interstitial fluid. These predictions were examined in 5 anesthetized, secretion infused (2.7 C. U./kg b.wt. h-1) pigs. Pancreatic juice was collected from a catheter in the pancreatic duct. Arterial pH was varied through i.v. HCl and NaHCO3 infusions and CO2 addition to inspired air. Before acetazolamide, HCO-3 secretion varied with plasma pH and averaged 298 +/- 30 mumol/min at control arterial pH. Acetazolamide (150 mg/kg, i.v.) reduced HCO3 secretion to 84 +/- 12 mumol/min and rendered secretion independent of arterial pH between pH 7.6 and pH 7.0. It is concluded that acetazolamide imposes a pH-independent transport maximum on pancreatic HCO-3 secretion, but does not reduce the capacity of the secretory mechanism to sustain a proton potential gradient between cells and interstitial fluid.

Acetazolamide↗
PubMed1982

Effect of intravenous infusion of hypertonic glucose solutions on pancreatic HCO3(-) secretion.

To examine why intravenous infusion of hypertonic non-electrolyte solutions inhibit pancreatic HCO3(-) secretion, the relationship between pancreatic HCO3(-) secretion and plasma pH was examined before and following intravenous infusion of hypertonic glucose to 5 anesthetized, secretin infused (2.7 C.U./kg b.wt.h-1) pigs. Hyperglycemia (plasma glucose 103 +/- 6 mmol/l) did not significantly change plasma pH, Na+, K+, Cl- and HCO3(-) concentrations. Hyperglycemia reduced pancreatic water flux by 48 +/- 5% and raised pancreatic juice HCO3(-) concentration by 43 +/- 4 mmol/l. Concurrently, HCO3(-) secretion fell by 34 +/- 5%. Acidosis, produced through intravenous HCl infusion and CO2 addition to inspired air, reduced HCO3(-) secretion by 40 +/- 6 mumol/min and 30 +/- 5 mumol/min per 0.1 pH unit reduction in plasma pH before and during hyperglycemia, respectively, and abolished HCO3(-) secretion at an estimated plasma pH of 6.51 +/- 0.06 before and a pH of 6.63 +/- 0.05 during hyperglycemia. We conclude that hypertonic glucose infusions inhibit pancreatic water flux and cause an increase in pancreatic juice HCO3(-) concentration which may inhibit HCO3(-) secretion through an effect on acid-base balance in secretory cells.

Acid-Base Equilibrium↗
PubMed1981

Mechanism of osmotic diuresis.

Mannitol might inhibit paracellular reabsorption of water and sodium chloride in the proximal tubules by reducing the osmotic driving force. We examined this hypothesis in anesthetized dogs. Bicarbonate reabsorption was kept constant by sodium bicarbonate infusion, and transcellular sodium chloride reabsorption was inhibited by ethacrynic acid. The glomerular filtration rate (GFR) was varied by altering renal perfusion pressure. Mannitol infusion reduced sodium chloride reabsorption from 62 +/- 5% to 33 +/- 5% of the filtered load. The calculated increase in reabsorbate osmolality, averaging 82 +/- 6 mOsm/kg H2O, was due to sodium bicarbonate and equalled the increase in plasma osmolality. Mannitol concentration averaged 81 +/- 7 mM in plasma and 101 +/- 12 mM in urine. A linear relationship between reabsorption and GFR (glomerulo-tubular balance) was maintained over the same range of GFR before and after mannitol infusion. Mannitol infusion reduced sodium chloride reabsorption from 2.6 to 1.4 moles for each mole of sodium bicarbonate reabsorbed. During mannitol infusion, acetazolamide inhibited sodium bicarbonate reabsorption as in control experiments, but reduced sodium chloride reabsorption less. We conclude that reduced water reabsorption increases sodium bicarbonate concentration in the paracellular fluid as much as mannitol concentration is raised in the plasma and glomerular filtrate. Along the proximal tubules, net osmotic force is progressively reduced as mannitol concentration rises, accounting for reduced water and sodium chloride reabsorption.

Acetazolamide↗
PubMed1981

Plasma Na+-iron concentration or pH as regulator of pancreatic HCO-3 secretion.

Pancreatic HCO-3 secretion is caused by proton flux from pancreatic cells to interstitial fluid which, hypothetically, may be derived by a Na-pump or a proton pump. A Na-pump would reabsorb protons from pancreatic duct in proportion with plasma Na+ concentration (PNa+). A proton pump would cause passive HCO-3 flux into pancreatic ducts that would vary with pancreatic jice HCO-3 concentration (CHCO-3). Because pancreatic ducts are water-permeable, CHCO-3 varies with plasma osmolarity. This phenomenon allows testing of the two hypotheses. Intravenous infusion of hypotonic salt solution to 5 anesthetized, secretin infused pigs (2.7 C.U./kg b. wt. H-1) lowered PNa+ by 20 +/- 2 mmol/l and CHCO-3 by 20 +/- 4 mmol/l and increased pancreatic HCO-3 secretion by 71 +/- 5 mumol/min. Intravenous infusion of hypertonic salt solutions to 5 other pigs raised PNa+ by 52 +/- 3 mmol/l and CHCO-3 by 54 +/- 3 mmol/l and reduced HCO-3 secretion by 86 +/0 26 mumol/min. Isotonic glucose infusion lowered PNa+ by 27 +/- 2 mmol/l and did not change CHCO-3 nor HCO-3 secretion rate in 5 pigs. These findings comply with the proton pump hypothesis and are at variance with the Na-pump hypothesis of pancreatic HCO-3 secretion.

Animals↗
PubMed1980

Relationship between plasma pH and pancreatic HCO3- secretion at different intravenous secretin infusion rates.

The relationship between pancreatic HCO3- secretion and plasma pH during acute systemic acid-base changes was investigated in 6 anesthetized, artificially ventilated pigs (20-25 kg) at 2 different, i.v. secretion infusion rates. At 0.45 C.U./kg b. wt. h-1 secretin infusion and plasma pH 7.40 +/- 0.01 pancreatic HCO3- secretion averaged 61+/- 12 mumol/min. Stepwise lowering of plasma pH through i.v. infusion of HCl and CO2 administration to inspired air proportionately reduced secretion rate; estimated zero HCO3- secretion occurring at plasma pH 7.01. Subsequent i.v. secretin infusion at 2.70 C.U./kg b. wt. h-1 increased HCO3- secretion to 249 +/- 42 mumol/min at plasma pH 7.33 + 0.04; stepwise lowering of plasma pH proportionately reduced HCO3- secretion to estimated zero at plasma pH 6.71. A reduction of plasma pH by 0.1 pH unit reduced HCO3- secretion during low and high rate of i.v. secretin infusion by 18 +/- 3 mumol/min and 35 +/- 8 mumol/min, respectively. Secretin infusion rate did not affect pancreatic chloride excretion. These findings support the view that secretin increases HCO3- secretion, and hence proton transport to the interstitial fluid, by augmenting the proton motive force developed by HCO3- secreting cells.

Animals↗
PubMed1979

Effect of plasma H+-ion concentration on pancreatic HCO-3 secretion.

The relationship between the rate of pancreatic HCO-3 secretion and plasma H+-ion concentration was investigated in 15 pentothal anesthetized, secretin infused pigs (1.8 C.U./kg b.w. h-1, intravenously) during acute metabolic and respiratory acid-base disturbances. Pancreatic HCO-3 secretion increasd to 196 +/- 10% of control during alkalosis and fell to 41 +/- 4% of control during acidosis. Partial metabolic compensation of respiratory acidosis restored HCO-3 secretion to 87 +/- 6% of control. A proportional relationship was found between HCO-3 secretion and plasma pH. Different, proportional relationships were found between HCO-3 secretion and plasma HCO-3 concentration during metabolic and respiratory acid-base changes. HCO-3 secretion was independent of H+-ion concentration in pancreatic juice. Plasma H+-ion concentration, therefore, seems to determine the rate of pancreatic HCO-3 secretion. This finding supports the hypothesis that a proton pump is responsible for pancreatic HCO-3 secretion.

Acid-Base Equilibrium↗
PubMed1979

Coupling of NaHCO3 and NaCl reabsorption in dog kidneys during changes in plasma PCO2.

To study the relationship between proximal tubular reabsorption of bicarbonate, sodium, and chloride, the effects of changes in plasma PCO2 were examined in anesthetized dogs. Distal tubular reabsorption was inhibited by ethacrynic acid; plasma bicarbonate concentration was kept constant at 33.4 +/- 0.3 mM; glomerular filtration rate (GFR) was varied over a wide range to examine glomerulotubular balance (constant fractional reabsorption). Hypercapnia (PCO2, 112.0 +/- 2.5 mmHg) increased bicarbonate reabsorption by about 30%, and hypocapnia (PCO2, 19.8 +/- 0.6 mmHg) decreased reabsorption of bicarbonate by more than 50% and altered reabsorption of sodium, chloride, and bicarbonate in the molar ratios 2.7:1.6:1, respectively. During hypercapnia the range of glomerulotubular balance was extended to a GFR 125% of control. During hypocapnia glomerulotubular balance was present only at GFR below 50% of control; reabsorption of bicarbonate sodium, and chloride was constant at GFR exceeding 50% of control. During metabolic acidosis hypercapnia had no significant effect on reabsorption of bicarbonate, sodium, and chloride. These observations support the hypothesis that bicarbonate reabsorption is the main driving force for osmotic reabsorption of water and NaCl in the proximal tubules.

Acidosis↗
PubMed1979

Skin necrosis between parallel abdominal incisions.

Four cases of skin necrosis between vertical abdominal incisions are presented. Even though many years may elapse between the abdominal operations, necrosis of the skin as well as of the underlying fascia may develop between new and old vertical incisions parallel with each other. Such necrosis probably takes place particularly in patients with impaired peripheral circulation.

Abdominal Muscles↗
PubMed1976

Effect of acetazolamide on glomerular balance and renal metabolic rate.

Glomerulotubular balance, defined as proportionality between filtered and reabsorbed sodium during inhibition of sodium reabsorption in the thick ascending limb of Henle's loop (diluting segment), was examined in anaesthetized dogs by gradual reduction of renal arterial pressure. In control experiments, glomerulotubular balance applied over the whole rante of glomerular filtration rate (GFR) examined but was absent after acetazolamide administration (30 mg/kg/body wt) at GFR above 50% of control. Hence, the inhibitory effect of acetazolamide varied with GFR. At control GFR, acetazolamide reduced tubular sodium reabsorption by 32 +/- 2% chloride reabsorption by 34 +/- 3%, and bicarbonate reabsorption by 52 +/- 2%; no significant effect was observed at GFR below 50% of control. For each bicarbonate ion, three sodium ions and two chloride ions were inhibited. Measurements of renal oxygen consumption and heat accumulation rates showed that acetazolamide did not reduce renal metabolic rate significantly. It is proposed that energy-requiring hydrogen ion secretion occurs at unchanges rate during variations in GFR but that back leakage of hydrogen ions varies with bicarbonate concentration in tubular fluid. Net secretion of hydrogen ions is associated with bicarbonate transport into the intercellular space and is linked with sodium reabsorption. The concentration difference of bicarbonate salts over the tight junction (zonula occludens), which is much less permeable to bicarbonate than to sodium chloride, provides the osmotic force for reabsorption of water and sodium chloride from the tubular lumen into the intercellular space. Glomerulotubular balance is mediated by variations in filtered amounts of bicarbonate.

Acetazolamide↗
PubMed1975

Renal autoregulation: evidence for the transmural pressure hypothesis.

Autoregulation of glomerular filtration rate (GFR) was examined during uteral orarterial constriction in anesthetized dogs after renal denervation. GFR was sustaineduntil ureteral pressure greater than 80 mmHg, provided renal arterial pressure exceeded 180 mmHg, but fell at ureteral pressure less than 54 mmHg when arterial pressure averaged 127 plus or minus 5 mmHg; renal blood rose as GFR declined. Ethacrynic acid, saline, or mannitol infusion increased tubular pressure without reducing GFR,but during subsequent ureteral constriction GFR fell at uteral pressure less than 40mmHg. During arterial constriction GFR was maintained at lower arterial pressures in hydropenic than in diuretic dogs. Because of thisdifference in the range of autoregulation, saline infusion increased GFR more in hydropenic than in diuretic dogs except at high arterial pressure. This response to reduced plasma oncotic pressure and the constancy of GFR over a wide range of proximal tubular and arterial pressure indicate constancy of thehydrostatic transmural pressure of glomerular capillaries. Afferent arteriolar resistance is, in addition to a regulation by transmural pressure, perhaps controlled by vascular stretch receptors in the glomeruli.

Animals↗