Amylase Excretion Research Articles

Effect of monensin supplementation on growth, feed digestibility and utilization in young calves

ABSTRACTTwo feeding trials were carried out with Israeli Friesian male calves, commencing at an average age of 7 to 10 days, and covering a suckling period of 30 days followed by a further 90 days. A conventional starter, or one that contained cotton hulls, was used. In each experiment one group of 10 animals served as a control and a similar group was monensin-supplemented. No coccidia were found in the animals. In experiments 1 and 2 monensin supplementation was associated with increased daily gains of 10% and 47% during the suckling period and of 6% and 17% during the next 90 days, but only the differences obtained in experiment 2 were significant. In both experiments, dry-matter intake relative to body weight was higher with monensin supplementation in period 1, but reduced in period 2. The effect of monensin on molar proportions of acetic and propionic acids was smaller than that reported by previous authors for older cattle.A separate digestibility trial showed that monensin administered to suckling calves, either with milk replacer or directly into the rumen, improved dry-matter digestibility, increased the excretion of amylase, and tended to reduce that of trypsin and chymotrypsin.

Does renal tubular dysfunction account for the enhanced CAmCCr ratio in acute pancreatitis?

To verify whether renal tubular dysfunction may account for the CAmCCr enhancement in acute pancreatitis (AP), we have measured the renal excretion of amylase, lysozyme, and gamma-glutamyl-transpeptidase (GGTP) in 22 patients with AP and in 8 with acute tubular necrosis. While the CAmCCr ratio was elevated in most patients with AP, the CLysCCr ratio fell within the normal range in 60% of these patients. The subdivision of patients with AP in subgroups with elevated and normal CLysCCr ratios revealed a mean CAmCCr not statistically different. Moreover, no correlation was present in AP between amylase vs. both lysozyme and GGTP clearances. These data suggest that tubular dysfunction does occur in some but not in all the patients with AP and seems not to play a major role in the pathogenesis of the increased CAmCCr ratio in this condition.

The renal handling of amylase in normal man.

The renal glomerular and tubular transport rate of amylase was studied by measuring the urinary excretion of this protein before and during inhibition of tubular protein reabsorption by lysine. The excretion of amylase was compared with the excretion of albumin, beta-2 microglobulin and free light chains of immunoglobulins. This investigation showed that amylase is reabsorbed by the tubular cells, but only to a very modest degree compared with the reabsorption of the other three proteins. In the case of amylase only about 45% of the filtered molecules are reabsorbed, whereas more than 90% of the filtered amount of the other molecules is reabsorbed by the tubular cells. The excretion of amylase rose after lysine injection only by a factor 1.8, whereas excretion rose by a factor 28 for albumin, 1,500 for beta-2 microglobulin, 16 for kappa chains and 8 for lambda chains. Minimal values for tubular reabsorption were found to be 5.5 +/- (SD) 4.3 U/min for amylase, 174.0 +/- 35.7 micrograms/min for albumin, 90.5 +/- 14.4 micrograms/min for beta-2-microglobulin, 70.4 +/- 17.4 micrograms/min for kappa chains and 24.2 +/- 9.2 micrograms/min for lambda chains.

Effect of Glucagon Infusion on the Renal Clearance of Amylase Relative to Creatinine

Recent data seem to support a tubular defect as the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon has been proposed by some to be an important factor in this phenomenon. To examine the role of glucagon as this "tubular dysfunction factor", we investigated the effect of intravenously infused glucagon on the fractional excretion of amylase and the tubular handling of a low molecular weight protein, beta2 microglobulin, in normal, healthy volunteers. At glucagon levels far in excess of those seen in pancreatitis, the clearance ratio of beta2 microglobulin relative to creatinine increased, whereas the clearance ratio of amylase relative to creatinine did not increase above the normal range. The dissociation between beta2 microglobulin clearance and amylase clearance allows one to question the theory that tubular dysfunction is the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon does not appear to be the sole factor responsible for the elevation of renal clearance of amylase relative to creatinine in acute pancreatitis.

Micropuncture Study of Postnatal Functional Maturation of the Rat Parotid

The postnatal function maturation of the rat parotid was investigated using micropuncture and microanalytical techniques. The cationic composition of the luminal fluid at different levels of the duct system, the net transductal fluxes of Na, K, and H2O and the salivary excretion of protein and amylase in immature and mature rats were determined.

Macroamylasaemia after treatment with hydroxyethyl starch.

After infusion of 500 ml of 6% hydroxyethyl starch into fifty-four patients an increase of serum amylase was observed which in fifty-one cases exceeded the upper limit of normal (190 U/l). In most cases serum amylase reached twice the basal value. Renal function influenced the duration of the increase in serum amylase, but not the maximum increase (201+/-15 U/l; mean+/-SEM). In patients with advanced renal failure (glomerular filtration rate (GFR) = 2-10 ml/min) serum amylase was still markedly elevated after 72 h (298+/-24 U/l; mean+/-SEM). In patients with normal renal function (GFR greater than 90 ml/min) serum amylase decreased to 183+/-40 U/l (mean+/-SEM) within 72 h without reaching basal values. After infusion of HES no changes were observed in serum lipase or in amylase or lipase activities in duodenal secretion. Amylase excretion in the urine decreased. The assumption of a macroamylasaemia caused by formation of an HES-amylase complex was confirmed by gel filtration. The elimination from plasma of this high molecular enzyme-substrate complex is slow and causes hyperamylasaemia. In no case was the macroamylasaemia associated with signs or symptoms. An awareness of this causal relationship seems to be important, to avoid the erroneous diagnosis of a pancreatic disease.

Evaluation of experimental canine pancreatitis

The usefulness of serum amylase determinations in evaluating and quantitating experimental canine pancreatitis is controversial. Serum amylase in the dog is normally 20 to 30 times higher than in man. On the other hand, some authors have stated that amylase is not normally excreted in dog urine. To evaluate the use of amylase determinations in experimentally produced canine pancreatitis, the pancreatic duct was ligated in five dogs, and serum and urine amylase measured daily for 9 days. The amylase methods used in this study had bypassed maltase activity, the cause of canine hyperamylasemia, but elevated serum levels were still found preoperatively. The techniques compared consisted of an automated Somogyi saccharogenic process expressed in maltose units percent, and an amyloclastic (Amylochrome) method; neither measured maltase. These methods correlated well; both serum and urine values had a P value at the 0.001 level. Postoperatively, serum amylase rose 30 to 40 times preoperative levels, and amylase appeared within 3 days after serum elevations in these animals. Possibilities for canine hyperamylasemia include a multienzyme complex producing erroneously high amylase values, increased amylase production, and lack of excretion or degradation of amylase. A fourth possibility, that of a macroamylase molecule in dog serum, was disproved by a rapid detection column method which revealed no abnormal amylase. The measurement of amylase clearance corrected by creatinine clearance was valueless because of decreased urine excretion. Whereas C Am/ C Cr percent in man is normally from 1 to 4%, it was found in this study that the canine preoperative average was 0.066%. These results emphasize again the marked differences in the behavior of the canine and human amylase systems, and for this reason, experimental studies of pancreatitis in the dog should be interpreted with caution.

Increased “bile duct-pancreatic fluid” flow in rats pretreated with carbon tetrachloride

Retrograde intrabiliary injection experiments in CCl 4-pretreated (1 ml/kg, ip, 24 hr) rats suggested that the retrogradely injected solution was being diluted in the common bile duct portion of the biliary tree. This dilution was substantiated in subsequent experiments by a double-cannulation technique. To collect hepatic bile, a PE 10 cannula was placed in the proximal portion of the common bile duct near the liver hilus. To collect “bile duct-pancreatic fluid,” the distal portion of the ligated common bile duct was cannulated near the duodenum. CCl 4 pretreatment produced a 40% decrease in hepatic bile flow (57 ± 6 mg/min/kg, control, vs 35 ± 4, CCl 4, mean ± SE) and a 600% increase in bile duct-pancreatic fluid flow (1.6 ± 0.3 mg/min/kg, control, vs 9.5 ± 1.8, CCl 4). The enhanced bile duct-pancreatic fluid flow did not involve a change in the rate of protein and amylase excretion from the pancreas. Also CCl 4 produced a decrease in the secretory pressure of hepatic bile and an increase in that of bile duct-pancreatic fluid. Thus, CCl 4 has the interesting action of increasing bile duct-pancreatic fluid flow at the same time it is decreasing hepatic bile flow.

Urinary kallikrein excretion in normal man. Relationships to sodium intake and sodium-retaining steroids.

The urinary excretion of kallikrein, a renal enzyme that cleaves the potent vasodilator kinin, kallidin, from kininogen, was measured in normal volunteers by three different assays, one of which was a bioassay. When sodium intake was changed from ad libitum or 109 mEq/day to 9 mEq/day, daily kallikrein excretion increased progressively in every subject to a mean maximal value that was 271% of control by day 7; an increase in sodium intake to 259 mEq/day resulted in the return of kallikrein excretion to control values. Urinary excretion of amylase, a protein with a molecular weight similar to that of kallikrein, did not change when sodium intake was changed, but plasma renin activity and aldosterone excretion changed appropriately. In subjects on a constant-sodium (109 mEq/day), constant-potassium (100 mEq/day) diet, fludrocortisone, 0.5 mg/day for 10 days, increased kallikrein excretion to a mean maximal value that was 203% of control. In subjects on a diet containing 9 mEq sodium/day, elevated kallikrein excretion decreased during treatment with spironolactone, 400 mg/day. Rapid administration of water (1 or 2 liters in 30 minutes, orally) or rapid infusion of 2.4 liters of normal saline did not significantly alter urinary kallikrein excretion despite large changes in urine volume or sodium excretion. Thus, kallikrein excretion appears to be directly related to the effective level of circulating sodium-retaining steroid. The findings are consistent with a role for the kallikrein-kinin system in the renal response to sodium-retaining hormones.

Influence of Renal Function on the Urinary Excretion of Amylase

Influence of Renal Function on the Urinary Excretion of Amylase

Influence of renal function on the urinary excretion of amylase. An experimental study in the rat.

Urinary excretion of endogenous amylase was studied during osmotic diuresis in normal rats and in rats with different kinds of induced kidney damage. In normal rats the amylase excretion varied almost proportionally with respect to plasma concentration of amylase and to glomerular filtration rate (GFR), estimated as clearance for polyethylene glycol 1000 (PEG 1000). The ratio between amylase clearance and GFR varied only slightly with body weight and was independent of urine flow in normal rats. Both increased glomerular permeability to proteins in aminonucleoside-nephrosis and tubular dysfunction after sodium maleate treatment augmented the ratio of amylase clearance to GFR. A considerable tubular reabsorption of amylase in normal rats is concluded. In unilateral pyelonephritis or unilateral ischemic kidney damage this ratio remained constant, but when the functional kidney mass was reduced by removal of the intact kidney, it increased considerably, possibly owing to decreased fractional reabsorption of ...

Biliary Amylase Excretion in Rats, Especially in Relation with Plasma Level of the Enzyme

Biliary Amylase Excretion in Rats, Especially in Relation with Plasma Level of the Enzyme

Urinary Amylase Excretion as Measured by Amylochrome Assay

Urinary Amylase Excretion as Measured by Amylochrome Assay

Simulation of macroamylasaemia by salivary-type ('S type') hyperamylasaemia.

Hyperamylasaemia with low or normal urinary amylase excretion in the face of normal renal function has been noted to be indirect evidence for the existence of macroamylasaemia. A more refined indicator is a low ratio of renal amylase clearance to creatinine clearance. This report describes observations made in three patients, each of whom displayed the indirect features suggestive of macroamylasaemia. In none of these patients, however, could a serum macroamylase be demonstrated by chromatography. Ultracentrifugation was also done in one of the patients and likewise failed to disclose a macroamylase in the serum. When the isozyme nature of the serum amylase in each of these patients was examined, there was found to be a marked rise in activity of the salivary-type isoamylase (;S-type amylase'). The pancreatic-type isoamylase (;P-type amylase') was normal in one patient and perhaps slightly above normal in the other two. These data indicate that (1) S-type hyperamylasaemia may exhibit the indirect criteria taken to indicate macroamylasaemia and thereby simulate the latter disorder; and (2) unequivocal identification of macroamylasaemia requires the direct demonstration of the presence in the serum of a macromolecular amylase complex.

The hourly rate of urinary amylase excretion, serum amylase, and serum lipase: Part II Patients with gastrointestinal and pancreatic disorders

The hourly rate of urinary amylase excretion, serum amylase, and serum lipase: Part II Patients with gastrointestinal and pancreatic disorders

The hourly rate of urinary amylase excretion, serum amylase, and serum lipase. I. In control subjects and patients with renal disease.

The rates of urinary amylase excretion/hour and the levels of serum amylase and lipase were measured in 190 normal subjects and patients with no evidence of renal or gastrointestinal disorder. The hourly rate of urinary amylase excretion/hour was found to have an upper limit of normal of 69 IU. The upper limit of normal for the serum amylase was 251 IU/litre and for the serum lipase 1.6 units/ml. Raised levels of serum amylase and lipase with a normal rate of urinary amylase excretion/hour were found in chronic renal failure.

Distribution, turnover, and mechanism of renal excretion of amylase in the baboon.

Pure amylase was isolated from pancreata and parotid glands of the baboon, an animal which has a serum amylase level and renal clearance of amylase (C(Am)) similar to man. After bolus injection, both pancreatic and salivary amylase rapidly disappeared from the serum in a monoexponential fashion with a mean serum half-time of approximately 83 min. Only about 24% of the amylase cleared from the serum appeared in the urine indicating that the majority of amylase was removed from the serum by an extraurinary mechanism. The C(Am) by the kidney was constant over a wide range of serum amylase levels and the ratio of C(Am)/C(In), which averaged 3.0%, was not influenced by mannitol diuresis. This suggests that the renal excretion of amylase results from glomerular filtration without appreciable tubular reabsorption. Pancreatic amylase was consistently cleared more rapidly by the kidney than was the baboon's endogenous amylase while salivary amylase was consistently cleared less rapidly than endogenous amylase. THE FINDINGS IN THIS STUDY PROVIDE INSIGHT INTO SEVERAL OF THE FOLLOWING CLINICALLY OBSERVED PHENOMENA: (a) the short serum half-time of amylase accounts for the transient nature of serum amylase elevations in pancreatitis; (b) the extra-urinary removal of amylase accounts for the maintenance of relatively normal amylase levels in uremia; and (c) the more rapid renal clearance of pancreatic amylase compared to salivary amylase may explain the disproportionate elevation of the urinary amylase excretion rate relative to the serum amylase level in acute pancreatitis.

The study of the mechanism of synthesis and excretion of amylase in pancreas

The study of the mechanism of synthesis and excretion of amylase in pancreas

A CASE OF MACROAMYLASAEMIA

A further case of macroamylasæmia is described. The two known forms of macroamylasæmia are discussed, and a review of clinical findings and ætiology is presented. Macroamylasæmia should be suspected in patients who have a persistently raised serum amylase level, but normal urinary amylase excretion, as surgical exploration is unnecessary in this condition.

Renal excretion of amylase and lipase by dogs.

Serum amylase and lipase determinations have long been a mainstay in the diagnosis of pancreatic disease. Many investigators 1-10 have indicated that the urinary output of amylase may be elevated more consistently in acute pancreatic disease than the serum concentration of either amylase or lipase. These earlier studies have been based on the following three assumptions: (1) that the concentration of both amylase and lipase in the blood is related to the state of function or injury of the pancreas; (2) that the quantity of enzyme excreted in the urine is related to the amount passing into the blood from the pancreas; and (3) that the amount of enzyme inactivated in the urine is either negligible or is a constant fraction of the total quantity of enzyme excreted. The purpose of the current investigation was to establish the relationship, if any, between serum concentration and urinary output of both amylase