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H Wald

Publications and source records attributed to H Wald.

At least 55 records · Page 3Linked to original sources
PubMed1987

Enhanced glomerular filtration and Na+-K+-ATPase with furosemide administration.

To evaluate the effect of furosemide on kidney function, glomerular filtration rate (GFR), urinary Na excretion (UNaV), Na reabsorption (NAR), and Na+-K+-ATPase in isolated nephron segments were measured in 1) rats treated with furosemide 10 mg X 100 g-1 X 24 h-1 ip for 7 days, and 2) rats receiving an oral Na load for 12 days. In furosemide-treated rats, GFR rose from 0.61 +/- 0.03 (mean +/- SD) to 0.83 +/- 0.06 ml/min (P less than 0.01), UNaV rose from 904 +/- 71 to 1,402 +/- 85 mueq/day (P less than 0.001), and net NAR rose from 87.5 +/- 3.7 to 116.7 +/- 9.0 mueq/min (P less than 0.01). Na+-K+-ATPase remained unchanged in the proximal convoluted tubule (PCT), proximal straight tubule (PST), cortical thick ascending limb of Henle's loop (cTALH), and medullary thick ascending limb of Henle's loop (mTALH), but was increased in the distal convoluted tubule (DCT) and in cortical collecting duct (CCD) from 48.5 +/- 1.2 to 75.3 +/- 0.7 (P less than 0.001) and from 18.6 +/- 0.7 to 27.1 +/- 2.7 (P less than 0.02) X 10(-11) mol X mm-1 X min-1, respectively. In Na-loaded rats GFR rose from 0.61 +/- 0.04 to 0.86 +/- 0.03 ml/min (P less than 0.001), UNaV rose from 1,064 +/- 118 to 18,532 +/- 2,045 mueq/day (P less than 0.001), net NAR from 88.1 +/- 3.0 to 107.8 +/- 3.9 mueq/min and Na-K-ATPase in the mTALH rose from 40.3 +/- 1.4 to 56.2 +/- 2.11 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

24,25(OH)2D3 enhances the calcemic effect of 1,25(OH)2D3 in PTX rats.

The effect of 24,25(OH)2D3 on 1,25(OH)2D3-induced hypercalcemia was studied in parathyroidectomized (PTX) rats for 10 days. Serum (S) and urinary Ca excretion (UCaV) were measured in (a) control rats, (b) rats receiving a daily sc injection of 54 ng 1,25(OH)2D3, (c) rats receiving 24,25(OH)2D3 in the same dose and same manner, and (d) rats receiving 1,25(OH)2D3 + 24,25(OH)2D3. Our results show that (i) 24,25(OH)2D3 alone does not increase SCa2+ in PTX rats, (ii) combined administration of 1,25(OH)2D3 + 24,25(OH)2D3 enhances the hypercalcemic response to 1,25(OH)2D3 without a parallel increase in UCaV, (iii) combined administration of 1,25(OH)2D3 + 24,25(OH)2D3 reduces the rise in urinary excretion of Ca2+ compared with that of rats receiving 1,25(OH)2D3 alone for 10 days, and (iv) these alterations are independent of parathyroid hormone.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

Sodium handling by the Sabra hypertension prone (SBH) and resistant (SBN) rats.

The acute and chronic renal handling of salt was evaluated in age matched Sabra hypertension-prone (SBH) and hypertension-resistant (SBN) rats. Acute oral (4 ml/100 g) and intravenous (3.3 ml/100 g) isotonic saline loading in unanesthetized normotensive animals maintained on normal diet elicited a significantly lesser diuretic and natriuretic response in SBH than in SBN. Intermittent studies in metabolic cages in rats aged 5 to 21 weeks showed that both strains consumed similar amounts of salt but that SBH excreted significantly less urinary sodium than SBN (F = 40, p less than 0.001). Twenty four hour clearance studies showed a similar filtered sodium load in the two strains but a lower total and fractional sodium excretion in SBH, suggesting increased tubular reabsorption. Under conditions of water diuresis, free water clearance was similar in the two strains, suggesting the site for disparate tubular sodium handling to be distal to the thick medullary ascending limb of the loop of Henle. Acute oral saline loading and long term studies in metabolic cages in rats prepared with deoxycorticosterone-acetate (doca) and salt showed no significant differences in sodium excretion between hypertensive SBH and normotensive SBN. These findings indicate disparate renal sodium handling between SBH and SBN rats, already apparent before the onset of hypertension, which dissipates during doca-salt treatment.

Age Factors↗
PubMed1986

Enhanced renal tubular ouabain-sensitive ATPase in streptozotocin diabetes mellitus.

The effect of streptozotocin-induced diabetes mellitus on rat renal ouabain-sensitive ATPase in six distinct nephron segments was studied. Twenty-four hours after administration of streptozotocin, blood glucose increased threefold (P less than 0.001), and glucosuria was evident. Aldosterone levels increased almost twofold (P less than 0.001). Ouabain-sensitive ATPase increased in the proximal segments PC (proximal convoluted tubule) and PS (proximal straight tubule) by 43 and 62%, respectively, (P less than 0.001) and CD (cortical collecting duct) ouabain-sensitive ATPase increased 77% (P less than 0.001). Ouabain-sensitive ATPase in the cortical (CTAL) and medullary (MTAL) thick ascending limbs of Henle's loop and in the DC (distal convoluted tubule) remained unchanged after 24 h of streptozotocin administration. Eight days after streptozotocin administration, when glomerular filtration rate (GFR) was already markedly elevated, ouabain-sensitive ATPase remained increased in the PC, PS, and CD but was significantly less compared with the activity after 24 h (P less than 0.05), whereas in the CTAL and MTAL a marked increase in ouabain-sensitive ATPase occurred by 54% in the CTAL and 65% in the MTAL (P less than 0.001). Aldosterone levels remained elevated compared with control but less than after 24 h. Pretreatment with deoxycorticosterone acetate abolished the increase in ouabain-sensitive ATPase in the CD. These findings show that streptozotocin-induced diabetes mellitus in the rat is associated with a substantial increase in ouabain-sensitive ATPase activity along most of the nephron. This increase in enzyme activity may represent a mechanism of physiological adaptation of the nephron to maintain electrolyte homeostasis in diabetes in face of the increased GFR and osmotic diuresis.

Aldosterone↗
PubMed1986

Resorption of soft tissue calcification: a possible mechanism of hypercalcemia.

In rats with intact parathyroid glands and normal renal function, extraskeletal Ca3(PO4)2 deposits cause an increase in serum Ca2+ concentration from 4.39 +/- 0.07 to 5.24 +/- 0.13 mEq/l (p less than 0.001) and an increase in urinary excretion of calcium. In rats with acute renal failure and secondary hyperparathyroidism, Ca3(PO4)2 deposits potentiate the pre-existing elevation of serum calcium from 4.9 +/- 0.08 to 5.4 +/- 0.13 mEq/1 (p less than 0.01). In parathyroidectomized rats, Ca3(PO4)2 produce a significant increase in serum calcium from 3.39 +/- 0.07 to 4.19 +/- 0.2 mEq/1 (p less than 0.005). Induction of acute renal failure elevated the serum calcium concentration both in intact rats from 4.39 +/- 0.07 to 4.9 +/- 0.08 mEq/1 (p less than 0.01) and in parathyroidectomized rats from 3.39 +/- 0.07 to 3.85 +/- 0.15 mEq/1 (p less than 0.02). In parathyroidectomized rats with acute renal failure, Ca3(PO4)2 deposits cause an increase in serum Ca2+ concentration from 3.85 +/- 0.15 to 4.26 +/- 0.15 mEq/1 (p less than 0.05).

Acute Kidney Injury↗
PubMed1985

Parallel changes in red blood cell and renal Na-K-ATPase activity in adrenal and electrolyte disorders in the rat.

To compare the activity of Na-K-ATPase in the red blood cells (RBCs) and in renal tissue in disorders of Na+ metabolism, the following groups of rats were studied: 1) control, intact rats, 2) adrenalectomized (ADX) rats, 3) intact rats treated with DOCA, 4) ADX DOCA-treated rats, 5) intact salt-loaded rats, 6) ADX salt-loaded rats, 7) intact dexamethasone-treated rats (DEXA), and 8) ADX DEXA-treated rats. After adrenalectomy (group 2) serum Na+ decreased and serum K+ increased. Renal Na-K-ATPase in cortex, medulla and papilla of the control group was 44 +/- 2.7 mumol Pi/mg prot/h, 128.2 +/- 5.9 and 44 +/- 3.2 respectively and in group 2 the enzyme activity was 32.5 +/- 2.0 (P less than 0.005), 81.7 +/- 4.5 (P less than 0.001) and 23.6 +/- 1.9 (P less than 0.001) respectively. RBCs Na-K-ATPase of control animals was 2.82 +/- 0.19 mumol Pi/mg prot/h, while in group 2 the activity was 1.43 +/- 0.24 (P less than 0.001). DOCA treatment of ADX rats (group 4) normalized serum electrolytes and Na-K-ATPase activity in the renal cortex and papilla and in the RBCs. In the renal medulla the correction by DOCA was only partial. Salt loading of ADX rats (group 6) normalized serum electrolytes and Na-K-ATPase activity in the renal medulla and RBCs. Salt loading of normal rats increased RBC Na-K-ATPase to 3.72 +/- 0.36 (P less than 0.02) and medullary Na-K-ATPase to 185.6 +/- 9.8 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1985

Water handling by the sabra hypertension prone (SBH) and resistant (SBN) rats.

The renal handling of water by SBH and SBN rats was evaluated under basal conditions and following various intervention procedures. During 17 weeks of unrestricted water intake, SBH rats drank less water and excreted less urine with a higher osmolality than SBN. The differences in urine volume and osmolality persisted during 2 weeks of paired water intake. Acute water loading elicited comparable dilution of the urine in the two strains. Water deprivation for 48 h resulted in a marked rise in urine osmolality, which tended to be higher in SBN. Administration of exogenous vasopressin in water loaded animals caused a similar rise in urine osmolality. Papillary solute and urea content was higher in SBH than in SBN, but comparable in water loaded animals. The results show that although SBH differ from SBN rats in the handling of water under basal conditions, their renal diluting and concentrating capacity is comparable at extreme conditions. GFR and RBF were equal in both strains. The data suggest that SBH rats have increased renal water reabsorption as compared to SBN, which may be mediated by ADH, PG or other mechanisms. This characteristic may be related to their propensity to develop hypertension.

Animals↗
PubMed1985

The effect of acute saline volume expansion on renal Na-K-ATPase.

To examine the role of Na-K-ATPase in the natriuresis that occurs after acute extracellular volume expansion, we performed acute clearance experiments and in vitro analysis of renal microsomal ATPase activity in rats receiving intravenous 0.9% sodium chloride (0.1 ml/100 g bw/min). Despite increased absolute reabsorption of filtered sodium (196 +/- 8.1 vs. 165 +/- 11.4 uEq/min, p less than 0.05), renal medullary microsomal Na-K-ATPase activity was decreased from 134 +/- 5.9 to 110 +/- 6.3 pmol Pi/mg protein/hour (p less than 0.02). No changes occurred in cortical or papillary regions and Mg-ATPase was unaffected. Similar results were obtained after adding 4 mEq/l potassium chloride to the infusion to prevent any fall in serum K+. These data suggest that a considerable percentage of sodium reabsorption is suppressed in acutely volume expanded animals and it is proposed that this is mediated by inhibition of medullary Na-K-ATPase.

Animals↗
PubMed1985

The effect of acutely reduced plasma osmolality on acute renal failure in rats.

The present study was designed to evaluate the effect of acute fall in plasma osmolality in three models of acute tubular necrosis in rats: (a) glycerol, (b) arterial clamping and (c) mercuric chloride. Plasma osmolality was reduced by a water loading during a mild anaesthesia from 305 +/- 7 to 270 +/- 12 mosmol/kg of water (P less than 0.01). In the ischaemic models of acute tubular necrosis (glycerol and arterial clamping), during the first 24 h in rats with reduced plasma osmolality, the respective creatinine clearance rates (CCR), 0.04 +/- 0.02 and 0.06 +/- 0.04 ml/min, were strikingly lower than those in rats with normal osmolality, 0.21 +/- 0.03 and 0.26 +/- 0.06 ml/min (P less than 0.001) respectively. The control CCR were 0.65 +/- 0.07 and 0.62 +/- 0.07 ml/min respectively. During the second day after induction of ischaemic (glycerol and arterial clamping) acute tubular necrosis, rats with reduced plasma osmolality exhibited a similar worsening in CCR as on the first day, when compared with that in rats with normal osmolality. In rats with acute tubular necrosis induced with mercuric chloride reduction in plasma osmolality did not aggravate the severity of renal failure. These results show that acute fall in plasma osmolality worsens the renal failure in the ischaemic but not in the nephrotoxic models of acute tubular necrosis.

Acute Kidney Injury↗
PubMed1985

Na-K-ATPase in isolated rabbit tubules after unilateral nephrectomy and Na+ loading.

Na-K-ATPase activity was studied in tubule segments from the cortex and medulla of rabbit kidneys under normal conditions, after unilateral nephrectomy, and after chronic salt loading. After unilateral nephrectomy kidney weight increased by 37% and Na-K-ATPase activity rose significantly in all nephron segments by 36-200% (P less than 0.01). Oral salt loading for 2 wk with 0.5% NaCl caused an increase in GFR and in absolute sodium excretion as well as reabsorption; plasma aldosterone decreased by 44% (P less than 0.005). In the proximal segments (PCT, CPST, OMPST, and TDL) there were no marked changes in Na-K-ATPase activity, whereas along the whole length of the ascending limb of Henle's loop (iMTAL, MTAL, and CTAL) there was a significant rise in the enzymatic activity of 30-200% (P less than 0.02). In the distal segments (DCT, CCD, and OMCD) there was a marked decrease of 50-60% (P less than 0.005) in Na-K-ATPase activity after the salt loading. We conclude that unilateral nephrectomy caused a general increase in Na-K-ATPase activity along the whole length of the nephron, and salt loading caused a selective increase in enzyme activity along the ascending limb of Henle's loop and decrease in the distal segments.

Adenosine Triphosphatases↗
PubMed1985

24,25(OH)2D3 enhances the calcemic effect of 1,25(OH)2D3.

The effect of 24,25(OH)2D3 on 1,25(OH)2D3-induced hypercalcemia was studied in normal rats. Serum (S) levels and urinary excretion of Ca2+ (UCaV) were measured in (a) control rats, (b) rats receiving a daily sc injection of 54 ng 1,25(OH)2D3, (c) rats receiving 24,25(OH)2D3 in the same dose and same manner, and (d) rats receiving 1,25(OH)2D3 + 24,25(OH)2D3. The animals were housed in metabolic cages and 24-hr urine specimens were collected. After 24 hr SCa2+ increased similarly with 1,25(OH)2D3 and with 1,25(OH)2D3 + 24,25(OH)2D3, while 24,25(OH)2D3 alone did not change SCa2+. UCaV after 24 hr increased significantly less (P less than 0.025) with 1,25(OH)2D3 + 24,25(OH)2D3 than with 1,25(OH)2D3 alone. After 5 days of 1,25(OH)2D3, SCa2+ rose from 5.1 +/- 0.15 to 6.29 +/- 0.08 whereas 1,25(OH)2D3 + 24,25(OH)2D3 effected a greater increase in SCa2+ up to 6.63 +/- 0.09 (P less than 0.01). 24,25(OH)2D3 alone did not change SCa2+. UCaV after 5 days of treatment rose similarly with 1,25(OH)2D3 and with 1,25(OH)2D3 + 24,25(OH)2D3. After 10 days of 1,25(OH)2D3 SCa2+ was 6.17 +/- 0.15 meq/liter while with the combination SCa2+ rose to 6.74 +/- 0.2 (P less than 0.025). 24,25(OH)2D3 alone did not change SCa2+. These results show that (a) 24,25(OH)2D3 alone does not alter SCa2+ in normal rats, (b) combined administration of 1,25(OH)2D3 + 24,25(OH)2D3 enhances the hypercalcemic response to 1,25(OH)2D3 without a parallel increase in UCaV, and (c) it is suggested that the effect of 24,25(OH)2D3 on serum Ca2+ level, at least partly, may result from its hypocalciuric effect.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

The effect of streptozotocin-induced diabetes mellitus on urinary excretion of sodium and renal Na+-K+-ATPase activity.

Renal sodium handling and microsomal Na+-K+-ATPase activity in kidney cortex, medulla and papilla of rats with streptozotocin-induced diabetes mellitus (DM) was studied. During 7 days following the administration of streptozotocin GFR, urinary excretion, filtered load and tubular reabsorption of Na+ averaged (mean +/- SE) 1.18 +/- 0.016 ml/min, 1.74 +/- 0.14, 177.3 +/- 8.9 and 175.6 +/- 8.9 mEq/min respectively in experimental rats as compared to corresponding rates of 0.85 +/- 0.04 (P less than 0.001), 0.85 +/- 0.03 (P less than 0.001), 129.8 +/- 5.8 (P less than 0.001) and 129 +/- 5.8 (P less than 0.001) respectively in the control rats. The activity of microsomal Na-K-ATPase in the kidney cortex, medulla and papilla of the control group was (mean +/- SE) 44.7 +/- 1.7, 150 +/- 7.5 and 37.4 +/- 3.6 (mumoles Pi/mg prot/h) respectively. 24 h after DM induction Na-K-ATPase activity in the cortex rose to 59.3 +/- 2.4 (P less than 0.001) and remained high after 3 and 7 days. Medullary Na-K-ATPase activity was unchanged 24 h after streptozotocin administration but was markedly increased to 260 +/- 9 (P less than 0.001) after 3 days and remained high after 7 days. These findings show that streptozotocin-induced DM in rats causes a substantial increase in GFR which is associated with a net increase in filtered and reabsorbed load of Na+ and natriuresis. These alterations are accompanied by a marked increase in Na-K-ATPase activity in renal medulla and in the cortex.

Absorption↗
PubMed1984

Renal refractoriness to PTH in experimental Fanconi syndrome: evidence for intact adenylate cyclase activation.

Previous studies demonstrated renal refractoriness to parathyroid hormone (PTH) in maleate-induced Fanconi syndrome (FS) in rats. In membrane fraction of renal cortex of parathyroidectomized (PTX) rats with FS, PTH increased adenylate cyclase (AC) activity from a basal value of 7.4 +/- 0.6 (mean +/- SE) to 16.8 +/- 3.5 pmoles cAMP/mg prot/min (P less than 0.01), similar stimulation by PTH was observed in control incubation with normal kidneys. In membrane fraction of renal cortex of PTX rats incubated with maleate, PTH increased AC from 5.7 +/- 0.42 to 10.7 +/- 1.08 (P less than 0.01) similar to control incubation without maleate. In cortical slices from PTX rates with FS incubated in vitro, PTH increased cAMP content only from 4.0 +/- 0.21 to 5.27 +/- 0.27 pmole cAMP/mg prot (P less than 0.005), while in slices from the control group the increment by PTH was from 3.9 +/- 0.43 to 10.7 +/- 0.93 pmoles cAMP/mg prot (P less than 0.001). For the difference in the increment between the control and FS group, P less than 0.001. In cortical tissue of PTX rats with FS, PTH injection failed to increase cAMP content: basal value 7.4 +/- 0.8 and with PTH 9.2 +/- 0.8 pmole cAMP/mg prot (P NS), as compared with controls: basal value 9.5 +/- 0.5 and with PTH 23.8 +/- 1.6 (P less than 0.001). ATP content of cortical slices fell from a control value of 2.3 +/- 0.18 in PTX rats to 1.0 +/- 0.14 nmol/mg prot in PTX rats with FS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Developmental aspects of sugar transport by isolated dog renal cortical tubules.

alpha-Methyl-D-glucoside (AMG) uptake was examined in isolated renal cortical tubules from newborn, 3-month-old, and adult dogs. All three age groups demonstrated active sugar transport. The initial rate of AMG uptake was similar in the 3-month-old and adult tubules which was twice that of the newborn. At steady-state, the adult and newborn tubules had achieved a similar intracellular AMG concentration which was 45% greater than that of the 3-month-old. Determination of the flux constants of these uptake patterns revealed that there was an age-dependent increase in both the net flux and the fractional influx rate constant. However, the 3-month-old had the highest fractional efflux rate constant and the newborn the lowest value with the adult in between. Kinetic analysis of AMG uptake showed a single saturable transport system for each age group. The newborn and adult had similar Km values but the 3-month-old had a value that was 60% higher. The 3-month-old tubules had the highest Vmax and the newborn tubules the lowest with the adult value in between. AMG uptake by tubules from each age group demonstrated a similar pattern of inhibition in a low sodium buffer and by glucose and phlorizin. This indicated that, aside from kinetic changes with maturation, the saturable transport system for AMG is similar in each age group.

Aging↗
PubMed1984

Effect of divalent ions on basal and hormone-activated renal adenylate cyclase/cyclic AMP system.

To elucidate the effect of Ca++ on adenylate cyclase (AC)/cyclic AMP system and its response to parathyroid hormone (PTH), experiments with parathyroidectomized rats' renal cortical tissue were performed in vitro. Increasing Ca++ from 0 to 5 mM reduced basal AC from 5.4 +/- (SE) 0.5 to 2.5 +/- 0.2 pmol cyclic AMP/mg protein/min (p less than 0.001). Raising Mg++ from 5 mM (basal concentration) to 20 mM restored AC to 5.7 +/- 0.55 (p less than 0.001). Adding 1 mM Mn++ to the incubation medium without Ca++ raised basal AC activity from 5.8 +/- 0.4 to 10.8 +/- 1.35 (p less than 0.01) and reversed the Ca++-induced inhibition. NaF-stimulated AC was reduced from 77.8 +/- 5.4 to 41.0 +/- 3.8 by 5 mM Ca++ (p less than 0.001), while adding Mg++ abolished this effect. PTH- and calcitonin-induced increase in AC was relatively resistant to Ca++ inhibition. Increasing Mn++ concentration from 0 to 5 mM (without Mg++) completely abolished PTH-induced increase in AC. The apparent Km of basal AC for Mg++ was 2.4, while in the presence of PTH the Km of AC for Mg++ was reduced to 1.1. The relative resistance of the PTH-induced increase in AC to Ca++ inhibition as opposed to the response of the basal activity to Ca++ may be explained by PTH-increased affinity of AC for Mg++.

Adenylyl Cyclases↗
PubMed1983

Blockade of the renal tubular effects of vitamin D by cycloheximide in the rat.

To further characterize the mechanisms by which 25(OH) vitamin D3 (25(OH)D3) and 1.25(OH)2 vitamin D3 (1,25(OH)2D3) suppress the phosphaturic action of parathyroid hormone (PTH) we have studied the effects of cycloheximide (cyclohex), a protein synthesis inhibitor, on the interaction between PTH and vitamin D metabolites in parathyroidectomized (PTX) rats, both in vivo and in vitro experiments. In clearance studies PTX PTH-infused rats were pretreated with cyclohex 2 h before the administration of vitamin D. In control, PTX PTH-infused rats not pretreated with cyclohex, the administration of 25(OH)D3 and 1,25(OH)2D3 was associated with a fall in fractional excretion of phosphate (CP/CIN) from 0.30 +/- 0.05 to 0.16 +/- 0.02 and from 0.31 +/- 0.05 to 0.13 +/- 0.01 (P less than 0.005) respectively. Cyclohex-pretreated PTX PTH-infused rats failed to respond to both 25(OH)D3 and 1,25(OH)2D3, and CP/CIN, which rose after PTH, remained 0.32 +/- 0.05 and 0.29 +/- 0.03 respectively. In vitro, both 25(OH)D3 and 1,25(OH)2D3 inhibited the PTH-induced activation of adenylate cyclase in the renal isolated membrane fractions. Pretreatment with cyclohex abolished this effect of vitamin D metabolites. These results show that cyclohex blocks the antiphosphaturic effects of both 25(OH)D3 and 1,25(OH)2D3 but does not alter the response to PTH. These findings are consistent with the possibility that the acute renal action of vitamin D depends on de novo synthesis of protein.

Adenylyl Cyclases↗
PubMed1983

Anatomical variations in hiatal and upper gastric areas and their relationship to difficulties experienced in operations for reflux esophagitis.

We have seen a number of patients whose initial operations for reflux esophagitis or hiatal hernia or both have failed. During the course of reoperation, the authors have been impressed that anatomic variation contributed to these failures. Therefore, a formal anatomic study was undertaken in 36 fresh cadavers without hiatal hernias or factors pertinent to operative maneuvers. The data from this study suggest that 1) mobilization of the left lobe of the liver is difficult in 30% of normal specimens; 2) the hiatal crura are very thin in early half of the specimens; 3) a "tethering ligament" (the gastrolienal ligament) between fundus and superior pole of the spleen is present in half of the specimens, but there is ample space (7-8 cm) "above" the highest short gastric artery; 4) the angle of His is highly variable in normal subjects; 5) the bare area of the stomach requires deliberate exposure and division in more than half of the subjects to obtain a wrap without tension; 6) the posterior gastric vessels can be a hazard in such mobilization. Attention to these matters should enhance the safety and success of transabdominal operation for reflux esophagitis.

Esophagitis, Peptic↗