Beauty is pain: pediatric burns resulting from hair curling and flat irons.

Ceramic and metal hair straightening and curling irons are common household items which reach up to 450°F in as little as five seconds. Of particular concern is the threat these devices pose to children. Our objective is to characterize and bring attention to this preventable injury in the pediatric population. Retrospective records from a high-volume level I trauma center and regional burn center from 2011-2015 were analyzed. Inclusion criteria were defined as patients <11 years of age, as those presenting with burns above this age were more likely to be utilizing the tools for hair styling. A total of 59 patients were identified with an average age of 2.4 years. The average burn size was 0.30%, with an average 0.24% 2nd degree TBSA. The etiology of the burns included touching a hair iron that was within reach (61%), pulling a hair iron's power cord (15%), stepping/rolling/jumping onto a hair iron left on the ground (17%), and hair irons falling (7%). The majority of households were comprised of unemployed (64%), single (60%) parents. CPS consult was required for 20% of patients. Grafting and excision was necessary for 20% of patients The pediatric population is at risk for accidental burns with household hair irons. These burns typically have a small TBSA, but may require excision and grafting and extended follow-up.

Les lisseurs et fers à friser, en céramique ou en métal, sont des objets courants au domicile. Leur température peut monter à plus de 230°C en quelques secondes. Le risque qu'encourent les enfants est préoccupant. Nous avons explorés ces brûlures afin de déterminer des stratégies de prévention. Nous avons analysé rétrospectivement les données d'un CTB régional, recueillies entre 2011 et 2015. Nous n'avons retenu que les brûlures atteignant les enfants de 11 ans au maximum (59 cas, âge moyen 2,4 ans), les enfants plus âgés étant susceptibles d'utiliser ces instruments à leur propre bénéfice. La surface brûlée était de 0,3 % dont 0,24 % de 2ème degré. La brûlure était consécutive au toucher d'un ustensile atteignable (61%), à la traction sur le cordon d'alimentation (15%), à la marche dessus (17%), à la chute de l'objet (7%). Les familles concernées étaient en majorité monoparentales (60%) sans emploi (64%). Les services de protection de l'enfance ont été sollicités dans 20% des cas. Les enfants sont particulièrement à risque de brûlures lors d'accidents domestiques, pouvant impliquer des fers à friser et des lisseurs. Ces brûlures sont typiquement peu étendues mais peuvent être profondes, nécessiter une greffe et un suivi prolongé.

Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion.

The effect of increased peritubule capillary oncotic pressure on sodium reabsorption by the proximal tubule of the dog was investistigated after extracellular volume expansion (ECVE) with Ringer's solution or during continued hydropenia. Control measurements were made after ECVE or during hydropenia and again during renal arterial infusion with hyperoncotic albumin solution. Absolute reabsorption by the proximal tubule was calculated from fractional reabsorption and single nephron filtration rates as determined by micropuncture. Direct measurements of efferent arteriole protein were used to determine efferent arteriolar oncotic pressure. Albumin infused into the renal artery after ECVE significantly increased efferent oncotic pressure by 17.6 plus or minus 5.3 mm Hg. Fractional and absolute reabsorption by the proximal tubule increased from 20 plus or minus 6 to 37 plus or minus 5% and from 22 plus or minus 6 to 36 plus or minus 7 nl/min, respectively. During hydropenia, the albumin infusion significantly increased efferent oncotic pressure by 15.0 plus or minus 4.4 mm Hg. However, in contrast to the effect seen during ECVE, neither fractional nor absolute reabsorption was changed, delta equals 0.3 plus or minus 1.5% and 3 plus or minus 5 nl/min, respectively. Single nephron filtration rates were not significantly different between the groups and were unchanged by the albumin infusion. Peritubule capillary hydrostatic pressures, measured with a null-servo device, were not changed by the albumin infusion in either group. Renal interstitial hydrostatic pressure, measured from chronically implanted polyethylene capsules, was decreased significantly from 7.2 plus or minus 0.9 to 3.4 plus or minus 0.6 mm Hg in the hydropenic group and from 0.6 plus or minus 0.6 to 4.8 plus or minus 0.7 mm Hg in the Ringer's expanded group. In the hydropenic group, the increase in efferent oncotic pressure was nearly compensated for by changes in interstitial forces so that the calculated net force for capillary uptake was almost unchanged, 17.8 mm Hg before vs. 21.4 mm Hg during the albumin infusion. The increased efferent oncotic pressure in the Ringer's expanded group was not compensated, so that the calculated net force for uptake was increased, 11.9 mm Hg before to 22.2 mm Hg during the albumin infusion. Thus, while the increase in efferent oncotic pressure during albumin infusion was not significantly different between the groups, absolute and fractional reabsorptions were increased only in the animals in which the extracellular volume was expanded. The results suggest that ECVE alters the effect of increased peritubule oncotic pressure on sodium reabsorption by the proximal tubule.

Collecting duct sodium reabsorption in deoxycorticosterone-treated rats.

In vitro studies of isolated, perfused, cortical collecting tubules have demonstrated that prior chronic deoxycorticosterone acetate (DOCA) treatment increases sodium reabsorption in this nephron segment, yet sodium balance in vivo is maintained. To evaluate the effect of chronic DOCA treatment on collecting duct sodium reabsorption in vivo, we compared fractional sodium delivery (FD(Na)%) out of the superficial late distal tubule with the fraction of sodium remaining at the base and the tip of the papillary collecting duct during extracellular fluid volume expansion in untreated, salt-treated, and DOCA-salt-treated rats. In untreated rats, FD(Na)% to the distal tubule was 6.5+/-1.0%, and to the base was 8.7+/-1.6% (Delta2.2+/-0.9%, P < 0.05). FD(Na)% to the tip was 4.9+/-1.1%, significantly less than FD(Na)% to the base (Delta3.7+/-1.1%, P < 0.01). In salt-treated rats, FD(Na)% to the distal tubule was 8.3+/-0.8%, and to the base was 10.4+/-1.1%. FD(Na)% to the tip was 5.9+/-0.6%, significantly less than FD(Na)% to the base (Delta 4.6+/-1.0%, P < 0.005). In DOCA-salt-treated rats, FD(Na)% to the distal tubule was 16.1+/-2.6% and to the base was 9.5+/-1.9% (Delta 6.6+/-1.7%, P < 0.005). FD(Na)% to the tip was 5.9+/-1.2%, also significantly less than FD(Na)% to the base (Delta 3.6+/-1.1%, P < 0.01). We conclude that (a) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than in untreated or salt-treated rats; (b) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than to the base of the papillary collecting duct, suggesting stimulation of sodium reabsorption in the cortical and(or) outer medullary collecting duct; and (c) sodium reabsorption by the papillary collecting duct is unaffected by chronic DOCA-salt treatment in the volume-expanded rat.

Effects of secretin on peritubular capillary physical factors and proximal fluid reabsorption in the rat.

The effects of secretin vasodilation on peritubular capillary Starling forces and absolute proximal reabsorption were examined in the rat. Secretin was infused at 75 mU/kg per min into the aorta above the left renal artery. Efferent plasma flow increased from 125 +/- 28 to 230 +/- 40 nl/min with secretin infusion. Single nephron filtration rate (44 +/- 6 vs. 44 +/- 7 nl/min) and absolute proximal reabsorption (21 +/- 5 vs. 21 +/- 4 nl/min) were not significantly changed. Peritubular capillary and interstitial hydrostatic pressures increased with secretin infusions (from 9 +/- 0.4 to 15 +/- 0.7 mmHg and from 3 +/- 0.2 to 4 +/- 0.2 mmHg, respectively). Both peritubular capillary and interstitial oncotic pressures decreased (from 25 +/- 2 to 20 +/- 2 mmHg and from 10 +/- 1 to 4 +/- 1 mmHg, respectively) during secretin infusion. The net reabsorption pressure for peritubular capillary uptake significantly decreased from 9 +/- 2 to 5 +/- 2 mmHg and the coefficient of reabsorption increased from 3 +/- 1 to 6 +/- 2 nl/min per mmHg. We conclude that although secretin causes a vasodilation and decreases net reabsorption pressure, absolute proximal reabsorption is unchanged. Peritubular capillary uptake is maintained, and since net reabsorption pressure is decreased, the coefficient of reabsorption is increased.

Low-dose angiotensin II increases free isoprostane levels in plasma.

Chronic intravenous infusion of subpressor doses of angiotensin II causes blood pressure to increase progressively over the course of several days. The mechanisms underlying this response, however, are poorly understood. Because high-dose angiotensin II increases oxidative stress, and some compounds that result from the increased oxidative stress (eg, isoprostanes) produce vasoconstriction and antinatriuresis, we tested the hypothesis that a subpressor dose of angiotensin II also increases oxidative stress, as measured by 8-epi-prostaglandin F(2alpha) (isoprostanes), which may contribute to the slow pressor response to angiotensin II. To test this hypothesis, we infused angiotensin II (10 ng/kg per minute for 28 days via an osmotic pump) into 6 conscious normotensive female pigs (30 to 35 kg). We recorded mean arterial pressure continuously with a telemetry system and measured plasma isoprostanes before starting the angiotensin II infusion (baseline) and again after 28 days with an enzyme immunoassay. Angiotensin II infusion significantly increased mean arterial pressure from 121+/-4 to 153+/-7 mm Hg (P<0. 05) without altering total plasma isoprostane levels (180.0+/-24.3 versus 147.0+/-29.2 pg/mL; P=NS). However, the plasma concentrations of free isoprostanes increased significantly, from 38.3+/-5.8 to 54.7+/-10.4 pg/mL (P<0.05). These results suggest that subpressor doses of angiotensin II increase oxidative stress, as implied by the increased concentration of free isoprostanes, which accompany the elevation in mean arterial pressure elevation. Thus, isoprostane-induced vasoconstriction and antinatriuresis may contribute to the hypertension induced by the slow pressor responses of angiotensin II.

Blunted pressure natriuresis in the Brattleboro diabetes insipidus rat.

Antidiuretic hormone is known to stimulate the renal synthesis of prostaglandins. These autacoids, in turn, modulate the pressure natriuresis phenomenon. Accordingly, the present study was done to test the hypothesis that, in the absence of antidiuretic hormone and antidiuretic hormone-dependent prostaglandin synthesis, the pressure natriuresis response is blunted. Experiments were performed on Brattleboro diabetes insipidus rats (n = 7) and Long Evans control rats (n = 14). A change in perfusion pressure in the Long Evans rats from 89.3 +/- 1.0 to 108.7 +/- 1.1 mm Hg (p less than 0.05) was associated with significant increases in the fractional excretion of sodium (1.1 +/- 0.2 to 2.3 +/- 0.3%) and the urinary prostaglandin excretion (32.6 +/- 6.8 to 56.6 +/- 10.0 pg/min). In contrast, a similar change in perfusion pressure in the diabetes insipidus rat from 88.6 +/- 1.4 to 106.2 +/- 1.5 mm Hg (p less than 0.05) resulted in no significant increases in either sodium or prostaglandin excretions. Treatment of a third group of diabetes insipidus rats (n = 9) with 1-desamino-8-D-arginine vasopressin (1 microgram/day) restored the natriuretic response to increases in renal perfusion pressure. Treated diabetes insipidus and Long Evans control rats had comparable natriuretic responses to increases in renal perfusion pressure. Untreated diabetes insipidus rats, on the other hand, had blunted responses. In summary, the pressure natriuresis response in diabetes insipidus rats is blunted compared with Long Evans control rats. We conclude that antidiuretic hormone is necessary for the complete expression of the pressure natriuresis response.

The effects of sequence and type of chemotherapy and radiation therapy on cosmesis and complications after breast conservation therapy.

PURPOSE: Chemotherapy plays an increasingly important role in the treatment of both node-negative and node-positive breast cancer patients, but the optimal sequencing of chemotherapy and radiation therapy is not well established. The purpose of this study is to evaluate the interaction of sequence and type of chemotherapy and hormonal therapy given with radiation therapy on the cosmetic outcome and the incidence of complications of Stage I and II breast cancer patients treated with breast-conserving therapy. METHODS AND MATERIALS: The records of 1053 Stage I and II breast cancer patients treated with curative intent with breast-conserving surgery, axillary dissection, and radiation therapy between 1977-1991 were reviewed. Median follow-up after treatment was 6.7 years. Two hundred fourteen patients received chemotherapy alone, 141 patients received hormonal therapy alone, 86 patients received both, and 612 patients received no adjuvant therapy. Patients who received chemotherapy +/- hormonal therapy were grouped according to sequence of chemotherapy: (a) concurrent = concurrent chemotherapy with radiation therapy followed by chemotherapy; (b) sequential = radiation followed by chemotherapy or chemotherapy followed by radiation; and (c) sandwich = chemotherapy followed by concurrent chemotherapy and radiation followed by chemotherapy. Compared to node negative patients, node-positive patients more commonly received chemotherapy (77 vs. 9%, p < 0.0001) and/or hormonal therapy (40 vs. 14%, p < 0.0001). Among patients who received chemotherapy, the majority (243 patients) received concurrent chemotherapy and radiation therapy with two cycles of cytoxan and 5-fluorouracil (5-FU) administered during radiation followed by six cycles of chemotherapy with cytoxan, 5-fluorouracil and either methotrexate (CMF) or doxorubicin(CAF). For analysis of cosmesis, patients included were relapse free with 3 years minimum follow-up. RESULTS: The use of chemotherapy had an adverse effect on cosmetic outcome compared to no chemotherapy, which was of borderline significance at 3 years (92% excellent or good cosmetic outcome vs. 96% respectively, p = 0.057); however, cosmesis was not different at 5 years (91 vs. 93% respectively, p = 0.67). Cosmesis was not significantly different between patients treated sequentially and those treated concurrently (3 year: 87 vs. 93% respectively, p = 0.33), nor was it different between patients who received CMF vs. CAF (3 year: 92 vs. 93% respectively, p = 0.89). Hormonal therapy did not influence cosmetic outcome (p = 0.78). The incidence of Grade 4 or 5 arm edema (> or = 2 cm difference in arm circumference) was 2% without chemotherapy vs. 8% with chemotherapy (p = 0.00002). However, the incidence of arm edema was not affected by sequencing or type of chemotherapy (all p > or = 0.52). Patients treated sequentially had a 10% incidence of Grade 4 or 5 arm edema vs. 7% in the patients treated concurrently (p = 0.52). The incidence was 7 vs. 9% in patients treated with CMF vs. CAF (p = 0.73). The incidence of clinical pneumonitis and rib fracture was not influenced by use of chemotherapy, sequence of chemotherapy or use of hormonal therapy (all p > or = 0.06). CONCLUSIONS: Chemotherapy can be given concurrently with radiation therapy in the treatment of Stage I and II breast cancer with breast-conserving therapy without seriously compromising cosmetic outcome or incidence of complications compared to patients receiving other sequences of chemotherapy. Hormonal therapy did not affect cosmesis or complications. The chemotherapeutic regimen of cytoxan and 5-FU concurrent with radiation therapy followed by more chemotherapy is one reasonable option for breast conservation therapy in patients requiring chemotherapy.

Management of superficial bladder cancer in a community setting.

Over the past four or five years, the urologist in private practice has gained experience using mitomycin in the treatment of superficial bladder cancers. Indications for use of mitomycin include carcinoma in situ (CIS), more than two or three recurrences on successive cytoscopic examinations of superficial transitional cell carcinomas, the presence of multiple transitional cell carcinomas at the time of initial examination when it was believed that all tumor could not be removed cystoscopically, and prophylaxis. The regimen for mitomycin has changed over time; currently the standard regimen is 40 mg mitomycin in 40 cc sterile water given intravesically once a week for eight weeks followed by routine cystoscopic examinations every three months and maintenance therapy, if indicated, of 40 mg mitomycin once a month. Results following use of this regimen in private practice have been most encouraging. Complications have been minimal. Only 1 patient had to discontinue therapy because of side effects, and 1 patient underwent radical cystectomy for recurrent disease after partial cystectomy and mitomycin therapy. Patients still receiving treatment include 1 patient who had not responded after initial treatment and who is being followed up for possible recurrence. Mitomycin therapy appears to be effective in controlling superficial bladder cancer and, possibly, carcinoma in situ, with minimal side effects and good patient compliance.

Adenosine induced fall in glomerular capillary pressure. Effect of ureteral obstruction and aortic constriction in the Munich-Wistar rat kidney.

The effect of acute ureteral obstruction (UO) and reduction of renal artery pressure (AC) on the adenosine-induced renal vasoconstriction was studied in the Munich-Wistar rat. Infusion of adenosine, 0.05 mumol/min . kg body weight, into the thoracic aorta, was associated with a fall of directly measured glomerular capillary pressure (Pgc) from 45.2 + 1.8 to 32.5 + 1.7 mm Hg, P less than 0.001. Elevation of ureter pressure to 39 + 2 mm Hg abolished the fall of Pgc following adenosine infusion, 51.3 + 1.7 vs. 50.0 + 1.3 mm Hg, NS. Reduction of renal artery pressure to 70 mm Hg by an aortic clamp above the renal arteries also prevented the fall of Pgc due to adenosine, 36.8 + 0.9 vs. 36.4 + 1.8 mm Hg, NS. Administration of indometacin (10 mg/kg i.v.) restored the ability of adenosine to reduce Pgc in UO from 41.5 + 1.1 to 25.9 + 2.6 mm Hg (P less than 0.001) and in AC from 34.0 + 3.4 to 28.2 + 75.7 mm Hg (P less than 0.02). Since previous studied have demonstrated that in UO and AC renal prostaglandin synthesis is enhanced the effects of indometacin suggest that prostaglandins could be antagonistic to the action of adenosine on the kidney. The data show that the renal vasculature becomes insensitive to the vasoconstrictive action of adenosine during elevated ureter pressure and reduced renal artery pressure.

Incidence and onset of critical illness polyneuropathy in patients with septic shock.

BACKGROUND: To estimate the incidence and onset of critical illness polyneuropathy (CIP) in patients in septic shock. METHODS: Prospective, observational study, no interventions, in a general 9-bed ICU of a large teaching hospital. Twenty-five patients consecutively admitted to the ICU for treatment of septic shock were studied. Within 72 h of admission to the ICU a complete neurological examination and electromyografic studies were done. Studies were repeated weekly until discharge of ICU or death or CIP confirmed. RESULTS: Nineteen patients developed CIP (76%), with a majority (80%) within 72 h after onset of septic shock. All twenty-two patients with multi organ dysfunction syndrome (MODS) had CIP. The three patients without MODS did not have CIP (P<0.01). CONCLUSIONS: In a group of patients suffering from septic shock the incidence of CIP is high (76%). The onset is early, within 72 h after onset of septic shock. CIP is an early feature of MODS, developing after septic shock.

Quetiapine in overdosage: a clinical and pharmacokinetic analysis of 14 cases.

Data on quetiapine overdosage are only sparsely available in the literature. This study provides additional data on the pharmacokinetics and clinical effects of intoxication with this atypical antipsychotic drug. The authors performed a retrospective analysis of all quetiapine intoxications reported to and screened by the toxicological laboratory of the Central Hospital Pharmacy The Hague between January 1999 and December 2003. Cases with known suggested amount of intake and medical outcome were included. From the patient's medical record and from the toxicological laboratory findings, patient demographic characteristics (gender, age), details of quetiapine intoxication (estimated time of ingestion, estimated amount of ingestion, and coingested drugs) and clinical parameters were obtained. Severity of intoxication was graded by the Poisoning Severity Score (PSS). Individual pharmacokinetic parameter values were calculated using a one-compartment open model and a Bayesian fitting procedure. Out of a total of 21 intoxications with quetiapine, 14 fulfilled the inclusion criteria. The ingested dose ranged from 1200 to 18,000 mg. The blood concentration ranged from 1.1 to 8.8 mg/L with a lag time of 1 to 26.2 hours between time of ingestion and blood sampling at the emergency ward. The most frequent findings were somnolence and tachycardia. The PSS was minor in 6 patients (43%), moderate in 5 patients (36%), and severe in 3 patients (21%). Severity of intoxication was not associated with a higher amount of quetiapine intake. The authors found no correlation between the serum concentration of quetiapine and the amount ingested. Elimination t(1/2) was not prolonged. It can be concluded that quetiapine intoxications appear to proceed mildly. Tachycardia and somnolence were the main clinical symptoms in our case series. No fatalities occurred. The severity of clinical symptoms was not associated with either a high serum concentration or the suggested amount ingested of quetiapine.

Role of hydrophobic partitioning in substrate selectivity and turnover of the ricinus communis stearoyl acyl carrier protein delta(9) desaturase.

Stearoyl acyl carrier protein Delta(9) desaturase (Delta9D) uses a diiron center to catalyze the NADPH- and O(2)-dependent desaturation of stearoyl acyl carrier protein (ACP) to form oleoyl-ACP. The reaction of recombinant Ricinus communis Delta9D with natural and nonnatural chain length acyl-ACPs was used to examine the coupling of the reconstituted enzyme complex, the specificity for position of double-bond insertion, the kinetic parameters for the desaturation reaction, and the selectivity for acyl chain length. The coupling of NADPH and O(2) consumption and olefin production was found to be maximal for 18:0-ACP, and the loss of coupling observed for the more slowly desaturated acyl-ACPs was attributed to autoxidation of the electron-transfer chain. Analysis of steady-state kinetic parameters for desaturation of acyl-ACPs having various acyl chain lengths revealed that the K(M) values were similar ( approximately 2.5-fold difference) for 15:0-18:0-ACP, while the k(cat) values increased by approximately 26-fold for the same range of acyl chain lengths. A linear increase in log (k(cat)/K(M)) was observed upon lengthening of the acyl chain from 15:0- to 18:0-ACP, while no further increase was observed for 19:0-ACP. The similarity of the k(cat)/K(M) values for 18:0- and 19:0-ACPs and the retained preference for double-bond insertion at the Delta(9) position with 19:0-ACP (>98% desaturation at the Delta(9) position) suggest that the active-site channel past the diiron center can accommodate at least one more methylene group than is found in the natural substrate. The DeltaDeltaG(binding) estimated from the change in k(cat)/K(M) for increasing substrate acyl-chain length was -3 kJ/mol per methylene group, similar to the value of -3.5 kJ/mol estimated for the hydrophobic partition of long-chain fatty acids (C-7 to C-21) from water to heptane [Smith, R. , and Tanford, C. (1973) Proc. Natl. Acad. Sci. U.S.A. 70, 289-293]. Since the K(M) values are overall similar for all acyl-ACPs tested, the progressive increase in hydrophobic binding energy available from increased chain length is apparently utilized to enhance catalytic steps, which thus provides the underlying physical mechanism for acyl chain selectivity observed with Delta9D.

Effect of meclofenamate or ketoconazole on the natriuretic response to increased pressure.

Increases in renal interstitial hydrostatic pressure (RIHP) by direct renal interstitial volume expansion (DRIVE) decrease proximal sodium reabsorption and increase urinary fractional sodium excretion (FENa). This natriuretic response is blunted by inhibition of the cyclooxygenase pathway. However, complicating the interpretation of the effects of cyclooxygenase inhibition on sodium excretion are the following: (1) products of the other pathways of arachidonic acid metabolism, such as the cytochrome P-450 metabolites, may be attenuated when cyclooxygenase activity is reduced; (2) the proximal tubule has a high biosynthetic capacity for cytochrome P-450 metabolites of arachidonic acid. Therefore, the purpose of the present study was to compare blockade of the epoxygenase products of the cytochrome P-450 pathway with ketoconazole to blockade of the cyclooxygenase pathway with meclofenamate on the natriuretic response to increased RIHP during DRIVE. RIHP, fractional excretion of lithium (FELi), FENa and glomerular filtration rate (GFR) were measured before and after DRIVE in control (n = 6), meclofenamate-treated (n = 6), and ketoconazole-treated (n = 5) rats. DRIVE was achieved by infusing 100 microL of 2.5% albumin solution directly into the renal interstitium. In control animals, DRIVE significantly increased RIHP (delta 2.8 +/- 0.6 mm Hg), FELi (delta 13.4% +/- 5.2%), and FENa (delta 1.29% +/- 0.31%). In the ketoconazole-treated group, RIHP (delta 3.9 +/- 0.8 mm Hg), FELi (delta 19.3% +/- 2.0%), and FENa (delta 1.73% +/- 0.43%) also significantly increased. However, the natriuretic response to DRIVE was blunted during cyclooxygenase blockade with meclofenamate when compared with control or ketoconazole-treated animals (FELi (delta 2.5% +/- 1.4%, not significant) and FENa (delta 0.07% +/- 0.18%, not significant), even though the response of RIHP was intact (delta 4.5 +/- 0.4 mm Hg, p < 0.001). These results suggest that the natriuretic response to increased RIHP is dependent on the presence of, but not necessarily the increased synthesis of, products of cyclooxygenase rather than the cytochrome P-450 epoxygenase pathway for arachidonic acid metabolism.

Effect of synthetic atrial natriuretic factor on superficial and deep proximal tubule sodium reabsorption.

The effects of synthetic atrial natriuretic factor (ANF) on sodium reabsorption by deep and superficial proximal tubules were examined in the rat. In response to ANF infusion (4 micrograms/kg/hr), the urinary fractional excretion of sodium increased from 1.21% +/- 0.53% to 3.48% +/- 0.48%, p less than 0.05 (n = 12). Fractional delivery of sodium (FDNa) from the deep proximal tubule was 25.9% +/- 3.7% before and 33.7% +/- 3.4% after ANF infusion. In time control animals, FDNa from deep proximal tubules was 34.3% +/- 3.0% and 28.5% +/- 4.0% respectively (n = 12). The change in FDNa from deep proximal tubules during ANF infusion (increase of 7.8% +/- 3.9%) was significantly different from the change in control animals (decrease of 5.8% +/- 3.1%) (ANF infusion vs control, delta 13.7% +/- 4.9%, p less than 0.05). No significant change was observed in FDNa in the superficial proximal tubule either during ANF infusion or in control animals. In summary, ANF infusion increased urinary fractional sodium excretion; however, fractional sodium reabsorption by the proximal tubule of superficial nephrons was unchanged. In contrast, sodium delivery to the point of micropuncture in the descending limb of Henle's loop of deep nephrons was increased, as compared with controls, suggesting inhibition of sodium reabsorption by proximal tubules of deep nephrons.