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Biomedical subjects

L L Norling

Publications and source records attributed to L L Norling.

At least 19 recordsLinked to original sources
PubMed1999

Postnatal transient renal insufficiency in the feto-fetal transfusion syndrome.

Twinning and higher-order multiple-gestation pregnancies have become relatively frequent in the current era of assisted reproductive techniques. Vascular interconnections are present in nearly all monochorionic twin placentae, yet hemodynamically significant arteriovenous anastomoses resulting in the feto-fetal transfusion syndrome occur in only 5%-18% of these. When arteriovenous connections through a shared placental cotyledon are present, variable amounts of blood may be transfused from one fetus to the other, and feto-fetal transfusion syndrome may result. While reports of renal failure due to a small non-functioning kidney in the donor infant pre- or postnatally have been published, recoverable renal insufficiency has not been previously delineated in feto-fetal transfusion syndrome. This article describes a case of postnatal transient renal insufficiency in a donor infant from a pair of monozygotic twins.

Acute Kidney Injury↗
PubMed1998

Feeding problems in cystinosis.

Nephropathic cystinosis, a rare autosomal recessive storage disease characterized by intracellular storage of free cystine due to a defect in lysosomal cystine transport, is the most common cause of Fanconi syndrome in childhood. Although manifestations of extrarenal organ involvement during the course of the disease are diverse, the spectrum of gastrointestinal (GI) problems has not yet been examined. In responses to a questionnaire from 70 (35%) of the 200 registered members of the Cystinosis Foundation, we found that GI symptoms are more common, more diverse, and occur at a younger age in patients with cystinosis than previously recognized. Ninety-three percent of interviewed subjects had GI symptoms at initial presentation, and the overall lifetime prevalence of GI problems in this group was 100%. Thirty percent have received gastric/jejunal tube feedings, and 7% required continuous or intermittent total parenteral nutrition. Fifty percent have been formally tested for GI abnormalities, and among these 77% have documented functional abnormalities (reflux/dysmotility, pseudo-obstruction, swallowing dysfunction). Early recognition and aggressive therapy of GI problems in cystinotic patients may ameliorate or prevent the development of disabling symptoms.

Adolescent↗
PubMed1998

Stored renin isoforms in the developing rat kidney.

Fetal rat kidney contains renin in renal microvasculature, whereas adult rat kidney contains renin predominantly in juxtaglomerular cells. It is hypothesized that renin isoforms stored within these renal tissues may differ chemically and functionally. To test this hypothesis, stored renin isoforms in fetal and adult rat kidney were compared by isolating renin from adult and fetal kidney homogenate with pepstatin agarose. Pepstatin-eluted renin isoforms were separated by relative molecular size using one-dimensional polyacrylamide gel electrophoresis (SDS-PAGE), or by isoelectric point (pI) and size using two-dimensional (2D) gel electrophoresis. Isoforms were identified either by silver staining or immunoblotting. One-dimensional polyacrylamide gel electrophoresis of pepstatin-treated kidney homogenates showed a silver-stained band in the range of approximately 45 kDa, which corresponded to a silver-stained spot consistently seen on 2D gels. In fetal kidney homogenate, the approximately 45 kDa band had a pI of 5.3 +/- 0.1, whereas the corresponding band in adult samples had a basic pI of 6.0 +/- 0.05. Angiotensin I generation was measured to assess renin enzymatic activity. There was significantly more inactive renin in fetal kidney homogenate than in adult kidney homogenate (60.2 +/- 22.4 v 9.6 +/- 4.0 ng AI/mg protein/h, P < .05). There was significantly less active renin in fetal kidney homogenate than in adult kidney homogenate (5.4 +/- 0.4 v 36.5 +/- 14.2 ng AI/mg protein/h, P < .05). The average total renin activity in fetal kidney homogenate was significantly higher than in adult kidney homogenate (65.6 +/- 22.3 v 46.0 +/- 15.2, P < .05). These results demonstrate major differences in the physical and enzymatic forms of stored renin found in fetal and adult kidney. It is speculated that these variations in stored renin isoforms play a role in the developmental differential regulation of the intrarenal renin angiotensin system.

Animals↗
PubMed1996

Persistent severe hypertension in an infant with posterior urethral valves.

Severe hypertension, an infrequent problem in pediatrics, usually has a single secondary cause. We report an infant with severe hypertension and left reflux nephropathy, a known cause of secondary hypertension. The severity of hypertension and poor response to pharmacological therapy prompted further investigation, including a renal arteriogram that showed a right segmental renal artery stenosis.

Angiography↗
PubMed1996

Accumulation of acidic renin isoforms in kidneys of cyclosporine-A-treated rats.

Chronic cyclosporin A (CsA) treatment results in major hemodynamic changes in the renal microvasculature and in expression of the intrarenal renin angiotensin system. Changes in renin expression in kidneys of CsA-treated rats include the recruitment of immunoreactive renin in afferent arterioles and in the juxtaglomerular apparatus. This study presents evidence that an acidic isoform of renin is increased in kidneys of CsA-treated rats. Immunoblots of rat kidney homogenate separated by polyacrylamide-gel electrophoresis and also by isoelectric focusing demonstrate the presence of an acidic isoform (pl 5.5 and estimated molecular weight of approximately 32 to 36 kd) seen in increased amounts in kidney homogenate from CsA-treated rats. Silver-stained two-dimensional gels of renin separated from kidney homogenate with pepstatin agarose confirm the presence of an acidic renin isoform in CsA-treated rats. In rats that received CsA for varied intervals of 1, 3, 5, and 8 wk, this acidic isoform is shown to significantly accumulate relative to duration of treatment with CsA when immunoreactive bands are analyzed by densitometric scanning (r2 = 0.90, P < 0.001). Renin enzymatic activity also increased in kidney homogenate of CsA-treated rats relative to duration of treatment with CsA (r2 = 0.486, P < 0.001). Prorenin in these same samples was significantly decreased compared with controls. The acidic renin isoform identified in kidney homogenate of CsA-treated rats may be involved in the vascular changes that are seen in this model.

Acids↗
PubMed1996

Abnormal glomerular response to atrial natriuretic peptide in rats with aortocaval fistulas.

Heart failure is characterized by a blunted natriuretic and diuretic response to atrial natriuretic peptide (ANP). To investigate this, a rat model of compensated high-output heart failure was used to determine whether glomerular response to ANP differs in animals with high cardiac output compared with control animals. An aortocaval (AC) fistula was made below the level of the renal arteries in male Sprague-Dawley rats. At 6 wk, one group of AC fistula (N = 6) and control rats (N = 6) was injected with radiolabeled microspheres for determination of hemodynamic parameters, including cardiac output, renal blood flow, and vascular resistance. Rats with AC fistulas had significant changes in cardiac output (218 +/- 17 versus 57 +/- 11 mL/min, P < or = 0.0001), renal blood flow (3.4 +/-0.7 versus 8.4 +/- 1.9 mL/min Left, P < or = 0.05; 3.0 +/- 0.4 versus 7.2 +/- 1.9 mL/min Right, P < or = 0.05), and total vascular resistance (0.6 +/- 0.1 versus 2.7 +/- 0.4 mm Hg/mL per min, P < 0.001) compared with control animals, respectively. In another group of animals, after 6 wk, glomeruli were isolated from kidneys. Extracellular (EC) and intracellular (IC) cGMP was measured as an indication of glomerular response to ANP. Early glomerular response to ANP (10(-8)mol/L) showed a similar acute 13- to 18-fold rise in IC cGMP after 30 sec exposure to ANP (P < or = 0.0001 versus no ANP; N = 4 AC fistula rats and N = 4 control rats). During 1-h incubations with ANP, glomerular response was characterized by a five- to sevenfold increase in EC cGMP. However, glomeruli of AC fistula rats produced significantly less EC cGMP than did those of control animals (21.3 +/- 2.5 versus 44 +/- 4.9 fMol cGMP/2000 glomeruli, P < = 0.005; N = 5 AC fistula rats and N = 5 control rats, respectively). Probenecid-sensitive transport of EC cGMP between AC fistula and control rats (86% decrease versus 82% decrease) was similar. However, glomeruli from AC fistula animals had significantly less phosphodiesterase activity compared with control animals (3.6 +/- 0.4 versus 5.4 +/- 0.7 nMol cGMP/mg protein per min, P < or = 0.01; N = 4 AC fistula rats and N = 5 control rats, respectively). It is speculated that reduced glomerular generation of cGMP in response to ANP contributes to sodium retention in heart failure, but may be compensated for in part by decreased phosphodiesterase-mediated hydrolysis of cGMP.

Animals↗
PubMed1995

Unilateral ureteral obstruction increases glomerular soluble guanylyl cyclase activity.

RBF and GFR are decreased in kidneys after ipsilateral unilateral ureteral obstruction (UUO) for 24 h. Despite net vasoconstriction, vasodilatory mechanisms respond to counterbalance the vasoconstriction: the inhibition of nitric oxide synthase activity is associated with a greater reduction in RBF with ipsilateral UUO. To determine whether the stimulation of soluble guanylyl cyclase differs between glomeruli from obstructed kidneys and normal kidneys, cGMP was measured after stimulation by 10(-3) M sodium nitroprusside (SNP) in glomeruli isolated from the kidneys of Sprague-Dawley rats after 24 h of UUO or sham operation. The generation of intracellular and extracellular (EC) cGMP (femtomoles of cGMP/100 glomeruli/per hour) was measured by RIA. After incubation with SNP, the EC accumulation of cGMP by UUO glomeruli was significantly greater than that by glomeruli from sham-operated rats (P < 0.05). When glomerular studies were repeated in the presence of the phosphodiesterase inhibitor isobutyl methylxanthine, there was no difference in the EC accumulation of cGMP. The direct measurement of cGMP hydrolysis by phosphodiesterase was significantly less in glomerular homogenate from UUO rats compared with sham-operated rats (P < 0.05). When 10(-5) M losartan, an angiotensin II receptor inhibitor, was included in glomerular incubations, there was a significant decrease in the EC glomerular cGMP response to SNP in UUO glomeruli (P < 0.05). This attenuated response was abolished by the addition of isobutyl methylxanthine. The addition of angiotensin II did not alter the accumulation of cGMP by UUO or sham glomeruli. These studies indicate that decreased phosphodiesterase activity in UUO glomeruli contributes to the enhanced accumulation of EC glomerular cGMP after the stimulation of soluble guanylyl cyclase by SNP. In addition, angiotensin II receptors modulate this response, suggesting a role for soluble guanylyl cyclase in countering angiotensin-mediated vasoconstriction due to UUO.

Angiotensin II↗
PubMed1995

Characterization of a synthetic peptide antibody recognizing rat kidney renin and prorenin.

A fourteen amino acid peptide from the cDNA predicted rat renin amino acid sequence was synthesized and used to produce a polyclonal antibody. The ability of this antibody to recognize rat renin was characterized and compared to that of a previously tested polyclonal anti-rat renin antibody raised against purified rat renin to verify its usefulness as a reagent in renin processing. The anti-renin peptide antibody and anti-rat renin antibody were evaluated for specificity of recognition of rat renin by immunohistochemical staining and immunoblotting. The ability of the anti-renin peptide antibody to inhibit renin enzymatic activity and to immunoprecipitate rat recombinant protein was also tested. Anti-renin peptide antibody and anti-rat renin antibody had identical recognition of rat renin and prorenin in immunohistochemical stains of rat kidney section and immunoblots. However the anti-renin peptide antibody does not inhibit renin enzymatic activity nor does it immunoprecipitate recombinant rat prorenin. We have produced and characterized an antirenin peptide antibody which recognizes denaturated rat renin and prorenin in a way that is identical to that of an antibody raised against native rat renin. The anti-renin peptide antibody does not recognize nondenatured renin because it did not inhibit renin enzymatic activity nor was it able to immunoprecipitate renin or prorenin. The technique of using synthetic peptides to produce antibody recognizing at renin is useful because low yields of native renin purified from rat kidney are generally insufficient for antibody production. This limits the widespread availability of antibodies that recognize rat renin.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Activation of calcium and calmodulin dependent protein kinase II during stimulation of insulin secretion.

Pancreatic islets contain an alloxan sensitive, calcium and calmodulin dependent protein kinase (CaM-PK) which may play an important part in the cellular control of insulin secretion. We have studied this activity in islets and the insulin secreting tumor cell line RINm5f with particular interest in the changes in kinase activity that accompany stimulation of secretion. Initial experiments showed that the CaM-PK activity enriched in microsomal preparations from RIN cells was similar to the islet cell kinase in terms of apparent endogenous substrates, Ca2+ and calmodulin dependence, and inactivation by alloxan. For studies of protein substrate specificity, tumor cell CaM-PK was isolated from other kinase activities and substantially purified by affinity chromatography with calmodulin-agarose. The major protein substrates of CaM-PK (54 kD and 57 kD) co-purified with the kinase activity, representing autophosphorylation of subunits of the enzyme. Exogenous substrates phosphorylated by these preparations included microtubule-associated protein 2, synapsin, and glycogen synthase; this pattern of substrate utilization identified the kinase as the Type II multifunctional kinase which has been extensively characterized in brain. A polyclonal antibody to rat brain CaM-PK II was employed to immunoprecipitate the kinase from RINm5f cells incubated with secretagogues to measure the effect of stimulation of secretion on autophosphorylation of CaM-PK (which reflects kinase activation). D-Glyceraldehyde (22 mM) and depolarizing concentrations of potassium increased autophosphorylation and insulin secretion in a parallel fashion. Potassium stimulated autophosphorylation was dose dependent and saturable, and was increased to near maximal levels at times as short as 1 min. These studies demonstrate that pancreatic islets and RINm5f cells contain a Type II CaM-PK which is activated during the secretion process.

Animals↗
PubMed1994

Maturation of A71915-dependent inhibition of atrial natriuretic peptide-stimulated cyclic GMP production in isolated rat glomeruli.

Atrial natriuretic peptide (ANP) regulates glomerular hemodynamics by interaction with biologic receptors (GC-A/ANP) that possess particulate guanylyl cyclase activity. In a previous study we have shown a developmental difference in glomerular response to ANP where preweaned glomeruli produced significantly less extracellular cGMP in response to ANP. Because of the possibility that functional differences in the ANP biologic receptor might exist during development, further characterization of GC-A/ANP receptor response in glomeruli of developing rats was done using a structural analogue of ANP. A71915 (Abbott Laboratories) is a structural analogue of ANP which has been shown to inhibit activation of ANP receptor-associated guanylyl cyclase in vascular smooth muscle cells. The purpose of this study was to investigate the ability of A71915 to inhibit ANP-stimulated cGMP response in isolated glomeruli of adult and preweaned rats. Isolated glomeruli from preweaned or adult rat kidneys were preincubated for 15 min with A71915 (10(-5) M) prior to addition of ANP (up to 10(-6) M). Glomerular response of production of intracellular and extracellular cGMP was measured by radioimmunoassay. Adult glomeruli produced significantly greater amounts of extracellular cGMP compared to preweaned glomeruli for concentrations of ANP > or = 10(-9) M. Infant glomeruli had a significant decrease in the production of ANP-stimulated intracellular cGMP in the presence of A71915 (10(-5) M), whereas extracellular cGMP production was unchanged. In contrast both ANP-stimulated intracellular and extracellular cGMP were significantly decreased by A71915 in adult glomeruli. These results demonstrate the maturation of the glomerular response to ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1993

Effect of CsA on the expression of renin and angiotensin type 1 receptor genes in the rat kidney.

To determine whether Cyclosporine A (CsA) alters the intrarenal expression of the renin and type 1 angiotensin II receptor genes, male adult Sprague-Dawley rats were given 25 mg/kg/day CsA s.c. for three weeks (CsA, N = 20) and were compared to pair-fed vehicle treated rats (Con, N = 20). The intrarenal distribution of renin and its mRNA was assessed by immunocytochemistry and in situ hybridization. In addition, kidney renin and type 1 angiotensin II (AT1) receptor mRNA levels were determined by Northern blot analysis. The percentage of juxtaglomerular apparatuses containing renin was higher in the CsA (84 +/- 5.5%) than in the Con (61 +/- 6.7%) group, (P < 0.05). The length of renin immunostaining along afferent arterioles was higher in the CsA (74 +/- 4.5 microns) than in the Con (37 +/- 5.1 microns) group, (P < 0.05). In contrast, neither renin mRNA levels nor its intrarenal distribution were altered by chronic CsA administration. Kidney AT1 receptor mRNA levels were lower in the CsA group than in the Con group. We conclude that chronic CsA: (1) induces recruitment of renin containing cells along the afferent arteriole, (2) causes no changes in intrarenal renin mRNA levels or distribution, suggesting that post-transcriptional events may be responsible for the persistence and/or uptake of renin by the preglomerular vasculature, (3) promotes a downregulation of AT1 receptor gene in the kidney, suggesting that local angiotensin II may control AT1 receptor gene expression by a negative feedback.

Animals↗
PubMed1993

Leukocytes synthesize angiotensinogen.

To determine whether leukocytes express the angiotensinogen gene, we subjected circulating rat leukocytes and murine bone marrow cells to Northern blot analysis and hybridization with homologous angiotensinogen complementary DNA. Angiotensinogen messenger RNA sequences were detected in circulating adult rat leukocytes, in murine-irradiated and nonirradiated bone marrow stromal cells, and in an adherent stromal cell line (preadipocyte). Western blot analysis of rat leukocyte homogenate showed that rat leukocytes contain two main angiotensinogen isoforms with approximate molecular weights of 46.5 and 53.9 kd. Synthesis and release of angiotensinogen protein by rat leukocytes was confirmed by immunoprecipitation of radiolabeled angiotensinogen from cell lysate and media of rat leukocytes that were metabolically labeled with 35S-L-methionine. In addition, the angiotensinogen protein present in media of rat leukocytes was enzymatically cleaved by hog renin, resulting in generation of angiotensin I (305 +/- 47 pg angiotensin I per milliliter of media per hour). We conclude that circulating rat leukocytes express the angiotensinogen gene and synthesize and release angiotensinogen with the capability to generate angiotensin. Expression of angiotensinogen by leukocytes may provide a mobile angiotensin-generating system of potential importance in the regulation of local inflammatory responses, tissue injury (i.e., myocardial infarction), and arterial hypertension.

Angiotensin I↗
PubMed1992

Maturation of cGMP response to ANP by isolated glomeruli.

Experiments were done to determine whether there is a maturational increase in production of guanosine 3',5'-cyclic monophosphate (cGMP) by glomeruli or in eggression of cGMP out of glomerular cells. Both preweaned and adult isolated rat glomeruli responded with an acute rise in intracellular cGMP after 0.5-min exposure to 0.1 microM ANP. However, at 4 h extracellular cGMP was significantly greater in ANP-treated adult compared with preweaned glomeruli (P less than 0.005). In the absence of 3-isobutyl-1-methylxanthine (IBMX) intracellular cGMP was significantly higher in preweaned glomeruli (P less than 0.05). Moreover, the specific activity of phosphodiesterases for cGMP hydrolysis was twofold less in preweaned glomerular membranes (P less than 0.004). Finally, probenecid decreased export of adult glomerular cGMP by 60 +/- 4%, whereas preweaned glomerular cGMP export decreased by only 27 +/- 4% (P less than 0.05). In conclusion, compared with adult, ANP-treated preweaned glomeruli export less cGMP out of glomerular cells, have a higher concentration of intracellular cGMP, and have lower cGMP-specific phosphodiesterase activity, and the organic ion transporter in preweaned glomerular cells exports cGMP less effectively. The limited transport of cGMP out of preweaned glomeruli may account for the blunted natriuretic and diuretic response following ANP stimulation of young rats.

Aging↗
PubMed1992

Colocalization and release of angiotensin and renin in renal cortical cells.

Angiotensin is generated within the kidney, but the precise loci for the formation of angiotensin I (ANG I) and angiotensin II (ANG II) have not been demonstrated. We performed electron microscopy immunocytochemistry in kidney sections of 10-day-old (newborn) and adult Wistar-Kyoto (WKY) rats using specific antibodies to renin, ANG I, ANG II, and angiotensinogen (AO). Renin, ANG I, ANG II, and AO were present in juxtaglomerular (JG) cells. Renin was largely confined to cytoplasmic granules; ANG I and ANG II were colocalized to these granules but also were present in the cytoplasm; AO was distributed throughout the cytoplasm. AO also was present in a renal cortical distribution in proximal tubular cells. Northern blot analysis demonstrated AO mRNA in total kidney and liver but not in renal microvessels. Using the reverse hemolytic plaque assay, we demonstrated release of ANG I and renin from individual renocortical cells of adult WKY rats. Under control conditions, the number of releasing cells was 11 +/- 1 for ANG I and 10 +/- 1 for renin. Addition of rat renin inhibitor (RI) (1 x 10(-5) M), which inhibited renin activity in the medium from 37 to 9 pg ANG I.ml-1.h-1, did not alter ANG I plaque number. Addition of rat AO increased ANG I plaque number to 17 +/- 2 (P less than 0.05). Incubation with both RI and AO prevented the increase in ANG I plaque number obtained with AO alone. Enalapril treatment (7 days; n = 5) increased the number of plaque-forming cells to 22 +/- 2 for ANG I (P less than 0.0005) and to 39 +/- 7 for renin (P less than 0.001). The results suggest an intracellular location for AO and angiotensin and release of renin and ANG I by renal cortical cells and suggest that released angiotensin is produced intracellularly and that secretion of ANG I is augmented by converting enzyme inhibition.

Angiotensin I↗
PubMed1991

Biochemical basis for the specificity of alloxan inactivation of calmodulin-dependent protein kinase II.

The specificity and biochemical basis of inactivation of calmodulin-dependent protein kinase II by alloxan was studied in dispersed rat brain cells and a partially purified kinase preparation from an insulin-secreting tumor-cell line, RINm5f. When mechanically dispersed rat brain cells were incubated with [32P]-phosphate to label endogenous ATP, depolarization with 44 mM KCl produced a significant (P = 0.03) increase in phosphorylation of endogenous synapsin (132 +/- 8% of basal). Pre-treatment of the brain cells with 1.5 mM alloxan reduced depolarization-sensitive synapsin phosphorylation (109 +/- 5%). Phosphopeptide mapping of depolarization-phosphorylated synapsin showed that alloxan pre-treatment reduced phosphorylation specifically at synapsin sites phosphorylated by calmodulin-dependent protein kinase II. The results demonstrate selective inactivation of calmodulin-dependent protein kinase II activity by alloxan in an intact cell system, which may be useful in the study of the Type II kinase in cells and tissues. Using a partially purified kinase preparation from RINm5f cells, alloxan (100 microM) inactivated 76 +/- 1% calmodulin-dependent protein kinase II activity in 5 min at 37 degrees C. Subsequent incubation with dithiothreitol restored most of the activity. 5,5'-Dithiobis (2-nitrobenzoic acid) (I50 = 2.5 microM) also inactivated the kinase. These results suggested that a sulfhydryl group was involved at the inactivation site. Iodoacetamide (1.0 mM) had no inhibitory effect; however, preincubation with iodoacetamide protected the kinase activity from subsequent inactivation by alloxan. Covalent binding of [14C]-alloxan to calmodulin-dependent protein kinase was demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Alloxan↗
PubMed1986

Sodium-lithium countertransport in erythrocytes of children and adolescents with hypertension.

We have investigated the sodium-lithium countertransport system as a screening test for hypertensive disease in children and adolescents using the method of Canessa et al. [New Engl. J. Med. 302: 772-776, 1980]. The sodium-lithium countertransport in erythrocytes was measured in patients, ages 4-18 years, having essential hypertension or secondary hypertension and compared with age-, weight-, sex- and race-matched normotensive controls. Children and adolescents with essential hypertension possessed a significantly higher erythrocyte sodium-lithium countertransport rate than the normotensive control group (0.39 +/- 0.18, n = 28, vs. 0.22 +/- 0.14 mmol Li/l red cells/h, n = 20, respectively; p less than 0.001). Children with secondary hypertension had intermediate values (0.31 +/- 0.15 mmol Li/l red cells/h; n = 17) which did not differ significantly from values of subjects with essential hypertension or normotensive controls. There was no correlation of counter-transport values with age, sex, or body weight in either hypertensive or normotensive groups. However, white normotensive children had significantly higher countertransport levels compared with black normotensives (0.32 +/- 0.14, n = 10, vs. 0.13 +/- 0.07 mmol Li/l red cells/h, n = 10, respectively; p less than 0.005). Similarly, white children and adolescents with essential hypertension had higher mean countertransport measurements than did black hypertensives (0.42 +/- 0.20, n = 21, vs. 0.27 +/- 0.05 mmol Li/l red cells/h, n = 7, respectively) although this difference did not reach statistical significance (p less than 0.1). Although children and adolescents with essential hypertension had a significant elevation of sodium-lithium countertransport when compared to normotensives, the large degree of overlap of countertransport values in these two groups, as well as the intermediate values of children with secondary hypertension, limits the usefulness of the sodium-lithium countertransport as a screening test for essential hypertension in this population. Taking into account the influence of racial differences on the countertransport assay does not sufficiently improve the discriminatory value of the test to render it clinically useful.

Adolescent↗
PubMed1986

Monoject Samplette capillary blood container with serum separator evaluated for collection of specimens for therapeutic drug assays and common clinical-chemical tests.

The Monoject Samplette (Sherwood) capillary serum-separator tube was evaluated for use in pediatric capillary blood collection. When patients' values for eight common clinical-chemical tests and five therapeutic drugs were compared with values from specimens concomitantly collected in plain Caraway tubes, only chloride and total CO2 were significantly different. The chloride differences (range 0-2 mmol/L) were considered to be clinically insignificant. Higher CO2 values in Samplette specimens were apparently ascribable to decreased loss to the atmosphere. Samplette values for therapeutic drugs were higher than corresponding Caraway values, but only the differences for digoxin were judged to be clinically significant. Both recoverable serum and the incidence of hemolysis were lower in Samplette specimens than in Caraway specimens. Storage of serum over the clots (with separator material interposed) in Samplettes for 24 h had no clinically significant effect on results for glucose or potassium. Storage of specimens for as long as 24 h had no effect on theophylline, phenytoin, and gentamicin concentrations, but phenobarbital reproducibly decreased after 24 h. We conclude that the Samplette serum-separator tube is suitable for the collection of capillary blood for many of the chemical tests commonly ordered for pediatric patients.

Adolescent↗