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J T Daugirdas

Publications and source records attributed to J T Daugirdas.

At least 55 records · Page 3Linked to original sources
PubMed1993

Second generation logarithmic estimates of single-pool variable volume Kt/V: an analysis of error.

The original formula proposed to estimate variable-volume single-pool (VVSP) Kt/V was Kt/V = -In(R - 0.008 * t - f * UF/W), where in the Kt/V range of 0.7 to 1.3, f = 1.0 (* denotes multiplication). This formula tends to overestimate Kt/V as the Kt/V increases above 1.3. Because higher Kt/V values are now commonly delivered, the validity of both the urea generation term (0.008 * f) and correction for UF/W were explored by solving VVSP equations for simulated hemodialysis situations, with Kt/V ranging from 0.6 to 2.6. The analysis led to the development of a second-generation formula, namely: Kt/V = -In(R - 0.008 * t) + (4-3.5 * R) * UF/W. The first and second generation formulas were then used to estimate the modeled VVSP Kt/V in 500 modeling sessions in which the Kt/V ranged widely from 0.7 to 2.1. An analysis of error showed that this second-generation formula eliminated the overestimation of Kt/V in the high ranges found with the first-generation formula. Also, total error (absolute value percent error + 2 SD) was reduced with the second-generation formula. These results led to the proposal of a new formula that can be used for a very wide range of delivered Kt/V.

Computer Simulation↗
PubMed1992

The vasorelaxant effects of acetate: role of adenosine, glycolysis, lyotropism, and pHi and Cai2+.

The mechanism of acetate vasorelaxation is unknown. In the rat caudal artery, acetate has a vasorelaxant effect and also increases cyclic AMP. Here we evaluate the role of adenosine, of possible glycolysis inhibition by acetate, of the lyotropic properties of acetate and other anions, and of intracellular calcium and pH. Adenosine per se did not relax the caudal artery in the range of 10(-8) to 10(-2) M. Preincubation with adenosine deaminase (ADA, 5.0 U/ml) or with 8-phenyltheophylline (8-PT, 10(-6) to 10(-4) M) increased, rather than blocked the vasorelaxant effect of acetate. Oxypurinol (10(-3) M) or the nucleoside transport inhibitor NBMPR (10(-4) M) had no effect on acetate relaxation. Whereas acetate increased tissue cyclic AMP content, 10(-3) M adenosine or 10(-6) M PIA had no effect. In strips studied under conditions of inhibited glycolysis (no glucose, with 11 mM 2-deoxyglucose, 1.0 mM pyruvate, and 0.5 mM 5-iodoacetate), acetate-induced relaxation, as well as acetate-induced cyclic AMP generation, tended to be reduced but not significantly so. Other anions relaxed vascular strips in relation to their lyotropic number, but only at higher doses, and they did not stimulate cyclic AMP formation. Acetate (10 mM) caused a transient fall in Ca2+i followed by a slight, sustained rise. A concomitant decrease in pHi was seen. DIDS, which blocks the relaxant and cyclic AMP effects of acetate, had no effect on the pHi decrease, but did decrease the rate of pHi recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1991

Vasorelaxant effects of short chain fatty acid salts in rat caudal artery.

Acetate relaxes rat caudal artery and increases tissue adenosine 3',5'-cyclic monophosphate (cAMP) levels. The present study's purpose was to determine whether related ultrashort chain (volatile) fatty acids, propionate (C3), butyrate (C4), and octanoate (C8) would do so as well. It was found that butyrate and propionate had very similar vasorelaxant profiles to acetate; they relaxed caudal artery strips precontracted with KCl, phenylephrine, arginine vasopressin, and prostaglandin F2 alpha. The vasorelaxation was endothelium independent, was not blocked by indomethacin, and was associated with a rise in tissue cAMP levels but not in guanosine 3',5'-cyclic monophosphate (cGMP) levels. The mean effective concentration for butyrate (0.8 mM) was lower than that for acetate (2.0 mM) or propionate (1.9 mM). Propionate-mediated relaxation was blocked by the stilbene inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Vasorelaxant effects of octanoate were also not dependent on endothelium and were not affected by indomethacin. Maximal vasorelaxant effect of octanoate was greater than that of acetate, propionate, or butyrate; vasorelaxant effect of octanoate was only slightly attenuated by DIDS and was associated with only a minimal effect on tissue cAMP levels. Results suggest that vasodilatory effects of acetate generalize to propionate and butyrate, but that vasorelaxant effects of octanoate may be occurring via a separate mechanism.

Animals↗
PubMed1991

Effect of H-8, an isoquinolinesulfonamide inhibitor of cyclic nucleotide-dependent protein kinase, on cAMP- and cGMP-mediated vasorelaxation.

We theorized that H-8, N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide, an inhibitor of cyclic nucleotide-dependent protein kinases, might be a useful probe to assess cyclic nucleotide-dependent relaxation of blood vessels. However, working in the rat caudal artery and aorta, we found that neither cyclic AMP- nor cyclic GMP-mediated relaxations were diminished by even large doses of H-8. For example, in the caudal artery, relaxation of a phenylephrine contraction by 8-bromo-cGMP (10(-5) M) was unaffected by H-8: control, 33 +/- 6.2%; 10 microM H-8, 41 +/- 12%; 30 microM H-8, 30 +/- 16% (p NS). The amount of relaxation by 8-bromo-cAMP (3 x 10(-4) M) was actually increased by H-8: control, 29 +/- 7.6%; 10 microM H-8, 34 +/- 7.4%; 30 microM H-8, 80 +/- 14%. In the rat aorta, H-8 also failed to diminish relaxation induced by 8-bromo-cGMP, or by atriopeptin II or sodium nitroprusside. In both caudal artery and aorta, H-8 of itself caused a dose-dependent suppression of alpha-adrenergic contraction: for example, in the caudal artery, with 10 or 30 microM H-8, peak contraction to phenylephrine was reduced to 70 (SEM) +/- 12% or 52 +/- 7% of control, respectively. The results suggest that the protein kinase inhibitor H-8 is not a useful probe to study cyclic nucleotide-dependent relaxation.

Animals↗
PubMed1990

L-lactate high-efficiency hemodialysis: hemodynamics, blood gas changes, potassium/phosphorus, and symptoms.

Hemodynamic changes were measured during high-efficiency hemodialysis (HEHD) using three dialysis solutions: L-lactate (46 mM), bicarbonate (35 mM + 4 mM acetate), and acetate (39 mM). Cardiac output was determined by changes in thoracic electrical bioimpedance. Although there appeared to be subtle differences in hemodynamic response to L-lactate versus bicarbonate, the blood pressure, cardiac output, and total peripheral resistance were affected less with either of these solutions than with acetate. In particular, neither L-lactate nor bicarbonate HEHD were associated with a change in cardiac output, whereas with acetate HEHD a marked (22%) increase in cardiac output was seen concurrently with a moderate fall in blood pressure and TPR. Both acetate and L-lactate HEHD were associated with hypoxemia, whereas with bicarbonate HEHD the PO2 did not change. With L-lactate HEHD, correction of pH and plasma HCO3 concentrations was delayed but these values were not significantly different from those obtained with bicarbonate HEHD by one hour after dialysis. Potassium removal was comparable with the three dialysis solutions. Phosphorus removal with L-lactate tended to be slightly less than with bicarbonate, but not less than with acetate. Our results suggest that L-lactate (46 mM) dialysis solution may be a suitable alternative to acetate for HEHD, being associated with a hemodynamic profile that is similar to that of bicarbonate and better than that of acetate. Our results further suggest that the hypoxemia associated with the use of acetate dialysis solution is not intrinsic to acetate, but is due either to a low dialysis solution PCO2 level or to accelerated consumption of oxygen during substrate metabolism.

Acetates↗
PubMed1990

Colon-cancer screening in dialysis patients.

The usefulness of colon-cancer screening using stool-guaiac testing has been established in large control populations, but not in dialysis patients. In 72 asymptomatic dialysis patients [51 treated with hemodialysis (HD), and 21 with peritoneal dialysis (PD)] who underwent outpatient stool occult blood testing, the test result was positive in 11 (15%) patients (8 HD and 3 PD). Eight of the 11 were investigated further by colonoscopy and, when deemed necessary by the treating physician, esophagogastroduodenoscopy and/or barium enema were also performed. A site of active bleeding was identified in three of the eight patients (hemorrhoids, telangiectasia, ulcerative colitis). In each of the five other patients, potentially bleeding lesions were identified: colonic polyps (two malignant and two benign) in four patients. Barrett's esophagus in one, diverticulosis in two, and colonic vascular deformities in two. These results were compared with those of a large ongoing fecal occult blood screening program in which the prevalence of positive stool occult blood tests is 5% and in which 42% of the positive patients have colonic neoplasms. Thus, although the baseline incidence of positive guaiac tests may be higher in dialysis patients than in nonuremic controls, our results suggest that stool guaiac testing of dialysis patients may not only be useful in detecting colonic polyps, but may also identify other previously unsuspected causes of gastrointestinal bleeding.

Adult↗
PubMed1990

Asymptomatic, nonketotic, severe hyperglycemia with hyponatremia.

We describe five patients with asymptomatic, nonketotic, severe hyperglycemia (serum glucose concentrations between 45.8 and 92 mmol/L) in the face of renal insufficiency are described. As opposed to most of the previously described patients with hyperglycemic, nonketotic, hyperosmolar coma, our patients were hyponatremic. The lack of symptoms in our patients may be related to the absence of cerebral cellular dehydration. Aggressive treatment of hyperglycemia in such patients is unnecessary. Attention to the serum sodium level as well as to the serum glucose concentration will allow recognition of this clinical entity.

Acute Kidney Injury↗
PubMed1989

The post: pre dialysis plasma urea nitrogen ratio to estimate K.t/V and NPCR: validation.

The ability of empirical formulae to predict K.t/V based on the ratio (R) of the postdialysis (Ct) to predialysis (Co) plasma urea nitrogen levels was tested. In 256 patients, 336 three-point modeling sessions were performed. The K.t/V and NPCR were derived by interative solution of equations for V and G according to the variable volume single-pool model. The modeled K.t/V values were compared to K.t/V predicted from the formula: K.t/V = -ln (R - 0.008.t-UF/W), where R is the Ct/Co ratio, t the session length (h), UF the ultrafiltrate volume (liters) and W the postdialysis weight (kg). Further, the ratio-derived K.t/V was used in conjunction with the Gotch nomogram for 3/week dialysis to estimate NPCR (NPCR-R/N); the latter value was compared to the NPCR from standard 3-point modeling (NPCR-MOD). The two K.t/V values were quite similar, although statistically separable: modeled K.t/V, 0.97 +/- 0.22 (SD), ratio-derived K.t/V 0.96 +/- 0.23, p less than 0.001. The mean percent error was -0.73% +/- 2.5 (range - 11 to + 4.8), and the correlation coefficient was 0.994, slope 1.01, int -0.016. Modifications of the prediction formula which incorporated UF/V instead of UF/W, and/or which weighted the UF/V term according to the expected K.t/V, produced only slight improvement in accuracy. The two values of NPCR were less similar, but still highly correlated: NPCR-MOD, 1.04 +/- 0.26 g/kg/day, NPCR-R/N, 0.94 +/- 0.23, p less than 0.001; mean percent error, - 8.2 +/- 16; r = 0.78, slope = 0.68, int = 0.23.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Urea Nitrogen↗
PubMed1989

L-lactate for high-efficiency hemodialysis: feasibility studies and a randomized comparison with acetate and bicarbonate.

We evaluated the feasibility of using L-lactate as a base for hemodialysis. In one study, acid-base changes using 40 mM L- or DL-lactate were compared. In a second study, acid-base status using various amounts of L-lactate exclusively was studied. The third study compared symptoms and acid-base changes during 9 weeks of high-efficiency dialysis when using L-lactate, acetate, or bicarbonate as base. In the first study, plasma bicarbonate changes were equivalent with 40 mM L-lactate and 40 mM DL-lactate, but overall correction of acidosis appeared to be suboptimal. In the second study, when compared to a bicarbonate control period, correction of acidosis was reduced when using 40 mM L-lactate + 4 mM acetate solution, but increased when using a 46 mM L-lactate + 4 mM acetate solution. In the third study, correction of acidosis was comparable when using 42 mM L-lactate + 4 mM acetate, 39 mM acetate, or 35 mM HCO3 + 4 mM acetate. Whereas 46% +/- 12 (SEM) treatments "failed" because of symptoms when using acetate, the percentages of "failed" treatments were only 7% +/- 4.2 with L-lactate (p less than 0.05) and 11% +/- 4.2 with bicarbonate (p less than 0.05). The results suggest that L-lactate is a suitable dialysis solution base that is capable of correcting chronic uremic acidosis. During high-efficiency dialysis, the incidence of intradialytic symptoms with L-lactate is comparable to that with bicarbonate and less than that with acetate.

Acetates↗
PubMed1989

Predicting need for surgical drainage of pericardial effusion in patients with end-stage renal disease.

The best approach to treatment of pericarditis accompanied by substantial pericardial effusion in end-stage renal disease (ESRD) patients is unknown. In a review of our experience, we found that ESRD patients with moderate-to-large or large (circa 250 mL or larger) pericardial effusions usually failed to improve with intensive dialysis and ultimately required surgical drainage of the effusion. Multivariate analysis revealed that effusion size was by far the most important factor predicting need for surgery. Since early pericardial drainage obviates the risk of sudden tamponade, we recommend that surgery without prior intensive dialysis therapy be considered in such patients.

Drainage↗
PubMed1989

The post: pre-dialysis plasma urea nitrogen ratio to estimate K.t/V and NPCR: mathematical modeling.

The mathematical basis of the relationship between K.t/V and the ratio of the postdialysis (Ct) to predialysis (Co) plasma urea nitrogen levels (Ct/Co = R) is the urea kinetic model. The R vs. K.t/V relationship is modulated by the patient's normalized protein catabolic rate (NPCR), the dialysis session length, and the predialysis plasma urea nitrogen level, due to urea generated during the dialysis session; the latter increases Ct and hence raises R. The relationship between R and K.t/V is also affected by the amount of ultrafiltrate removed during the dialysis session, because convective urea removal, which is a part of K, does not result in a lowering of the (Ct). In stable adult maintenance dialysis patients receiving 3 treatments/week, with an NPCR of less than or equal to 1.1 g/kg/day and zero residual renal function, the target K.t/V is 1.05 and the target R will be about 0.41. In patients who require different K.t/V values, corresponding values of R can be computed. Based on an empiric examination of the urea kinetic equations, several formulas are proposed for estimating K.t/V from R and vice versa, which depend only on the dialysis session length t, the amount of ultrafiltrate UF, and the postdialysis weight W or V; e.g., K.t/V = - ln (R - 0.008.t-UF/W). After K.t/V has been estimated from R, t, UF and W, one can then estimate the NPCR in the residual renal urea clearance (Kru) has also been measured. From the estimated K.t/V, the Kru, and an estimated V, the total urea clearance over time corrected for V ("KT") is computed.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Urea Nitrogen↗
PubMed1988

Depressant effect of acetate in isolated cardiac tissue.

Because acetate may have cardiodepressant properties in vitro, but previous studies have not separated out effects of acetate from possible effects of osmolality, sodium concentration, or calcium complexing, the effects of isosmotic acetate substitution (at a constant calcium concentration) on contractility were studied in isolated rat atrial tissue and in an isolated perfused non-working whole heart preparation. In spontaneously contracting right atrial tissue acetate induced dose dependent inhibition of isometric tension in the clinically important dose range of 4 to 16 mmol.litre-1. Bath acetate concentrations of 4, 16, or 64 mmol.litre-1 reduced peak tension (mean(SEM] to 78(2.7)%, 56(2.5)%, or 61(4.6)% respectively of control values. Because the calcium concentrations of the acetate baths were set equal to that of the control bath, calcium complexing by acetate could not have accounted for acetate's cardiodepressant effect. The inhibitory action was demonstrable with both isosmotic and hyperosmotic acetate solutions. Acetate had no effect on the spontaneous rate of atrial contraction. Inhibition of contractility (+dP/dt) by acetate in the whole heart preparation was also demonstrable at bath acetate concentrations of 8 and 16 mmol.litre-1. The results suggest that acetate has a myocardial depressant effect in vitro at concentrations achievable in the plasma during haemodialysis. The myocardial depressant action is not dependent on calcium complexing or on changes in bath osmolality or sodium concentration.

Acetates↗
PubMed1988

Alkalinization of peritoneal dialysis solutions with sodium hydroxide or sodium bicarbonate.

Peritoneal dialysis solution containing 1.5% dextrose was titrated with either sodium hydroxide or sodium bicarbonate. The titratable acidity was approximately 1.5 mmol/L as determined by sodium hydroxide titration. Generation of carbon dioxide on addition of sodium bicarbonate resulted in a titration curve that was shifted downward and to the right compared with the curve for sodium hydroxide addition. The information presented can be used to guide the amount of base to be added when partial or complete neutralization of peritoneal dialysis solution is desired.

Bicarbonates↗