K. S. Nelson

Renal and hemodynamic effects of intravenous fenoldopam versus nitroprusside in severe hypertension.

The renal and hemodynamic effects of intravenously administered fenoldopam mesylate, a novel dopamine-1 receptor agonist, were compared with those of sodium nitroprusside in 28 patients (18 male; 26 black, two white; average age, 49 +/- 3 years) with an average blood pressure of 219/137 mm Hg, most of whom presented with acute target organ damage. Fenoldopam and nitroprusside lowered blood pressure safely to an average pressure of 176/105 mm Hg; highly significant dose-response relations were found for the 13 patients receiving fenoldopam and the 15 receiving nitroprusside. Volume and sodium, potassium, and creatinine concentrations were measured in freely voided urine specimens both before and during intravenous therapy. In the fenoldopam-treated patients, there were significant increases in urinary flow (92 +/- 21 to 168 +/- 37 ml/hr, p less than 0.003), sodium excretion (227 +/- 73 to 335 +/- 90 mu eq/min, p less than 0.001), and creatinine clearance (70 +/- 11 to 93 +/- 13 ml/hr, p less than 0.003). In the nitroprusside-treated group, however, all these parameters decreased, but not significantly. For direct comparison of the two agents, the increments in urinary flow rate (+76 +/- 20 vs. -16 +/- 15 ml/hr, fenoldopam vs. nitroprusside), sodium excretion (+109 +/- 28 vs. -39 +/- 28 mu eq/min), and creatinine clearance (+23 +/- 6 vs. -11 +/- 7 ml/min) were significantly greater (p less than 0.001 for each) in the fenoldopam-treated group. Significant differences were also obtained when these parameters were calculated as percentage increase over baseline. Fenoldopam and nitroprusside are effective therapies for severe, accelerated, or malignant hypertension, but fenoldopam had additional salutary renal effects in these patients.

Evidence for the decay sigma+ --> pmu+ mu-.

We report the first evidence for the decay Sigma(+)-->pmu(+)mu(-) from data taken by the HyperCP (E871) experiment at Fermilab. Based on three observed events, the branching ratio is B(Sigma(+)-->pmu(+)mu(-))=[8.6(+6.6)(-5.4)(stat)+/-5.5(syst)]x10(-8). The narrow range of dimuon masses may indicate that the decay proceeds via a neutral intermediate state, Sigma(+)-->pP(0),P0-->mu(+)mu(-) with a P0 mass of 214.3+/-0.5 MeV/c(2) and branching ratio B(Sigma(+)-->pP(0),P0-->mu(+)mu(-))=[3.1(+2.4)(-1.9)(stat)+/-1.5(syst)]x10(-8).

Observation of CP violation in K(L) ---> pi+ pi- e+ e- decays

We report the first observation of a manifestly CP violating effect in the K(L)->pi+pi-e+e- decay mode. A large asymmetry was observed in the distribution of these decays in the CP-odd and T-odd angle phi between the decay planes of the e+e- and pi+pi- pairs in the K(L) center of mass system. After acceptance corrections, the overall asymmetry is found to be 13.6+-2.5 (stat) +-1.2 (syst)%. This is the largest CP-violating effect yet observed integrating over the entire phase space of a mode and the first such effect observed in an angular variable.

A determination of the cabibbo-kobayashi-maskawa parameter |VUS| using KL decays

We present a determination of the CKM parameter |Vus| based on new measurements of the six largest KL branching fractions and semileptonic form factors by the KTeV (E832) experiment at Fermilab. We find |Vus| = 0.2252 +- 0.0008(KTeV) +- 0.0021(ext), where the errors are from KTeV measurements and from external sources. We also use the measured branching fractions to determine the CP violation parameter |eta+-| = [2.228 +- 0.005(KTeV) +- 0.009(ext)]E-3.

Effects of selective dopamine-1 receptor activation on intraocular pressure in man

The lack of specific agonists and antagonists has, until recently, precluded investigation of a role for dopamine receptors in the control of intraocular pressure. In the present study, we have examined the effects of fenoldopam, a novel selective dopamine1 (DA1) receptor agonist, on intraocular pressure, in eight healthy human volunteers. Fenoldopam, infused intravenously at 0.5 micrograms kg-1 min-1, increased intraocular pressure from 14.6 +/- 0.9 to 17.6 +/- 1.4 mmHg (P less than 0.05) while a control saline infusion had no effect. Pupil diameter and blood pressure did not change. In the same subjects, i.v. norepinephrine or angiotensin II both increased intraocular pressure--from 13.8 +/- 1.4- to 17.6 +/- 1.4 mmHg and from 13.4 +/- 1.3- to 17.5 +/- 1.7 mmHg respectively (P less than 0.05), and mean arterial pressure by about 20 mmHg. These data suggest that: (1) DA1 receptor activation can modulate intraocular pressure; (2) the intraocular pressure effects of the DA1 receptor agonist, fenoldopam, are independent of changes in systemic blood pressure, in contrast to those of norepinephrine or angiotensin II where intraocular and systemic blood pressures increase in parallel; (3) the ability of a DA1 receptor antagonist to lower intraocular pressure merits investigation.

Observation of the decay K- ---> pi- mu+ mu- and measurements of the branching ratios for K+- ---> pi+- mu+ mu-

Using data collected with the HyperCP (E871) spectrometer during the 1997 fixed-target run at Fermilab, we report the first observation of the decay K--->pi(-)mu(+)mu(-) and new measurements of the branching ratios for K+/--->pi(+/-)mu(+)mu(-). By combining the branching ratios for the decays K+-->pi(+)mu(+)mu(-) and K--->pi(-)mu(+)mu(-), we measure Gamma(K+/--->pi(+/-)mu(+)mu(-))/Gamma(K+/--->all) = (9.8+/-1.0+/-0.5)x10(-8). The CP asymmetry between the rates of the two decay modes is [Gamma(K+-->pi(+)mu(+)mu(-))-Gamma(K--->pi(-)mu(+)mu(-))]/[Gamma(K+-->pi(+)mu(+)mu(-))+Gamma(K--->pi(-)mu(+)mu(-))] = -0.02+/-0.11+/-0.04.

Measurements of K(L) branching fractions and the CP violation parameter |eta+-|

We present new measurements of the six largest branching fractions of the KL using data collected in 1997 by the KTeV experiment (E832) at Fermilab. The results are B(KL -> pi e nu) = 0.4067 +- 0.0011 B(KL -> pi mu nu) = 0.2701 +- 0.0009 B(KL -> pi+ pi- pi0) = 0.1252 +- 0.0007 B(KL -> pi0 pi0 pi0) = 0.1945 +- 0.0018 B(KL -> pi+ pi-) = (1.975 +- 0.012)E-3, and B(KL -> pi0 pi0) = (0.865 +- 0.010)E-3, where statistical and systematic errors have been summed in quadrature. We also determine the CP violation parameter |eta+-| to be (2.228 +- 0.010)E-3. Several of these results are not in good agreement with averages of previous measurements.

A Measurement of the K(L) charge asymmetry

We present a measurement of the charge asymmetry delta(L) in the mode K(L)-->pi(+/-)e(-/+)nu based on 298 x 10(6) analyzed decays. We measure a value of delta(L) = [3322+/-58(stat)+/-47(syst)]x10(-6), in good agreement with previous measurements and 2.4 times more precise than the current best published result. The result is used to place more stringent limits on CPT and DeltaS = DeltaQ violation in the neutral kaon system.

Measurement of the decay K(L) ---> pi0 gamma gamma

We report on a new measurement of the decay KL -> pi0 gamma gamma by the KTeV experiment at Fermilab. We determine the KL -> pi0 gamma gamma branching ratio to be (1.68 +/- 0.07 +/- 0.08)x10**-6. Our data shows the first evidence for a low-mass gamma gamma signal as predicted by recent O(p**6) chiral perturbation calculations that include vector meson exchange contributions. From our data, we extract a value for the effective vector coupling aV = -0.72 +/- 0.05 +/- 0.06.

Search for the decay KL → π0e+e-

We report on a search for the decay Kl -> pi0 e+ e- carried out by the KTeV/E799 experiment at Fermilab. This decay is expected to have a significant CP violating contribution and the measurement of its branching ratio could support the CKM mechanism for CP violation or could point to new physics. Two events were observed in the 1997 data with an expected background of 1.06 +-0.41 events, and we set an upper limit Br(Kl -> pi0 e+ e-) < 5.1 x 10^-10 at the 90% confidence level.