Comparative hepatic in vitro depletion and metabolite formation of major perfluorooctane sulfonate precursors in arctic polar bear, beluga whale, and ringed seal Letcher, Robert J; Shaogang ChuauthorEcotoxicology and Wildlife Health Division, Wildlife and Landscape Science Directorate, Science and Technology Branch, National Wildlife Research Centre, Environment Canada, Carleton University, Ottawa, ON K1A 0H3, Canada; Melissa A. McKinneyauthorEcotoxicology and Wildlife Health Division, Wildlife and Landscape Science Directorate, Science and Technology Branch, National Wildlife Research Centre, Environment Canada, Carleton University, Ottawa, ON K1A 0H3, CanadaDepartment of Chemistry, Carleton University, Ottawa, ON K1S 5B6, Canada ...
2015
Journal Article
A series of 4-coordinate, neutral, approximately square planar (1,3-bis(2$\sp \prime$-pyridylimino)isoindolinato)Ni(II)(phenylcyanamido) complexes (i.e.(PVP)Ni(pcyd)) have been prepared and ...characterized by $\sp1$H NMR, electronic absorption, and infrared spectroscopies and X-ray crytallography. Increasing the $\pi$-donating ability of the phenylcyanamido ligand results in a diamagnetic to paramagnetic change in magnetic properties of the complexes. Tetrahedral distortion from the square plane is demonstrated by a crystal structure of (PVP)Ni(2-Clpcyd) which also shows ordered molecular stacking in the crystal lattice. The PVP$\sp\ominus$ centered $\pi$-$\pi\sp\ddagger$ electronic transitions of the (PVP)Ni (pcyd) complexes in low donating solvents shows a " mixing" effect attributed to an extension of conjugation resulting from $\pi$ donation of the phenylcyanamido ligand mediated by a common Ni(II) $\pi$ symmetry orbital within a square planar geometry. Temperature dependent, reversible solvent coordination equilibria exist for the (PVP)Ni(pycd) complexes. The proportions of non-solvated and solvated complexes are characterized by changes in the apparent $\pi$- mixing effect from which thermodynamic parameters are derived.
The relationships among blood pressure (BP), blood viscosity and echocardiographic left ventricular (LV) muscle mass were evaluated in 24 patients with essential hypertension and in 13 normotensive ...control subjects. LV mass was greater in the hypertensive patients than in the control subjects (225 +/- 69 vs 170 +/- 31 g, p less than 0.02) as was blood viscosity at a shear rate of 104 sec-1 (4.7 +/- 0.1 vs 4.3 +/- 0.2 cp, p less than 0.005). Among the hypertensive patients, LV mass was most closely related to viscosity at 104 sec-1 (r = 0.80, p less than 0.001), whereas only weak correlations were found between LV mass and systolic or diastolic BP (r = 0.45, p less than 0.05 for both). The 14 hypertensive patients with normal LV mass had viscosity similar to that in control subjects (4.5 +/- 0.3 vs 4.3 +/- 0.2 cp), whereas viscosity was consistently increased (5.0 +/- 0.4 cp, p less than 0.02) in hypertensive patients with LV hypertrophy. Thus, increased blood viscosity may be a determinant of or a response to hypertensive cardiac hypertrophy.
Blood pressure and components of blood viscosity were measured in 49 normal subjects and in 49 untreated patients with essential hypertension. Blood viscosity values measured at six different shear ...rates were significantly correlated with blood pressure (r = 0.432 to 0.505, p less than 0.001). Blood viscosity was higher in hypertensive patients. This was due to both higher plasma viscosity (1.29 +/- 0.08 standard deviation versus 1.24 +/- 0.05 centipoise (cPs), p less than 0.001) and increased hematocrit values (44.4 +/- 4 percent versus 41.5 +/- 3 percent, p less than 0.005). When blood viscosity was evaluated in subgroups of normal and hypertensive subjects with matched hematocrit values, it remained higher in the hypertensive patients, and the relationship between blood pressure and viscosity was still significant. Regardless of the hematocrit value, fibrinogen levels were elevated in hypertensive patients (p less than 0.006) and, in association with the increased globulin concentration, fibrinogen was largely responsible for the increased plasma viscosity in hypertensive patients. Since the viscosity of defibrinated blood was similar in normal and hypertensive subjects with matched hematocrit values, the elevated fibrinogen level also affected whole blood viscosity. Defibrinated blood viscosity and arterial pressures were not correlated. These studies demonstrate a direct correlation between blood pressure and blood viscosity among normotensive and hypertensive subjects. This relationship is, in part, due to the rheologic effects of an elevated fibrinogen level and to an increased hematocrit value. The basis for hyperfibrinogenemia in hypertensive patients is unclear.
In patients with borderline hypertension, total peripheral resistance (TPR) is either elevated or abnormally related to cardiac output. Since blood viscosity is one determinant of TPR, we compared ...various components of blood viscosity in 25 patients with borderline hypertension and 25 normal subjects. Under all experimental blood flow conditions examined, blood viscosity directly correlated with systolic and diastolic blood pressure (p less than 0.05 or better) and was greater in the hypertensive than in normal subjects. Venous hematocrit and plasma viscosity were higher in the hypertensive patients. These latter rheologic abnormalities accounted for the increased blood viscosity at higher shear rates. At lower shear rates, increased red cell aggregation, primarily mediated by elevated fibrinogen concentration, accounted for the higher blood viscosity in the hypertensive subjects. We conclude that even relatively small elevations in arterial pressure are associated with increased viscous resistance of blood to flow, and that the increased blood viscosity is a consequence of increased hematocrit, plasma viscosity, and red cell aggregation.
Recent research shows that the renin-angiotensin-aldosterone axis either maintains or causes some or all of the high blood pressure of most patients and demonstrates anew that renin-sodium profiling ...defines this involvement. Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions. For the remaining majority with essential hypertension, renin profiling exposes the relative participation of either vasoconstriction or volume factors, thereby guiding simpler, more specific, and predictably effective antirenin or antivolume treatments. Renin profiling identifies those in whom treatment should begin with a beta-blocker as opposed to a diuretic while not infrequently also providing baseline information about severity and prognosis in individual patients.
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