Search

The normal transmyocardial tissue hematocrit distribution (i.e., subepicardial greater than subendocardial) is known to be affected by red blood cell (RBC) aggregation. Prior studies employing the use of infused large macromolecules to increase erythrocyte aggregation are complicated by both increased plasma viscosity and dilution of plasma. Using a new technique to specifically alter the aggregation behavior by covalent attachment of Pluronic F-98 to the surface of the RBC, we have determined the effects of only enhanced aggregation (i.e., Pluronic F-98-coated RBCs) versus enhanced aggregation with increased plasma viscosity (i.e., an addition of 500 kDa dextran) on myocardial tissue hematocrit in rapidly frozen guinea pig hearts. Although both approaches equally increased aggregation, tissue hematocrit profiles differed markedly: 1) when Pluronic F-98-coated cells were used, the normal transmyocardial gradient was abolished, and 2) when dextran was added, the hematocrit remained at subepicardial levels for about one-half the thickness of the myocardium and then rapidly decreased to the control level in the subendocardial layer. Our results indicate that myocardial hematocrit profiles are sensitive to both RBC aggregation and to changes of plasma viscosity associated with increased RBC aggregation. Furthermore, they suggest the need for additional studies to explore the mechanisms affecting RBC distribution in three-dimensional vascular beds. myocardium; plasma viscosity; Pluronic F-98; dextran

Objectives Prolidase plays a major role in collagen turnover, matrix remodeling, and cell growth. Benign prostatic hyperplasia (BPH) may be associated with an increased extracellular matrix deposition. Therefore, the present study was designed to investigate the plasma prolidase activity, oxidative status, and peripheral mononuclear leukocyte DNA damage in patients with BPH. Patients and methods Twenty-six male patients with BPH and 24 healthy male subjects were included in this study. Blood samples were collected from antecubital vein after an overnight fasting period, and the plasma was separated. Plasma prolidase activity, total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. The peripheral lymphocyte oxidative DNA damage was determined using an alkaline single cell gel electrophoresis assay (comet assay). Results The plasma prolidase activity, TOS levels, OSI values, and peripheral mononuclear leukocyte DNA damage were significantly higher (P < 0.001), while the TAC levels were significantly lower (P < 0.001) in patients with BPH than controls. In BPH patients, the prolidase activity was significantly associated with TAC levels (r = −0.366, P < 0.05), TOS levels (r = 0.573, P < 0.001), and OSI (r = 0.618, P < 0.001) and peripheral mononuclear leukocyte DNA damage (r = 0.461, P < 0.001). Conclusions Our results showed that BPH might be associated with an increased oxidative stress, and also an increased plasma prolidase activity. Increased prolidase activity might play an important role in the etiopathogenesis and/or progression of BPH. [ABSTRACT FROM AUTHOR]

Red blood cells (RBC) in normal human blood undergo reversible aggregation at low flow or stasis. The extent and kinetics of this phenomenon have been studied using various optical and electrical methods, yet results using such methods are not always in concordance. This study employed a horizontal glass tube in which blood flow could be established, then abruptly stopped. Normal blood and RBC suspensions with enhanced or decreased aggregation were studied. Light transmittance (LT) and electrical impedance at 100 kHz were recorded during high-shear flow and for 120 s after flow was abruptly stopped during which RBC aggregation occurs. Capacitance values were also obtained based on the imaginary part of impedance data and recorded. Various aggregation parameters were calculated, using the time course of LT, impedance, and capacitance, then compared with each other and with results from laboratory aggregometers. RBC aggregation parameters were calculated, using the time course of impedance data often failed to correlate with known changes of aggregation, even reporting aggregation for cells in nonaggregating media (i.e., RBC in buffered saline). Alternatively, RBC aggregation parameters based upon the time course of capacitance data are in general agreement with those derived from LT data and with RBC aggregation indexes, measured using commercial instruments. [ABSTRACT FROM AUTHOR]

3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are the most commonly used cholesterol-lowering drugs, with recent clinical trends usually aimed at achieving the lowest possible plasma cholesterol levels. Although the effects of increased plasma cholesterol have been previously reported, it is not obvious how very low plasma cholesterol levels would affect membrane composition and the deformability of red blood cells (RBC). The present study investigated the effects of hypocholesterolemia achieved by atorvastatin therapy on RBC membrane and mechanical properties in guinea pigs fed a normal diet. Two groups of animals were used (atorvastatin-treated, n=12; control n=12), and atorvastatin given orally in isotonic phosphate-buffered saline (PBS) at a dose of 20 mg/kg/day for a 21-day period. Our results indicate that the atorvastatin-treated group had significantly lower plasma total cholesterol (17.42±1.70 mg/dl), low-density lipoprotein cholesterol (5.25±2.22 mg/dl) and triglycerides (42.60±3.78 mg/dl) than the control group (34.08±1.72, 21.17±1.41 and 60.64±2.43 mg/dl, respectively). In addition, membrane cholesterol content was lower (p<0.0001) and phospholipid content higher (p<0.0001) in the atorvastatin-treated group, thus decreasing the cholesterol to phospholipid ratio; a significant enhancement in sodium-potassium-ATPase activity also occurred. However, in spite the marked changes of plasma and RBC membrane composition, there was no change of RBC deformability. Note that although our results indicate no adverse rheological alterations, extension of our findings to humans requires caution. [ABSTRACT FROM AUTHOR]

The normal transmyocardial tissue hematocrit distribution (i.e., subepicardial greater than subendocardial) is known to be affected by red blood cell (RBC) aggregation. Prior studies employing the use of infused large macromolecules to increase erythrocyte aggregation are complicated by both increased plasma viscosity and dilution of plasma. Using a new technique to specifically alter the aggregation behavior by covalent attachment of Pluronic F-98 to the surface of the RBC, we have determined the effects of only enhanced aggregation (i.e., Pluronic F-98-coated RBCs) versus enhanced aggregation with increased plasma viscosity (i.e., an addition of 500 kDa dextran) on myocardial tissue hematocrit in rapidly frozen guinea pig hearts. Although both approaches equally increased aggregation, tissue hematocrit profiles differed markedly: 1) when Pluronic F-98-coated cells were used, the normal transmyocardial gradient was abolished, and 2) when dextran was added, the hematocrit remained at subepicardial levels for about one-half the thickness of the myocardium and then rapidly decreased to the control level in the subendocardial layer. Our results indicate that myocardial hematocrit profiles are sensitive to both RBC aggregation and to changes of plasma viscosity associated with increased RBC aggregation. Furthermore, they suggest the need for additional studies to explore the mechanisms affecting RBC distribution in three-dimensional vascular beds.