Biomedical subjects

S L Harper

Publications and source records attributed to S L Harper.

39 records · Page 3Linked to original sources

PubMedDate not supplied

An automated system for producing uniform surface deposits of dry particles.

A laboratory system has been constructed that uniformly deposits dry particles onto any type of test surface. Devised as a quality assurance tool for the purpose of evaluating surface sampling methods for lead, it also may be used to generate test surfaces for any contaminant that uses particles or dust as a transport mechanism. Additionally, it may be used to spike surfaces for studies concerning particle transport, resuspension, reentrainment, and exposure. The electromechanical system includes a rugged aluminum chamber housing deposition equipment, a computer-controlled positioning system, and a 0.61 x 0.61 m target surface area (2 x 2 ft). Media used to evaluate the system have included glass beads of various size fractions (physical diameters between 30 and 500 microm), and Arizona Test Dust (aerodynamic diameters between 1 and 80 microm). Presieved particle size fractions may be used individually to study the effects of monodisperse particles, or may be mixed to create custom polydisperse size distributions. Using arrays of 16 coupons placed on the surface to collect representative samples from every test, the uniformity of the particle deposition can be quantified. The system achieved an average coefficient of variation of less than 20% for the 16 coupons for the particle types and sizes mentioned above and for a variety of total surface loadings (0.3-19 g/m2). Calculations of the system's repeatability (as the average coefficient of variation of mass gains for individual coupon locations compared across multiple identically configured runs) yielded approximately 10 +/- 5% (one standard deviation). Tests of the system's accuracy, defined as the absolute percentage difference between predicted surface loadings and actual loadings, yielded 3.7 +/- 1.3% (one standard deviation).

Aerosols↗

PubMedDate not supplied

Microvascular adaptation in the cerebral cortex of adult spontaneously hypertensive rats.

The purpose of this study was to determine the microvascular characteristics that cause cerebral cortical blood flow autoregulation to shift to a higher range of arterial pressures during established hypertension in spontaneously hypertensive rats (SHR). An open-skull technique with constant suffusion of artificial cerebrospinal fluid (PO2 = 40-45 mm Hg, PCO2 = 40-45 mm Hg, pH = 7.35-7.45) was used to view the parietal cortex of 18- to 21-week-old SHR and Wistar Kyoto (WKY) normotensive control rats. The resting inner diameters of first (1A)-, second (2A)-, and fourth (4a)-order arterioles were significantly (p less than 0.05) smaller, and the wall thickness/lumen diameter ratios were significantly (p less than 0.05) larger in SHR compared to WKY. Only 1A and 4A has significantly (p less than 0.05) increased vessel wall cross-sectional area in SHR. At the resting mean arterial pressures of WKY and SHR, the passive (10(-4) M adenosine, topical) diameters of comparable types of arterioles were not significantly different (p greater than 0.05). At reduced arterial pressures, however, the arterioles in SHR had smaller maximum diameters than in WKY. Cortical blood flow in WKY and SHR was constant at arterial pressures from 70-150 mm Hg and 100-200 mm Hg, respectively. Resting arteriolar pressures in 1A, 2A, and 3A of SHR were substantially and significantly (p less than 0.05) elevated, although pressures in the smallest arterioles and venules of WKY and SHR were similar. Therefore, it is possible that cerebral capillary pressure is only slightly elevated, if at all, in SHR as a result of the vasoconstriction. The number of arterioles per unit area of brain surface at rest was equal in WKY and SHR. In addition, the number of vessels was equal in WKY and SHR during maximal dilation, and neither type of rat demonstrated an opening of previously closed vessels upon maximum dilation. Therefore, the cerebral arteriolar constriction in SHR, which was probably potentiated by vessel wall hypertrophy of the largest and smallest arterioles, was the major contributor to an upward shift in the autoregulatory range, the protection of exchange vasculature pressures, and the increase in vascular resistance.

Adaptation, Physiological↗

PubMedDate not supplied

Effects of antihypertensive treatment on the cerebral microvasculature of spontaneously hypertensive rats.

Experiments were performed in anesthetized 18-19-week-old spontaneously hypertensive rats (SHR) to evaluate the effects of delayed antihypertensive treatment on cerebrovascular function. Animals were treated for 25 +/- 1 days with an oral antihypertensive regimen consisting of hydralazine, reserpine, and chlorothiazide, resulting in normotension within 2 weeks. Cerebral arterioles were examined via a constantly suffused open cranial window and video microscopy. Resting cerebral blood flow was measured using radioactive microspheres and the reference organ method. While untreated SHR exhibited reductions in arteriolar diameter compared with normotensive Wistar Kyoto rats (WKY), treatment restored arteriolar dimensions to normal. Increments in microvascular wall area, associated with medial hypertrophy in untreated SHR, were completely reversed in treated SHR to a magnitude not different from control. Resting cerebral blood flow was, however, decreased in treated SHR compared with both untreated SHR and WKY; this was due to an increase in total cerebrovascular resistance compared with WKY. Additionally, microvascular pressure in the largest arterioles in treated SHR was reduced compared with both WKY and untreated SHR. There was a significant increase in the relative pressure drop accounted for by the arterial vessels upstream from the cerebral microcirculation in treated SHR. These results suggest that 1) cerebral microvascular abnormalities induced by chronic hypertension are reversed by delayed antihypertensive therapy, and 2) there is a persistent elevation in cerebrovascular resistance upstream from the microcirculation representing large vessel adaptations that may not be readily reversible with treatment.

Animals↗