PubMed · 5725232
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B W Zweifach. Vasoactive agents in the microcirculation.. https://pubmed.ncbi.nlm.nih.gov/5725232/
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BACKGROUND: Alcohol consumption protects against coronary heart disease by as yet unclear mechanisms. The aim of this study was to determine the effect of ethanol on vascular smooth muscle cell (SMC) migration which plays an important role in the pathogenesis of atherosclerosis. MATERIALS AND METHODS: Cultures of human SMC under static (no flow) or pulsatile flow conditions (perfused transcapillary culture system) were pretreated in the absence or presence of ethanol (EtOH) whereupon their random migration (chemokinesis) was assessed by Transwell assay. RESULTS: Ethanol pretreatment (24 h) dose dependently inhibited migration of HuSMC from static cultures with a maximal inhibition of 60.8 +/- 4.4% observed at 40-80 mM, in the absence of any effect on cell adhesion or cell viability as assessed by trypan blue exclusion. In HuSMC exposed to pulsatile flow (0.3 to 25 ml/min, 24 h), there was a flow-dependent increase in migration ranging from a 1.3 +/- 0.16- to 2.67 +/- 0.26-fold increase, compared to static cells, concomitant with a significant increase in urokinase-type plasminogen activator (uPA) mRNA levels. Ethanol pretreatment (20-80 mM, 24 h) dose dependently inhibited the flow-induced increase in SMC migration but did not affect uPA mRNA expression. CONCLUSIONS: The inhibitory effect of ethanol on basal and flow-stimulated SMC migration may be relevant to its cardiovascular effects in vivo.
BACKGROUND: Low ocular perfusion pressure (two thirds of mean arterial pressure minus intraocular pressure) and myopia have been associated with protection of the retina from clinical diabetic retinopathy. This prompts the question as to whether myopia's protective role could also be a pressure effect, given that pressure could be dissipated in the longer arteriole tree of the myopic eye. METHODS: We combined the Ohm, Poiseuille, and Murray laws to derive the following new formulation: the pressure attenuation along a vessel varies directly with its length and inversely with its diameter. A mean pressure attenuation index was calculated for 22 healthy control subjects, 25 patients with axial myopia, and 6 patients with retinitis pigmentosa using digitized fundus images. RESULTS: The myopic arteriolar tree would produce a 16% greater pressure attenuation than that of controls (P = .002), with a linear relationship between mean pressure attenuation index and axial length (r = 0.93). Mean pressure attenuation index of the group with retinitis pigmentosa is increased 67% above that of controls, which is calculated to contribute an additional 10 mm Hg of pressure dissipation along their retinal arteriolar system. CONCLUSIONS: Pressure attenuation in retinal arterioles is directly proportional to the length and inversely proportional to the diameter of the arteriole segment being measured. CLINICAL RELEVANCE: A pressure attenuation index may be important in light of the entities known or presumed to protect the retina from diabetic retinopathy. The results support the hypothesis that low-end arteriolar pressure is a common denominator for many protective conditions in diabetic retinopathy.
We consider the thermal response of the body to radiofrequency (RF) energy, with emphasis on partial-body exposure, to assess potential thermal hazards. The thermal analysis is based on Pennes' bioheat equation. In this model, the thermal response is governed by two time constants. One (tau1) pertains to heat convection by blood flow and is (for physiologically normal perfusion rates) on the order of 3 min. The second (tau2) characterizes heat conduction, and varies as the square of a distance that characterizes the spatial extent of the heating. We examine three idealized cases. The first is a region of tissue with an insulated surface, subject to irradiation with an exponentially decreasing SAR, which models a large surface area of tissue exposed to microwaves. The second is a region of tissue in contact with a hemispherical electrode that passes current into it, which models exposure from contact with a conductor. The third is a region of tissue with an insulated surface, subject to heating from a dipole located close to it. In all three cases, we estimate the maximum steady-state temperature increase as a function of the relevant electrical and thermal parameters and the thresholds for thermal hazard. We conclude that thermal models are a potentially fruitful but underutilized means of analyzing thermal hazards from RF fields. A quantitative analysis of such hazards enables the development of data-based uncertainty factors, which can replace arbitrary "safety factors" in developing exposure limits. Finally, we comment on the need to marry quantitative modeling of data and risk assessment, and to incorporate contemporary approaches to risk assessment into RF standards development.