The purpose of this study was to characterize the nucleotide profiles of a normal porcine elastic and muscular artery. Tissue samples (50 to 150 mg) were excised from the descending thoracic aorta and from the femoral artery of 14 normocholesterolemic, anesthetized minipigs. In three animals, transmural myocardial samples were also obtained. Nucleotide and nucleoside concentrations were analyzed by using a recently developed ion-pairing, reverse-phase, high-performance liquid chromatographic method. The arterial samples contained relatively low concentrations of adenosine triphosphate, approximately one-eighth that of the myocardial counterpart. Relative to the femoral artery, the aortic samples had significantly lower adenylate energy charges and higher levels of adenosine diphosphate, adenosine monophosphate, adenosine, and inosine. These baseline aortic levels did not change after in vitro exposure to 95% oxygen. The different energy states observed in the two arteries may reflect functional or metabolic differences in their medial smooth muscle cell populations. Alternatively, the lower energy state observed in the thicker walled aorta may be a manifestation of inadequate medial oxygen delivery that persists despite oxygen enrichment in vitro. We conclude that arterial energy states exhibit regional variation. This information will serve as a point of departure for the investigation of the role energy states may play in the atherosclerotic process.

Animals↗

PubMedDate not supplied

Topographic study of sudanophilic lesions in cholesterol-fed minipigs by image analysis.

A new morphometric technique using image analysis has been developed to express the topographic distribution of atherosclerotic lesions in unambiguous statistical terms. Computer-stored images of opened Sudan IV-stained aortas and iliac and coronary arteries from hypercholesterolemic minipigs (n = 39) were used in this study. The image processing methods included transformation of the data to standard templates, automated image segmentation, and creation of probability-of-occurrence maps. These maps have shown that sudanophilic lesions are localized with a characteristic topography along the aortas and iliac and coronary arteries. Areas of high probability are associated with the entrance regions of vessels and the lateral leading edges of the major flow dividers. Regions immediately distal to large branches were found to be areas of low probability. Despite the association of areas of sudanophilia with entrance regions and branch points, a major portion of sudanophilic lesions was not associated with any orifice region (e.g., ductus scar, dorsolateral surface of abdominal aorta, and ventral surface of terminal aorta). The present study provides the necessary information for the development of a rational sampling strategy for the experimental study of the distribution of localizing factors (e.g., hemodynamic, biochemical, cellular, mass transport, histological) and their relationships to putative atherogenic mechanisms.

Animals↗

PubMedDate not supplied

Uptake of low density lipoprotein, albumin, and water by deendothelialized in vitro minipig aorta.

The purpose of this research was to study the effect of pressure on arterial hydration in vitro and the effect of pressure and flow (stirred reagent) on the in vitro transport of 125I-albumin and 125I-LDL into deendothelialized minipig aortas over a 24-hour period. It was found that the arterial hydration (fractional mass of water) was 0.740 +/- 0.0043 SEM for control tissue; after 24 hours this rose to 0.745 +/- 0.0038 for 0 mm Hg, 0.752 +/- 0.0046 for 100 mm Hg, and 0.755 +/- 0.0065 for 200 mm Hg. In the transport studies, the following effects were found. The reagent radioactivity concentration and composition did not change with pressure or stirring over the 24-hour period. For unpressurized tissue, the 24-hour normalized uptake [uptake (M mg cm-2) divided by reagent concentration (co mg cm-3)] of albumin was (4.86 +/- 0.43 cm) X 10(-3) from stirred and (5.46 +/- 0.36 cm) X 10(-3) from nonstirred reagent; that of LDL was (0.31 +/- 0.02 cm) X 10(-3) from stirred and (0.37 +/- 0.02 cm) X 10(-3) from nonstirred reagent. Pressurization (100 mm Hg) of the tissue increased albumin uptake by 52% from stirred and by 125% from nonstirred reagent and the LDL uptake by 52% from stirred and 241% from nonstirred reagent. Pressure increased the intimal surface concentration of albumin and LDL at the nonstirred, but not at stirred, interfaces. The electrophoretic properties of the intimal surface fluid showed only minor differences from those of the bulk reagent. These data demonstrate that pressure causes a slight, but significant, increase in arterial hydration and that radiolabeled albumin and LDL appear to be sieved by the superficial intimal layers of the deendothelialized porcine aorta under the in vitro conditions of this study.

Albumins↗

PubMedDate not supplied

Mass transport, atherogenesis, and risk.

If the local chemically-active interstitial concentration (chemical activity) of a particular atherogenic molecule (atherogen) is considered to be one of the fundamental driving forces in a system of reactions that produces an associated local atherogenic change, then the chemical activity may be used as a measure of the potential for lesion development or local "risk." A model of steady-state, combined, diffusive and convective transport of an assumed atherogen across a multilayered arterial wall was used to illustrate mechanisms by which transport processes interact with tissue barriers to determine the transmural (x axis) chemical activity distributions [a(x), mol cm-3]. The model was used to evaluate the effects of increased endothelial gap fractional area (increased endothelial permeability), elevated blood pressure, elevated serum concentration of the atherogen, internal elastica fenestration, and preexisting intimal thickening on a(x). It was found that sites along the arterial tree that are characterized by "mild" increases in endothelial gap fractional area and concomitant subjacent interstitial sieving of the atherogen developed high a(x), in some cases much higher than that (a0) of the blood, and therefore were at high risk even in the absence of other risk factors. Moreover, the risk at such sites was dramatically increased with hypertension and/or elevated serum atherogen concentration and/or preexisting intimal thickening. However, if either condition, i.e., opened endothelial intercellular junctions or subjacent interstitial sieving, was absent, these other risk factors were ineffective. Finally, the response of the model was shown to be consistent with a variety of well-known, as well as puzzling, observations suggesting that transport processes may play roles in determining both the architecture of the atherosclerotic lesion and its rate of development.

Arteriosclerosis↗