Abstract. -We explored the extent to which the soil seed bank differed genetically and spatially in comparison to two actively growingstages in a natural population of Plantago lanceolata. All seedbank seeds, seedlings,and adults of P. lanceolata within eight subunits in a larger population were mapped, subjected to starch gelelectrophoresis, and allozyme analysis in 1988. Gel electrophoresis was also used to estimate the mating system in two years, 1986 and 1988. The spatial distributions of seeds, seedlings, and adults were highly coincident. Allele frequencies of the dormant seeds differed significantly from those of the adults for four of the five polymorphic loci. In addition, a comparison ofthe genotype frequencies of the three life-history stages indicated that the seed bank had an excessofhomozygotes. Homozygosity, relative to Hardy-Weinberg expectations, decreased during the life cycle (for seed bank, seedlings, and adults respectively: F;t = 0.19, 0.09, 0.01; F;, = 0.14, 0.04, -0.12). Spatial genetic differentiation increased sixfold during the life cycle: (for seed bank, seedling and adults: F" = 0.02, 0.05, 0.12). The apparent selfingrate was 0.01 in 1986 and 0.09 in 1988. These selfingrates are not large enough to account for the elevated homozygosity of the seed bank. Inbreeding depression, overdominance for fitness, and a "temporal Wahlund's effect" are discussed as possible mechanisms that could generate high homozygosity in the seed bank, relative to later life-history stages. In Plantago lanceolata, the influence of the mating system and the "genetic memory" of the seed bank are obscured by the time plants reach the reproductive stage.

We have developed a guinea pig model of iron overload toxicity. Animals were administered intraperitoneal iron dextran 3 times a week to achieve total body iron load of 0.25,0.5 1.0, 1.5, and 2.0 g Fe/kg body weight in less than 30 days. Quantitation of tissue iron levels with atomic absorption indicated increased iron deposition in liver and heart of the iron-loaded guinea pigs (p -= 0.001). Additionally, the iron-loaded pigs demonstrated decreased nuclear magnetic resonance spectropscopy T1 relaxation times in both liver and heart (p < 0.001). Serum iron, total body iron capacity, and transfenin saturation values were also determined in guinea pigs treated with 0.25,0.5, and 1.0 g Fe/kg body weight. Serum iron and total iron-binding capacity were significantly increased at 0.5 and 1.0 g Fe/kg; transfemn saturation was elevated at 0.25 and 1.0 g Fe/ kg. Histologic examination of liver, heart, and bone marrow as well as ultrastructural studies on liver and heart confirmed increased iron deposition in treated animals. At the low iron dose level of 0.5 g Fe/kg, liver iron particles were primarily confined to Kupffer cells with minimal hepatocellular localization. Increased hepatocellular iron deposition was observed with larger doses of loaded iron. Myocardial iron was most prominent in interstitial cells of the epicardium, endocardium, myocardium, and coronary adipose tissue. Ultrastructurally, the presence of iron particles in pennuclear, membrane-bound structures (consistent with lysosomes) was confirmed using x-ray microanalysis. These morphological studies suggest that in this animal model siderosis of hepatic mononuclear phagocyte and myocardial interstitial cells may be the initial lesions leading to further biochemical and functional abnormalities. Correlation between tissue iron measurements and both light and electron microscopic changes, presented in this report, serve to introduce the iron-loaded guinea pig as a model for the study of iron-induced tissue damage.

Under light ether anesthesia, blood of male guinea pigs (Hartley strain, 330-410 g, Simonsen, Gilroy, CA) or rats (Sprague-Dawley, 230-575 g, Simonsen) was withdrawn into sodiun citrate (0.38% w/v). Platelet rich plasm (PRP) was then prepared by a rapid centrifugation procedure. Aggregation induced by ADP (1.6 μg/ml) was then examined in 0.15 or 0.25 ml aliquots of PRP at various time intervals from 5-60 min after blood withdrawal. A spontaneous time-dependent rise in aggregation response occurred that was similar to that observed when PGI2 (0.5-3ng) was added to PRP in vitro. In both species, intraperitoneal ackninistration of indanethacin (100 mg/kg, 1h previously) failed to interfere with the spontaneous rise in aggregation although vascular PGI2 formation was shown to be virtually abolished. Similar results were seen in essential fatty acid (EFA) deficient rats that had been chronically maintained on a fat free diet. In these animals, vascular PGI2 product ion was less than 15% that of controls. These results clearly indicate that any basal levels of PGI2 present in the arterial circulation are less than those (0.3-1ng/ml) necessary to appreciably inhibit aggregation. This conclusion coincides with that of Steer, et al. (Nature, 283, 194, 1980) who failed to detect biologically active amounts of PGI2 in hiimn venous blood and of several other groups who have failed to detect significant blood levels of the PGI2 breakdown product, 6-keto-PGF1α.

Male guinea pigs of 350-500 g (Hartley strain, Simonsen, Gilroy, CA) were anesthetized with pentobarbitone sodium (32.5 mg/kg, i.p.) and restrained head downwards on a plexiglass board tilted at an angle of 45° to the horizontal. Both ears were held down on the surface of the board using adhesive tape (Scotch brand #810). The upper surface of each ear was then superfused at 5 ml/min with warmed (37°C) sterile 0.9% (w/v) NaCl solution, delivered via a 14 g hypodermic needle. The tip of the needle was lowered in a standardized manner to puncture a small ear artery. From the time of incision, serial 10 sec. aliquots of bloodstained superfusate were collected into tubes containing 10 ml of particle-free saline with EDTA (‘Isoton’, Coulter) to inhibit coagulation and platelet clumping. After bleeding had ceased, the tube contents were allowed to sediment overnight. The following day, platelets in the upper (plateletrich) layer were counted electronically (Coulter). After shaking and further dilution the red blood cells were similarly counted. Effects of 500U heparin and 20 mg/kg aspirin (i.p., 1h. before bleeding) were examined. Both drugs markedly increased platelet and RBC efflux from the hemostatic site, but with characteristic differences in the time curves observed. An unexpected finding was that an incision in one ear could suppress bleeding from an incision subsequently made in the second ear. A previously undiscovered reflex or blood-borne hormone may be responsible.