Water—filled treeholes provide an experimental setting for examining processes within an ecosystem, and influences of external factors on those processes. Using a limnological, experimental approach involving both natural tree holes and laboratory microcosms of the tree hole ecosystem, we identified and studied interacting, biotic processes, including dynamics of bacterial populations and variation in concentration of inorganic nutrients in tree hole water, and density—dependent competition for food among larvae of the mosquito Aedes triseriatus. We characterized the influence of external factors (inputs of leaf detritus and stemflow) on those processes. Analyses of water samples over time showed that tree hole water was rich and dynamic in nutrients (nitrite, nitrate, ammonium, phosphate, and sulfate); ammonium was the dominant form of inorganic nitrogen. Variation in nutrient concentrations in microcosms depended upon exogenous inputs (leaf detritus and stemflow water), dilution of nutrients by stemflow, nutrient cycling processes (nitrification, dentrification, and sulfate reduction), and ammonium excretion by mosquito larvae. The densities of bacteria in tree hole water, obtained using direct counts of DAPI—fluorochrome stained samples and epifluorescence microscopy, ranged from 2.0 ° 106 to 6.0 ° 107 cells/mL, and in microcosms from 4.6 ° 105 to 2.6 ° 108 cells/mL. Experimentation involving microcosms revealed that bacterial abundance was reduced by mosquito feeding and stemflow flushing. Further experiments showed that stemflow flushing increased mosquito productivity from microcosms several—fold and released mosquitoes from density—dependent competition. This effect was likely related to nutrient input and the simultaneous removal of toxic metabolites owing to inputs of stemflow water. We conclude that disturbance by a physical factor, stemflow, has a major influence on the interactions of nutrient dynamics, bacterial populations, and mosquito productivity in temperate tree—hole ecosystems.

Increased levels of an endogenous inhibitor of tissue-plasminogen activator (t-PA) have been thought to relate to the genesis of acute myocardial ischemia. To examine the role of the rapid inhibitor of t-PA, plasma samples were analyzed from 75 patients with chest pain syndrome undergoing coronary angiography (mean age 57 years), 24 patients with clinically documented coronary artery disease (unstable angina, positive exercise stress test or previous history of myocardial infarction; mean age 58 years) and 15 young normal subjects (mean age 26 years). Plasma t-PA inhibitor levels were similar in age-matched patients regardless of the absence or presence (and degree) of coronary artery disease. Plasma t-PA inhibitor levels correlated significantly with age (r - 0.46, p less than 0.005), suggesting an age-dependent decrease in fibrinolytic activity. Plasma t-PA inhibitor levels also correlated significantly with serum triglyceride levels (r - 0.60, p less than 0.001), but not with coronary risk factors such as serum cholesterol, diabetes, hypertension, serum uric acid levels or body weight. Association of high levels of inhibitor of t-PA with hypertriglyceridemia may be of importance in the development of coronary thrombosis, especially in elderly patients. Nonetheless, this study does not suggest a pathogenic role of t-PA inhibitor in coronary atherosclerosis.

It has been proposed that atherosclerotic arteries produce less prostacyclin (PGI2) than nonatherosclerotic arteries do, thereby predisposing arteries to vasospasm and thrombosis in vivo. We reexamined this concept by measuring spontaneous as well as arachidonate-induced PGI2 biosynthesis in aortic segments from nonatherosclerotic and cholesterol-fed atherosclerotic New Zealand White rabbits. Thromboxane A2 (TXA2) generation was also measured. Formation of PGI2, as well as TXA2, as measured by radioimmunoassay (RIA) of their metabolites, was increased in atherosclerotic aortic segments relative to nonatherosclerotic segments (P S 0.05) at 0, 5, 10, 15, and 30 min of incubation with arachidonate. Pretreatment of arterial segments with indomethacin inhibited PGI2 as well as TXA2 formation, whereas pretreatment with the selective TXA2 inhibitor OKY-046 inhibited only TXA2 release, thus confirming the identity of icosanoids. To confirm the RIA data, aortic segments were incubated with ['4C] ["'C]thromboxane B2 were similar in the two types of aortic segments. Thus, synthesis of PGI2 as well as TXA2 is increased in atherosclerosis, and this alteration in arachidonate metabolism is related to increased release of arachidonate.Decreased prostacyclin (PG12) biosynthesis and release by atherosclerotic compared to normal vessels was described by Dembinska-Keic et al. in 1977 (1). These initial observations in rabbit vessels were subsequently confirmed in the postmortem examination of human atherosclerotic vessels by D'Angelo et al. (2) Thromboxane A2 (TXA2) production is also increased in experimental (5) and human atherosclerosis (6-8). Accordingly, it has been proposed that a relative excess of TXA2 and deficiency of PG12 may predispose atherosclerotic vessels to vasospasm and platelet aggregation in vivo (9, 10).Although the plasma concentrations of 6-ketoprostaglandin Fla (6-keto-PGFia), the stable hydrolysis product of PGI2, are extremely low in normal plasma (-4 pg/ml) (11), it has been reported that these concentrations are increased in patients with atherosclerosis (8, 12 Since many previous studies employed bioassay or only radioimmunoassay (RIA) for measurement of PGI2, the present studies were designed to reexamine the concept of altered PGI2 generation in atherosclerosis. We examined the uptake and incorporation of labeled arachidonic acid into the phospholipids of the vessel wall and subsequent arachidonate release and conversion to major metabolites of PGI2 and TXA2 in both normal and atherosclerotic vessels.MATERIALS AND METHODS Induction of Atherosclerosis. New Zealand White male rabbits weighing 2.26-2.70 kg were fed an atherogenic diet of 1% cholesterol and 5% (wt/wt) lard (Bio-Serve, Frenchtown, NJ) for 2 weeks, which caused an increase of serum cholesterol to 981-1368 mg/dl (mean = 1191 mg/dl). Thereafter, the rabbits were anesthetized (acepromazine at 0.5 mg/kg, Rompun at 3 mg/kg, and ketamine at 50 mg/kg), and their right groins were explored to isolate the right femoral artery. After arter...

Previous studies indicate impairment of coronary arterial ring relaxation in response to acetylcholine (ACh) following coronary reperfusion, mediated via loss of endothelium-derived relaxing factor (EDRF). To examine if coronary vasodilator reserve is reduced following coronary ocdusionreperfusion in intact animnk, 16 open-chest mongrel dogs were subjected to 1 hour of total left circumflex (Cx) coronary artery ocduskm followed by reperfusion for 1 hour. Prior to Cx occlusion, coronary blood flow increased and vascular resistance decreased (both p<0.01) in response to ACh and bradykinin (BK). Following reperfusion, increase in Cx coronary flow in response to both vasodilators was significantly (p^O.Ol) unpaired. Myocardial histology showed extensive neutrophil infiltration and capillary plugging by neutrophils in the Cx compared with the left anterior descending coronary artery-supplied myocardium. Myocardial myeloperoxidase activity was also increased in the Cx compared with the left anterior descending region (p<0.02). Pretreatment of four dogs with indomethadn partially reduced the vasodilator response to BK but not to ACh. However, indomethadn did not affect reperfusion-induced attenuation of BK or ACh's coronary vasodilator effects. To determine if calcium blocker verapamil would modify reperfusion-induced impairment in coronary vasodilator reserve, six dogs were treated with verapamil. Although verapamfl enhanced coronary vasodilator effects of ACh and BK, it did not modify reperfusioninduced attenuation of coronary vasodilator reserve. Myocardial neutrophil accumulation and myeloperoxidase activity was also similar in control, indomethadn, and verapamil-treated dogs. These observations suggest that coronary reperfusion impairs coronary vasodilator reserve in intact dogs. This impairment is not modified by prostaglandin inhibition or by caldum blockade. Received February 22, 1988; accepted June 15, 1988. relaxation evoked by acetylcholine (ACh). Subsequent studies showed that the coronary artery ring relaxation by thrombin is converted to constriction when dog coronary arteries are subjected to total occlusion followed by reperfusion. 5 VanBenthuysen et al 6 have also shown attenuation of ACh-induced relaxation of coronary arterial rings from dogs subjected to temporary coronary occlusion. In those studies, electron microscopy demonstrated focal areas of endothelial cell injury with partial detachment of the cells from the underlying subendothelium.Recent studies have shown extensive capillary plugging by neutrophils in the myocardium of dogs following coronary occlusion and reperfusion, 78 which may relate to the microvascular origin of the "no-reflow" phenomenon. 9 Neutrophil capillary plugging reduces the cross-sectional area of the microvascular bed and could reduce coronary vasodilator reserve. Bradykinin (BK) dilates coronary arteries in a dose-dependent manner by stimulating release of EDRF as well as another potent vasodilator from the vessel wall, prostacyclin (PGI2).10 " Pretreatment of t...

This study investigated the effects of changes in the physical, chemical, and microbiological characteristics of decomposing pignut hickory (Carya glabra) leaves on the consumption rate, assimilation efficiency, and growth rate of the detritivore Tipula abdominalis. Larval growth was highest on leaves that had undergone decomposition for intermediate time periods. During this period maximum concentrations in leaf nitrogen, microbial biomass (ATP), and changes in microbial community structure associated with the decomposing leaves were observed. Laboratory feeding studies that investigated the role of these factors on larval growth established that microbial biomass, estimated by 15N enrichment, and leaf nitrogen concentration did not influence larval growth. However, microbial community structure had a significant influence on T. abdominalis consumption rate, assimilation efficiency, and growth rate. Results suggest that for normal growth T. abdominalis requires a microbial community composed of at least fungi and bacteria within its diet, but for reasons other than as a direct source of carbon and nitrogen.

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Previous studies indicate impairment of coronary arterial ring relaxation and loss of coronary vasodilator reserve after coronary artery occlusion and reperfusion. These changes are mediated in part through loss of endothelium-derived relaxing factor (EDRF) and/or myocardial neutrophil accumulation. To examine if superoxide dismutase (SOD), a scavenger of superoxide radicals, would modify the diminished coronary vasodilator reserve after temporary coronary occlusion in the intact animal, open-chest mongrel dogs were subjected to 1 hour of circumflex (Cx) coronary artery occlusion followed by 1 hour of reperfusion and treated with saline or SOD. Before Cx occlusion, coronary blood flow increased, and vascular resistance decreased (both p<0.01) in response to EDRF-dependent vasodilator acetylcholine as well as EDRF-independent vasodilator nitroglycerin. After Cx reperfusion, resting Cx coronary blood flow and vascular resistance were similar to the preocclusion values. In the saline-treated animals, there was evidence of myocardial dysfunction, which was measured by segmental shortening (-6±2% vs. 10±2%). Furthermore, increase in Cx coronary blood flow and reduction in vascular resistance in response to both vasodilators were significantly (p<0.01) impaired; these occurrences suggested loss of coronary vasodilator reserve. Myocardial histology showed extensive capillary plugging by neutrophils in the Cx-supplied myocardium. Myocardial myeloperoxidase activity, an index of neutrophil infiltration, was also increased in the Cx compared with the left anterior descending coronary artery region (p<0.02). Treatment of dogs with SOD, started at the end of Cx occlusion and continued during reperfusion, exerted significant (p<0.01) protective effect against reperfusion-induced attenuation of coronary vasodilator reserve in response to both acetylcholine and nitroglycerin. Loss of myocardial function (segmental shortening 5±1% vs. 10±l%) was less than in the saline-treated animals (p<0.01). Cx region-myocardial neutrophil accumulation and myeloperoxidase activity were also less (p<0.02) in the SOD-treated than in the saline-treated dogs. These observations suggest that coronary reperfusion impairs coronary vasodilator reserve in intact dogs. This impairment can be modified by treatment of animals with SOD before reperfusion. Capillary plugging by neutrophils may contribute to the altered coronary vasodilator reserve observed in the immediate postreperfusion period, and SOD modifies this reperfusion-induced impairment. {Circulation Research 1989;65:1283-1295) E ndothelium participates in the maintenance of coronary arterial tone by releasing vasodilator and vasoconstrictor substances. One of the most potent vasodilator substances, endothelium-derived relaxing factor (EDRF), 1 isFrom the Veterans Administration

The floodplain has been viewed as a transitional system or ecotone between aquatic and terrestrial habitats. This research has evaluated the role of floodplain macroinvertebrates in the degradation of leaf litter in a Michigan woodland floodplain, and examined the interrelationships among floodplain-stream macroinvertebrates, microbial colonization and selected environmental factors. Although taxonomically different decomposer groups operate in both systems, their functional roles as leaf litter detritivores are basically the same. Leaf litter processing rates were compared and contrasted between the stream and adjacent floodplain using leaf packs and litter bags, respectively. In the stream, the major time period for detritus processing by invertebrates is in the fall and winter, while in the floodplain it is during the spring. Therefore, the sequence of events involved in processing are similar, yet the timing and rate of these events are strikingly different. An understanding of the significant ecological processes linking the stream and floodplain as complementary systems is discussed within the context of watershed management.