Could a residential wood ash recycling programme be part of the solution to calcium decline in lakes and forests in Muskoka (Ontario, Canada)?

One possible solution to the recent decline of calcium (Ca) concentrations in Canadian Shield forests and lakes in eastern North America is the addition of Ca-rich wood ash to watersheds. We investigated the feasibility of using small, mainly residential sources of non-industrial wood ash (NIWA) for this purpose by quantifying concentrations of its major nutrients and metals, its toxicity to Daphnia in aqueous extracts, and estimating the amount of NIWA available in the District of Muskoka in central Ontario. Locally collected NIWA averaged 30% Ca, and also contained smaller but significant amounts of K, Mg, Na, and P. Of these, K was so soluble that it was toxic to Daphnia over 48 h in the concentrate and 10-fold dilution; however, sedimented ash was not toxic over 15 d. Most metal levels in NIWA were below targets permitting unrestricted land application. However, Cu and Zn were just above these targets, but well below those for conditional use. Muskoka residents generate about 235 000 kg of NIWA annually, not enough to treat all central Ontario areas affected; however, a NIWA recycling programme implemented across southern Ontario could generate enough ash to solve the Ca decline problem in Muskoka’s forests and lakes.

Abstract 56: Growth Hormone Releasing Hormone Improves Sarcomere Relaxation and Calcium Decline in Cardiomyocyte From a Mouse Model of Heart Failure With Preserved Ejection Fraction

Heart failure with preserved ejection fraction (HFpEF) is characterized by impaired relaxation, ventricular stiffening and fibrosis. Growth hormone releasing hormone (GHRH) agonists reduce fibrosis in rat and swine models of ischemic myocardial injury. However, their effect on cardiomyocytes is not known. We hypothesized that activation of GHRH receptor signaling improves impaired cardiomyocyte relaxation in a mouse model of HFpEF. C57BL6N mice (n=4-5) were implanted with a mini-osmotic pump to deliver angiotensin-II (Ang-II: 0.8 mg/kg/day) for 4 weeks and received daily injections of GHRH-Agonist (GHRH-A [MR-409]: 100 μg/kg) or vehicle (DMSO+propylene-glycol). Cardiomyocytes were isolated and calcium and sarcomere shortening assessed. Ang-II-treated cardiomyocytes exhibited reduced sarcomere length, indicating an inability to completely relax, despite lower resting calcium. These cardiomyocytes also exhibited impaired ability to contract with no changes in calcium transient amplitude, deficient relaxation and delayed calcium decay. MR-409 treatment restored resting calcium and resting sarcomere length; improved sarcomere shortening and completely abrogated Ang-II-induced delay in calcium decline and relaxation (see figure 1). Our findings demonstrate that chronic administration of Ang-II mediates structural and functional changes consistent with HFpEF and suggest that activation of the GHRH receptor signaling pathways prevents HFpEF-associated cardiomyocyte performance alterations.