Zn plays an important role in maintaining the anti-oxidant status within the heart and helps to counter the acute redox stress that occurs during myocardial ischaemia and reperfusion. Individuals with low Zn levels are at greater risk of developing an acute myocardial infarction; however, the impact of this on the extent of myocardial injury is unknown. The present study aimed to compare the effects of dietary Zn depletion with in vitro removal of Zn (N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN)) on the outcome of acute myocardial infarction and vascular function. Male Sprague–Dawley rats were fed either a Zn-adequate (35 mg Zn/kg diet) or Zn-deficient (<1 mg Zn/kg diet) diet for 2 weeks before heart isolation. Perfused hearts were subjected to a 30 min ischaemia/2 h reperfusion (I/R) protocol, during which time ventricular arrhythmias were recorded and after which infarct size was measured, along with markers of anti-oxidant status. In separate experiments, hearts were challenged with the Zn chelator TPEN (10 µm) before ischaemia onset. Both dietary and TPEN-induced Zn depletion significantly extended infarct size; dietary Zn depletion was associated with reduced total cardiac glutathione (GSH) levels, while TPEN decreased cardiac superoxide dismutase 1 levels. TPEN, but not dietary Zn depletion, also suppressed ventricular arrhythmias and depressed vascular responses to nitric oxide. These findings demonstrate that both modes of Zn depletion worsen the outcome from I/R but through different mechanisms. Dietary Zn deficiency, resulting in reduced cardiac GSH, is the most appropriate model for determining the role of endogenous Zn in I/R injury.

With visible disabilities, observers tend to overgeneralise from the disability. In contrast, with invisible disabilities such as traumatic brain injury and stroke, observers often fail to allow for challenges resulting from the disability. Persons who have suffered a stroke claim that people misunderstand their symptoms and stigmatise them as a result of these symptoms. This misunderstanding, which happens particularly with young survivors of stroke, may reflect people's causal attributions for symptoms that follow a stroke. Using a scenario design, this cross-sectional study examined whether people attribute ambiguous symptoms that may result from stroke to other causes (the stroke survivor's personality and age) and whether these attributions reflect the age of the stroke survivor. Participants (N = 120) read scenarios describing a male who was aged either 22, 72, or whose age was unstated and who showed four symptom changes: fatigue, depression, irritability and reduced friendships. For each symptom change, participants rated three causal attributions: the person's age, his personality and stroke. The age of the person in the scenario affected attributions; when the person in the scenario was 22, participants attributed his symptoms significantly more to his personality than to his age or stroke, whereas when he was 72, participants attributed his symptoms more to his age than to his personality or stroke and when his age was unstated, they attributed his symptoms equally to age, stroke and personality. Because misattributions for stroke symptoms hinder rehabilitation, therapy can target people's misattributions to enhance rehabilitation for survivors of stroke.