Choice of biodiversity index drives optimal fire management decisions.

Preservation of biodiversity is a central goal of conservation management, yet the conditions that promote persistence may differ for the species in the community. For systems subject to stochastic disturbances such as fire, understanding which management practices promote persistence for all species in a community is complex. Before deciding on the best course of action, an objective must be specified. Yet an overarching goal of species persistence can be specified into a measureable objective many different ways. We investigated four alternative management objectives for maximizing species persistence that use common biodiversity indices: (1) attaining the minimally acceptable mix of successional vegetation states to support species' relative abundances, (2) maximizing the arithmetic mean abundance of species, (3) maximizing the geometric mean abundance of species, and (4) minimizing the average extinction risk of species. We used stochastic dynamic programming to model successional changes in vegetation in the presence of both planned and unplanned fires, and utilize an extensive data set on the occurrence of birds, reptiles, and small mammals in different successional states in semiarid Australia. We investigated the influence the choice of objective function and taxonomic focus has on the optimal fire management recommendations. We also evaluated a recent hazard reduction policy to annually burn a fixed amount of the landscape and compare results to the optimal solution. The optimal management strategy to maximize species persistence over a 100-year period is predominantly to minimize wildfires. This is because the majority of species are more likely to occur in intermediate, and late successional vegetation. However the optimal solution showed sensitivity to the objective and the species included in the analysis. These results highlight the need for careful consideration when specifying an objective to represent overarching conservation goals. Using the extinction risk objective, we show that a policy to annually burn 5% of the landscape could increase the average probability of extinction for the modelled species by 7% over the next 100 years compared to the optimal management scenario.

Spectroscopic identification and direct imaging of interfacial magnetic spins.

Using x-ray absorption spectromicroscopy we have imaged the uncompensated spins induced at the surface of antiferromagnetic (AFM) NiO(100) by deposition of ferromagnetic (FM) Co. These spins align parallel to the AFM spins in NiO(100) and align the FM spins in Co. The uncompensated interfacial spins arise from an ultrathin CoNiOx layer that is formed upon Co deposition through reduction of the NiO surface. The interfacial Ni spins are discussed in terms of the "uncompensated spins" at AFM/FM interfaces long held responsible for coercivity increases and exchange bias. We find a direct correlation between their number and the size of the coercivity.

An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness.

Decreased elasticity of the cardiovascular system is one of the hallmarks of the normal aging process of mammals. A potential explanation for this decreased elasticity is that glucose can react nonenzymatically with long-lived proteins, such as collagen and lens crystallin, and link them together, producing advanced glycation endproducts (AGEs). Previous studies have shown that aminoguanidine, an AGE inhibitor, can prevent glucose cross-linking of proteins and the loss of elasticity associated with aging and diabetes. Recently, an AGE cross-link breaker (ALT-711) has been described, which we have evaluated in aged dogs. After 1 month of administration of ALT-711, a significant reduction ( approximately 40%) in age-related left ventricular stiffness was observed [(57.1 +/- 6.8 mmHg x m(2)/ml pretreatment and 33.1 +/- 4.6 mmHg x m(2)/ml posttreatment (1 mmHg = 133 Pa)]. This decrease was accompanied by improvement in cardiac function.

Nonplatelet effects of aspirin during acute coronary occlusion: electrophysiologic and cation alterations in ischemic myocardium.

BACKGROUND: Mortality after acute myocardial ischemia has been reduced by aspirin (ASA) but mechanisms other than the antiplatelet effect have not been established. This article evaluates an antiarrhythmic action during sympathetic stimulation in the intact anesthetized dog with and without ischemia. METHODS AND RESULTS: The ventricular fibrillation threshold (VFT) was examined before and after epinephrine (E) in normals (group I). A VFT reduction during E was normalized after 1 week of ASA (P<.01). Regional myocardial ischemia for 1 hour resulted in similar hypoperfusion in controls of group II and after ASA. Action potential responses in isolated superfused ischemic tissue showed prolonged repolarization (APD90) in response to E, which was normalized after ASA (P<.01). To assess the antiarrhythmic role of the anion in group III, Na salicylate was given. During 1 hour of ischemia, the VF incidence was reduced and cation abnormalities diminished in ischemic myocardium compared with untreated ischemia. CONCLUSIONS: ASA antagonizes the reduction of the VFT induced by catecholamine in normals as well as the repolarization abnormality elicited by E during acute ischemia. The salicylate anion appears to be the active component in view of the efficacy in preventing VF during the early ischemic period.

Effects of glucose intolerance on myocardial function and collagen-linked glycation.

In experimental diabetes, diastolic dysfunction of the left ventricle has been associated with collagen-linked glycation. To determine whether less severe hyperglycemia may have similar effects, we gave alloxan to mongrel dogs (group 2) to induce impaired glucose tolerance (IGT) for comparison with normal subjects (group 1). After 6 months, hemodynamic studies were performed in the anesthetized animals. Basal heart rate, aortic pressure, and ejection fraction were comparable in the two groups, but calculated chamber stiffness was increased in group 2, associated with a reduced end diastolic volume and increased pressure. During infusion of dextran, the volume and pressure responses were similarly abnormal in group 2. In the myocardium, the collagen concentration rose with an increased interstitial distribution histologically. To assess glycation, collagen was extracted, digested with collagenase, and measured for fluorescence. Advanced glycation end products were increased in group 2 to 10.6 +/- 1.6 vs. 6.9 +/- 0.7 fluorescent units (FU)/mg collagen in group 1 (P < 0.01). To assess whether this could be pharmacologically prevented, we administered enalapril to inhibit ACE during the 6 months of glucose intolerance to group 3. This resulted in normal glycation and significant reduction in chamber stiffness increment. We gave group 4 animals aminoguanidine daily for 6 months, which prevented abnormal collagen glycation and chamber stiffness. Thus, in animals with IGT, collagen-linked glycosylation appeared to be a major factor affecting diastolic function and was shown to be amenable to pharmacological intervention.

Influence of nicotine on myocardial stiffness and fibrosis during chronic ethanol use.

Cardiomyopathy related to ethanol abuse is often accompanied by cigarette use. To examine if the major cardioactive component may intensify the abnormal function and composition induced by chronic ethanol, nicotine was administered orally, 2.5 mg bid, to a canine model receiving 36% of calories as ethanol for 6 months (group III). These animals were compared with group II receiving ethanol alone, group IV on nicotine alone, and controls (group I). In the intact, ventilated, anesthetized dog, left ventricular pressures and volumes were measured before and after dextran infusion and related to left ventricular collagen alterations. Basal heart rate, aortic pressure, and ejection fraction were comparable with controls. End-diastolic pressure and diastolic chamber stiffness (KPV) were significantly higher in the basal state and during dextran infusion in the three experimental groups, compared with group I. The increment was largest in the ethanol-nicotine group. Analysis of left ventricular myocardium revealed a rise of collagen concentrations in all three experimental groups, with an interstitial distribution on histochemical examination. Moreover, determination of advanced glycosylation endproducts, as a measure of alterations in collagen cross-links, revealed higher concentrations versus controls. The greater increase of diastolic stiffness in the nicotine-ethanol group occurred despite a similar concentration of fluorescent products as group II. Because the former had a larger increase of collage concentration, total cross-linked collagen content was presumably greater after the combined use of nicotine-ethanol. Thus, nicotine in relatively high dose when combined with ethanol, elicited a modest further increase in the left ventricular chamber stiffness and collagen concentration.

Effect of acute ketoacidosis on the myocardium in diabetes.

Abnormalities of left ventricular function are often present in patients with diabetes who are in a stable metabolic state. To determine whether acute metabolic abnormalities may contribute to pathogenesis, patients with diabetes and ketoacidosis (Group 1) or hyperglycemia without ketosis (Group 2) were studied. They were assessed noninvasively for evidence of acute injury or dysfunction of the myocardium. Left ventricular function was assessed on admission and after clinical recovery. Myocardial enzyme release was examined during the acute phase. In Group 1, plasma glucose averaged 32 mM/L and carbon dioxide content 12.4 mEq/L. On echocardiography, the initial circumferential shortening velocity of 1.85 + 0.07 circumferences per second was significantly higher than the final circumferential shortening velocity of 1.31 + 01 (P < 0.005). The systolic time interval ratio, pre-ejection period/left ventricular ejection time, was significantly lower on the initial day compared with the second study. These data are consistent with enhanced ventricular performance. In group 2, plasma glucose averaged 29 mM/L, and carbon dioxide content was normal. The initial circumferential shortening velocity of 1. 1 circumferences per second and pre-ejection period/left ventricular ejection time ratio of 0.38 were normal and remained unchanged. There was no significant alteration of heart rate or arterial pressure in either group. In both groups, total serum lactate dehydrogenase and creatinine phosphokinase levels, as well as their cardiac isoenzymes, were within normal limits. Therefore, the initial increase of myocardial performance and subsequent restoration to normal, as well as the lack of cardiac enzyme increase in plasma, support the view that shortterm ketoacidosis does not contribute to the abnormalities of ventricular function in diabetes.

Cardiac consequences of diabetes mellitus.

A variety of disciplines including noninvasive and invasive cardiac methodologies, as well as epidemiologic studies, have provided information that has altered our view on the relation of diabetes to cardiac disease. Instead of an exclusive focus on coronary artery disease, it is now recognized that heart muscle can be independently involved in diabetic patients. In diabetics without known cardiac disease, abnormalities of left ventricular mechanical function have been demonstrated in 40 to 50% of subjects, and it is primarily a diastolic phenomenon. Left ventricular hypertrophy may eventually appear in the absence of hypertension. The diastolic dysfunction appears related to interstitial collagen deposition, largely attributable to diminished degradation. The presence of even moderate obesity intensifies the abnormality. Reversibility of this process is not readily achieved with chronic insulin therapy. Experimental studies have indicated normalization of the collagen alteration by endurance training, begun relatively early in the disease process. General measures of management include the control of other cardiac risk factors and a reasonable program of physical activity. The high mortality during an initial acute myocardial infarction has been attributed to heart failure, which is managed as in nondiabetic patients. Recently, the early introduction of aspirin, thrombolysis, and beta-adrenergic blockade has reduced mortality during the initial infarction. Chronic use of the latter agent over the subsequent years has also proven to be more beneficial in diabetic patients with acute myocardial infarction compared with nondiabetic patients.

Diabetic cardiomyopathy: experimental and clinical observations.

Heart failure, arrhythmia, or chest pain can be a consequence of diabetes independent of coronary disease or hypertension. Diastolic myocardial dysfunction is common, contributing to the high mortality during acute infarction. The authors discuss diabetic cardiomyopathy and its management.

Anti-arrhythmic efficacy of beta-adrenergic blockade during acute ischemia in myocardium with scar.

Ventricular arrhythmia production in the ischemic heart is considered to be influenced by prior infarction. Although beta-adrenergic blockade is known to have beneficial effects during acute ischemia, its anti-arrhythmic efficacy during post-infarction ischemia is not known. To explore this question, we have used a model with a relatively high incidence of ischemic arrhythmias. Mongrel dogs 2 to 3 years of age were studied intact under anesthesia. An irreversible injury of the infero-posterior myocardium was produced with an electrode catheter 1 week earlier. The arrhythmic response to acute ischemia was assessed using serial, transient 15-minute occlusions of the left-anterior descending coronary artery with a balloon catheter. During ischemia alone, the incidence of ventricular fibrillation in animals who underwent all phases of the study was 6 of 9; with atenolol (0.2 mg/kg intravenously) and ischemia, 1 of 9 (p < 0.05). To assess the role of the bradycardic response, the latter was repeated 1 week subsequently during atrial pacing at the heart rate that existed before ischemia. Fibrillation occurred in 8 of 9, a significant reversal of the therapeutic effect. To exclude the potential artifact of a fixed intervention protocol, a study was undertaken with the short-acting esmolol, in which three ischemic periods were alternated at 1-hour intervals: (A) ischemia without treatment, (B) ischemia with continuous infusion of 150 micrograms/kg/min esmolol, and (C) same as B except that heart rate was maintained by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic cardiomyopathy.

Clinical observations over the past two decades have pointed to the relationship between heart disease and alcohol abuse, usually without evident malnutrition or cirrhosis. While the prevalence of heart failure in the alcoholic population is now known, subclinical abnormalities of left ventricular function in noncardiac alcoholics who were normotensive have a high prevalence with or without some degree of ventricular hypertrophy by echocardiogram. This is frequently a diastolic rather than systolic abnormality. Congestive cardiomyopathy is not infrequently associated with high diastolic arterial blood pressures. Intoxication itself may contribute to blood pressure elevation. Angina pectoris in the absence of significant coronary disease is another presentation. Although the history may not be readily obtained, the major diagnostic feature in this entity is the history of ethanol ingestion in intoxicating amounts for at least 10 years, often marked by periods of spree drinking. While the course of congestive cardiomyopathy may be progressively downhill in individuals who continue to be actively alcoholic after the onset of heart failure, in one series one third of the patients became abstinent. These patients had a 4 year mortality that was persistently one-sixth of the alcoholic group. Management of heart failure is traditional in these patients. Atrial arrhythmias have been shown to occur during the early ethanol withdrawal phase in patients without other clinical evidence of heart disease. Sudden death in a segment of the alcoholic population is considered arrhythmia related and is commonly associated with cigarette use. Identification of the addicted individual is the essential element to management.

Myocardial inositol and sodium in diabetes.

Although inhibition of Na(+)-K+ ATPase has been described in the diabetic heart, K+ loss from myocardium has not been observed in a canine model of mild diabetes. The finding of tissue Na+ accumulation and a potential relation to alteration of left ventricular inositol as observed in other tissues in diabetes form the basis of this investigation. Diabetes was induced with alloxan in three groups of male mongrel dogs who were studied after 1 yr. In the initial experiment the tissue compartment volumes, determined with intravenous 51Cr EDTA as a marker, were found to be normal. Calculated cell sodium was increased to 32.8 +/- 2.6 mEq/kg cell H2O vs 18.7 +/- 1.1 in controls (p < 0.01). Cell potassium in diabetes was normal. In the second group, myocardial polyols were analyzed by gas-liquid chromatography. Inositol was diminished in diabetes to 0.61 +/- 23 microM/g of left ventricle, vs the respective control levels of 1.9 +/- 0.57 microM/g (p < 0.02). Sorbitol concentration was unaltered. Left ventricular sodium increments were not associated with altered tissue calcium. In group III the hypothesis that inhibition of Na(+)-K+ ATPase in diabetes might not elicit the expected alteration of K+ transport was assessed during intracoronary infusion of acetyl strophanthidin. No difference in cation responses from control was observed. It is postulated that a change in the conformation of Na(+)-K+ ATPase, with high affinity sodium binding sites facing the intracellular compartment, may render sodium less releasable from cell membrane.

Increased ventricular vulnerability in a chronic ethanol model despite reduced electrophysiologic responses to catecholamines.

An increased incidence of sudden death has been reported in chronic alcoholism. To assess electrical vulnerability of the heart, action potential responses, and the role of the sympathetic system, a well-nourished canine model has been studied intact under chloralose anesthesia after 1 year of ethanol consumption at 36% of caloric intake. Two alcoholic groups were compared with controls (Group 1). In Group 2 myocardial vulnerability was assessed after chronic EtOH and superimposed acute administration. In Group 3 basal vulnerability was related to circulating norepinephrine and release of neurohormone from the myocardium. Subsequently the responsiveness to catecholamine infusion was determined. To assess vulnerability an electrode catheter was placed in the right ventricular apex. The basal ventricular fibrillation threshold (VFT) was reduced to 27 +/- 3 ma in Group 2 versus 43 +/- 1.0 in Group 1. Acute infusion of ethanol in Group 2 further reduced the threshold. Group 3 had a reduced basal VFT. Baseline arterial plasma levels of norepinephrine were 8-fold higher and coronary venous levels 13 times higher in the alcoholic group than in Group 1. However, VFT was not responsive to infused epinephrine, compared with Group 1 controls. In vitro study of superfused ventricular tissue from Group 3 revealed that basal action potential amplitude, overshoot, and resting potential were comparable with normals. Basal repolarization time (90%) was 198 +/- 12 msec in Group 3 versus 215 +/- 6 msec in Group 1 (p less than 0.05). After acute EtOH, repolarization time was shortened to 170 +/- 8.6 in Group 1 at 90 mg% ethanol (p less than 0.002), with minimal further change up to 280 mg%.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol-induced brain changes in dogs.

We studied the neuropathologic effects of chronic alcohol ingestion on the brains of healthy, well-nourished, male mongrel dogs. Five experimental dogs were provided 36% of their calories as ethyl alcohol for 1 year. Following killing, their brains were weighed, photographed, sectioned, and processed for computerized morphometric determinations of ventricular size, cortical thickness, and neocortical neuron and glial cell populations. Compared with a similarly handled control group, the alcoholic dog brains showed lateral ventricular enlargement, cortical thinning in the temporal lobe only, and fewer glial cells in the temporal and frontal cortices. There were no statistically significant differences between the alcoholic and control groups in brain weight, frontal or parietal cortical thickness, or neocortical neuron populations. These results imply a disproportionate vulnerability of white matter to the damaging effects of alcohol with consequent lateral ventricular enlargement, and some regional variation in neocortical susceptibility to alcohol-induced cortical thinning and glial cell loss. In general, such changes are consistent with those described in neuroradiologic imaging studies of human alcoholics.

Alcohol and the cardiovascular system.

Ethanol has long been recognized as a toxic agent that has acute and chronic effects on cerebral and hepatic function. Over the past two decades important influences on the cardiovascular system have been either rediscovered or observed for the first time. The combined use of tobacco cigarettes and alcohol appears to increase the risk of many of these clinical abnormalities. While many individuals addicted to ethanol have subclinical abnormalities of the heart, somewhat less than a majority develop symptomatic cardiac problems. These include heart failure and arrhythmias. In addition to supraventricular arrhythmias that often normalize spontaneously, there is an increased incidence of sudden death that peaks at about 50 years of age in the alcoholic population. A significant degree of blood pressure elevation occurs in individuals who abuse alcohol. This appears to be transient and is normalized in most individuals during abstinence. The increased incidence of hemorrhagic and nonhemorrhagic stroke in middle age also appears to decline when alcohol abuse is interrupted. A preventive effect of mild to moderate drinking on coronary artery disease is, at present, equivocal, largely due to the question of appropriate controls.