The economic dimensions of integrating flood management and agri-environment through washland creation: a case from Somerset, England.

In many river floodplains in the UK, there has been a long history of flood defence, land reclamation and water regime management for farming. In recent years, however, changing European and national policies with respect to farming, environment and flood management are encouraging a re-appraisal of land use in rural areas. In particular, there is scope to develop, through the use of appropriate promotional mechanisms, washland areas, which will simultaneously accommodate winter inundation, support extensive farming methods, deliver environmental benefits, and do this in a way which can underpin the rural economy. This paper explores the likely economic impacts of the development of flood storage and washland creation. In doing so, consideration is given to feasibility of this type of development, the environmental implications for a variety of habitats and species, and the financial and institutional mechanisms required to achieve implementation.

Contrasting success in the restoration of plant and phytophagous beetle assemblages of species-rich mesotrophic grasslands.

Over the last 60 years changes to the management of species-rich mesotrophic grasslands have resulted in the large-scale loss and degradation of this habitat across Europe. Restoration of such grasslands on agriculturally improved pastures provides a potentially valuable approach to the conservation of these threatened areas. Over a four-year period a replicated block design was used to test the effects of seed addition (green hay spreading and brush harvest collection) and soil disturbance on the restoration of phytophagous beetle and plant communities. Patterns of increasing restoration success, particularly where hay spreading and soil disturbance were used in combination, were identified for the phytophagous beetles. In the case of the plants, however, initial differences in restoration success in response to these same treatments were not followed by subsequent temporal changes in plant community similarity to target mesotrophic grassland. It is possible that the long-term consequences of the management treatments would not be the establishment of beetle and plant communities characteristic of the targets for restoration. Restoration management to enhance plant establishment using hay spreading and soil disturbance techniques would, however, still increase community similarity in both taxa to that of species-rich mesotrophic grasslands, and so raise their conservation value.

Electrophysiological characteristics of repetitive ischemic preconditioning in the pig heart.

S-T segment changes have been cited as evidence for preconditioning in the human heart during repeated angioplasty inflations. Opening of preformed collaterals, however, could explain these observations. We have measured the profile of S-T segment and monophasic action potential (MAP) changes in a species with low collateralization. Open-chested pigs were subjected to two cycles of 8-min LAD occlusion and 8-min reperfusion prior to 60-min ischemia and 2-h reperfusion. Two epicardial ECGs and MAP were continuously recorded from the ischemic zone and one ECG from the normal zone. Flow was measured using Xenon washout. Infarct (IS) and risk zone (RZ) sizes were assessed after reperfusion in a subset of six pigs and confirmed profound protection with preconditioning (IS/RZ = 14 +/- 9% v 42 +/- 3% in controls, P < 0.05). S-T segment elevation was smaller early in the 2nd or 3rd (0-3 min) ischemic cycles than in the 1st. In contrast, in the 1st ischemic cycle, MAP duration after 3 min was reduced to 90 +/- 2% control and this was further reduced in the 2nd and 3rd ischemic episodes to 74 +/- 4% and 77 +/- 3% respectively. Thus, preconditioning increased APD shortening while simultaneously decreasing S-T segment elevation during the early minutes of ischemia. It therefore seems unlikely that the ability of preconditioning to limit S-T segment changes is related to limitations in APD shortening. All electrophysiological differences were lost later during ischemia. Collateral flow during the three ischemic cycles was 4.8 +/- 3.7, 5.8 +/- 2.3 and 5.6 +/- 2.9% (n = 5/grp, ns) respectively. Thus, in the absence of a significant increase in collateral flow. S-T segment and MAP changes provide an index of preconditioning but only during the first few minutes of occlusion. S-T segment changes observed during PTCA may therefore reflect genuine preconditioning in man although the contribution of ischemia-induced increases in collateral flow cannot be ignored.

Anti-arrhythmic protection by ischaemic preconditioning in isolated rat hearts is not due to depletion of endogenous catecholamines.

OBJECTIVES: The present study addresses whether the mechanism of anti-arrhythmic protection by ischaemic preconditioning involves depletion of myocardial catecholamines. METHODS: In a randomised series of studies isolated rat hearts, perfused with whole blood, underwent episodes of regional ischaemia and reperfusion induced with a snare around the left coronary artery. Control hearts (Group 1, n = 12) were subjected to 40 min aerobic perfusion, 30 min ischaemia and 10 min reperfusion. Preconditioned hearts (Group 2, n = 12) were subjected to 10 min aerobic perfusion, three cycles of ischaemia and reperfusion (5 min each), 30 min ischaemia and 10 min reperfusion. Cardiac rhythm was recorded continuously and arrhythmias quantified during the final periods of ischaemia and reperfusion. At the end of the experiment samples of right ventricular (RV; non-ischaemic) and left ventricular (LV; ischaemic territory) tissue were separated and frozen. In 5 additional groups (n = 6/group) tissue samples were taken after 10 min aerobic perfusion, after 10 min aerobic perfusion followed by 1, 2 or 3 preconditioning cycles and after 40 min of aerobic perfusion. All tissue samples were analysed for catecholamine content. RESULTS: Preconditioning resulted in reductions in the incidence of ischaemia-induced VF from 67% in Group 1 to 8% in Group 2, the incidence of ischaemia-induced VT from 100% to 17% and the number of ischaemia-induced VPBs from 246 +/- 25 to 59 +/- 19 (each P < 0.05). The mean content of noradrenaline and adrenaline was consistently higher in RV than LV tissue. Within the LV, however, neither preconditioning nor prolonged ischaemia had any significant effect upon tissue catecholamine content at any time in the experimental protocol. CONCLUSIONS: Depletion of myocardial catecholamines is not involved in the mechanism of anti-arrhythmic protection by ischaemic preconditioning in isolated rat hearts.

Preconditioning and reperfusion arrhythmias in the isolated rat heart: true protection or temporal shift in vulnerability?

OBJECTIVE: The relationship between arrhythmia severity during reperfusion and the duration of preceding ischaemia is bell shaped. Although ischaemic preconditioning can protect against reperfusion induced arrhythmias it is not clear if this is achieved by a true reduction in arrhythmia severity or by a temporal shift in the bell shaped relationship occurring as a consequence of increased ischaemic tolerance. METHODS: Isolated rat hearts (n = 12 per group) were Langendorff-perfused with whole blood from a support rat. Regional ischaemia and reperfusion were induced using a ligature around the left main coronary artery. Cardiac rhythm was recorded continuously. RESULTS: Repeated cycles of preconditioning (5 min ischaemia and 5 min reperfusion) led to a progressive reduction in the incidence of reperfusion induced ventricular fibrillation following 10 minutes of ischaemia (92%, 66%, 42%, and 8% following 0, 1, 2, and 3 cycles respectively). Three cycles of preconditioning reduced the incidence of reperfusion induced ventricular fibrillation after each of 10 (83% to 17%; p < 0.05), 15 (92% to 42%; p < 0.05), 20 (67% to 25%), 30 (33% to 0%), and 40 (25% to 0%) minutes of ischaemia. Preconditioning also led to a reduced incidence of reperfusion induced ventricular tachycardia following 10 minutes of ischaemia (100% to 42%; p < 0.05). There was no evidence of a temporal shift in the bell shaped relationships: peak incidences of reperfusion induced ventricular fibrillation and ventricular tachycardia each occurred after 15 minutes of ischaemia in both control and preconditioned groups. CONCLUSIONS: In isolated blood perfused rat hearts serial preconditioning cycles provide cumulative protection against reperfusion induced ventricular arrhythmias. This protection occurs over a wide range of ischaemic durations without altering the temporal relationship between the duration of ischaemia and arrhythmia severity. This may indicate that antiarrhythmic protection is not a consequence of anti-ischaemic mechanisms.

"Dose"-dependency and temporal characteristics of protection by ischaemic preconditioning against ischaemia-induced arrhythmias in rat hearts.

Brief episodes of ischaemia and reperfusion (preconditioning) can increase the resistance of the myocardium to ischaemic injury. We investigated the temporal characteristics of anti-arrhythmic protection by preconditioning. Rat hearts underwent regional ischaemia (+/- reperfusion) of the left coronary territory. Control isolated blood-perfused hearts underwent 40 min ischaemia; in the preconditioned groups this was preceded by one, two or three cycles of 5 min ischaemia and 5 min reperfusion. Control anaesthetized rats underwent 60 min ischaemia; this was preceded by three cycles of 3 min ischaemia and 3 min reperfusion in the preconditioned group. Preconditioning led to: (i) the abolition of ventricular fibrillation in both in vivo and in vitro preparations; (ii) a reduced incidence of ventricular tachycardia (from 100% to 8% in vitro and 100% to 25% in vivo); and (iii) a reduced incidence of ventricular premature beats (from 246 +/- 36 to 8 +/- 5 in vitro and 85 +/- 21 to 24 +/- 13 in vivo). In isolated hearts protection was proportional to the number of preconditioning cycles. Although preconditioning caused a dramatic reduction in the severity of arrhythmias it did not result in any significant alteration in their temporal profiles. We conclude that protection by preconditioning against ischaemia-induced arrhythmias is "dose"-dependent in rat hearts in vitro and results in an absolute reduction in the severity of ischaemia-induced arrhythmias rather than an alteration in their time-course, both in vivo and in vitro.

Early and late effects of leukopenic reperfusion on the recovery of cardiac contractile function. Studies in the transplanted and isolated blood-perfused rat heart.

BACKGROUND: Since there is considerable evidence that leukocytes contribute to tissue injury during ischemia and reperfusion, the present study was designed to: (1) determine whether reperfusion in vivo with leukopenic blood affords protection in a model of reversible hypothermic ischemia, (2) determine the duration of any protection, (3) characterize the relation between protection and duration of leukopenic perfusion, and (4) assess the effect of leukopenic reperfusion on myocardial glutathione content. METHODS AND RESULTS: Rat hearts (n = 12 per group) were excised, immediately arrested with an infusion (2 minutes at 4 degrees C) of St Thomas' cardioplegic solution, and subjected to 4 hours of global ischemia (4 degrees C). The hearts were then transplanted (1 hour additional ischemic time) into the abdomen of saline-treated or leukopenic recipients. Leukopenia was induced by intraperitoneal administration of mustine hydrochloride (2 mg/kg) 3 days before study. Hearts were then reperfused in situ for 1, 4, or 24 hours, after which they were excised and either processed for histological examination (n = 4 per group) or perfused aerobically with bicarbonate buffer for 20 minutes, and contractile function was assessed (n = 8 per group); at the end of this period, some hearts (n = 5 per group) were taken for metabolite analysis. After 1 hour of reperfusion, contractile function in the saline-treated control group was significantly reduced compared with aerobic controls that had not been subjected to ischemia (left ventricular developed pressure [LVDP], 108 +/- 5 vs 126 +/- 3 mm Hg at an end-diastolic pressure of 12 mm Hg; P < .05). However, in the hearts with leukopenic reperfusion, LVDP (119 +/- 2 mm Hg) was similar to that of aerobic controls. This benefit, however, was lost after 4 and 24 hours of reperfusion. Cardiac compliance was not influenced by leukopenia. Coronary flow recovered significantly better in the leukopenic hearts during the first 4 hours of reperfusion (11.8 +/- 0.5 vs 9.3 +/- 0.4 mL/min at 1 hour and 10.0 +/- 0.5 vs 8.0 +/- 0.4 mL/min at 4 hours, P < .05), but again this benefit was lost after 24 hours of reperfusion. The myocardial contents of reduced and oxidized glutathione after 1, 4, and 24 hours of reperfusion were similar in saline-treated and leukocyte-depleted animals. In additional studies, the period of ischemia was extended to 8 hours, and similar results were obtained, with improved recovery of contractile function and coronary flow but not cardiac compliance in the leukopenic group after 1 hour of reperfusion. In further studies with the isolated blood-perfused rat heart, ischemia was induced for 8 hours; this was followed first by reperfusion for 0, 2, 10, 30, or 60 minutes with leukopenic blood and then by perfusion with blood from saline-treated animals for 60, 58, 50, 30, or 0 minutes, respectively. Reperfusion with leukopenic blood for 2 minutes did not improve the recovery of LVDP (106 +/- 7 vs 96 +/- 10 mm Hg in controls; NS) but when continued for 10, 30, or 60 minutes resulted in significant improvements (137 +/- 5, 138 +/- 3, and 150 +/- 10 mm Hg, respectively). Although coronary flow tended to be greater in all leukopenic groups, by the end of 60 minutes of reperfusion, only those hearts reperfused with leukopenic blood for the entire reperfusion period showed a significant improvement (3.4 +/- 0.3 vs 2.5 +/- 0.2 mL/min in controls; P < .05). Histological studies revealed no intravascular aggregation of leukocytes or features of myocyte necrosis. CONCLUSIONS: Reperfusion with leukopenic blood accelerated the rate of recovery of cardiac function after reversible myocardial injury but did not lead to a sustained increase in the eventual extent of recovery. Reperfusion with leukopenic blood for the first 10 minutes of reflow is sufficient to obtain this benefit.

Preconditioning and post-ischaemic contractile dysfunction: the role of impaired oxygen delivery vs extracellular metabolite accumulation.

The aim of the present study was to identify components of ischaemia involved in the induction of preconditioning. Isolated rat hearts (n = 8 per group) were perfused with bicarbonate buffer. Following 10 min aerobic perfusion they were randomised and subjected to 5 min periods during which the perfusion conditions were: (i) normal aerobic perfusion (controls); (ii) zero flow ischaemia; (iii) low flow ischaemia (10% of control O2 delivery); (iv) hypoxia (10% of control O2 delivery); or (v) acidosis (pH 6.4). After these periods of "preconditioning", all hearts underwent 5 min aerobic perfusion followed by 40 min zero flow global ischaemia and 35 min reperfusion. Contractile function was measured at the beginning and at the end of the experiment. Despite profound differences in coronary flow during preconditioning, substantial and similar protection was observed in all groups preconditioned by transiently limiting oxygen delivery. Recovery of cardiac output was 66.7 +/- 6.3%, 58.7 +/- 5.1% and 62.6% +/- 3.3% in the zero flow, low flow and hypoxic groups, respectively, vs 31.0 +/- 3.0% in controls (all P < 0.05). In hearts subjected to acidosis there was no protection (recovery of cardiac output 38.1 +/- 2.7%). Impairment of oxygen delivery appears to be the principle component of ischaemia responsible for the induction of preconditioning. Metabolite accumulation appears to play no significant role.

The antiarrhythmic action of ischaemic preconditioning in rat hearts does not involve functional Gi proteins.

OBJECTIVE: Ischaemic preconditioning has been reported to be mediated by inhibitory G (Gi) proteins in rabbits; however, the mechanism of preconditioning in rats appears to differ from that in other species. The aim of this study was to determine whether functional Gi proteins are required for the antiarrhythmic action of preconditioning in rats. METHODS: Donor rats were randomised to receive pertussis toxin (25 micrograms.kg-1 intravenously) or saline. After 48 h the hearts were isolated and Langendorff perfused with blood from untreated support rats. Cardiac rhythm was recorded continuously. Ischaemia and reperfusion were induced by occluding and releasing a snare around the left coronary artery. Following 10 min of aerobic perfusion hearts were further randomised to: (1) control groups (n = 12 per group) which underwent a further 30 min of aerobic perfusion, or (2) preconditioned groups (n = 12 per group) which were subjected to three cycles of 5 min of ischaemia and 5 min of reperfusion. All hearts subsequently underwent 30 min of regional ischaemia and 10 min of reperfusion during which arrhythmias were quantified. RESULTS: In hearts not pretreated with pertussis toxin, preconditioning limited the severity of ischaemia induced arrhythmias. The incidence of ventricular tachycardia was reduced from 100% to 33% and the mean number of ventricular premature beats from 164(SEM 42) to 23(14) (each p < 0.05). Although pretreatment with pertussis toxin completely abolished the bradycardic response to both acetylcholine and adenosine (indicating functional blockade of Gi proteins), it did not significantly influence the degree of antiarrhythmic protection afforded by preconditioning. In pretreated hearts preconditioning reduced the incidence of ventricular tachycardia from 83% to 33% and the mean number of ventricular premature beats from 267(66) to 62(32) (each p < 0.05). CONCLUSIONS: The antiarrhythmic action of preconditioning in isolated blood perfused rat hearts does not require functional Gi proteins.

Initial experience with excimer laser angioplasty for coronary ostial stenoses.

The excimer laser has several potential advantages over conventional balloon angioplasty in the management of stenoses of the native coronary arteries and of the ostia of saphenous vein grafts. Its use in nine patients, eight of whom were classed as high risk, is described. Four lesions involved the ostia of saphenous vein grafts, three of protected left main stems, and two of native right coronary arteries. Stand alone laser was used in seven cases and laser with additional balloon angioplasty was used in two vein graft stenoses. Acute laser success was achieved in all cases, with a mean reduction of stenosis from 82% to 34% after laser alone and to 28% when balloon angioplasty was used as well. One patient died during laser angioplasty to a non-ostial lesion (procedural success rate 89%) and a second died ten weeks after the procedure. In one patient recurrent angina developed (clinical recurrence rate 25%) and restenosis was confirmed on angiography. Follow up angiography was also performed on the other six surviving patients, all of whom were symptom free and none of whom showed evidence of significant restenosis (restenosis rate 14%). With a mean follow up of 19.7 months the overall success rate was 67%.

Functional aortic coarctation caused by thrombosis within a thoracic aortic aneurysm.

A 67 year old male arteriopath presented with chest pain, a new systolic murmur at the lower left sternal border and loss of leg pulses. Mitral regurgitation and ventricular septal defect were excluded by echocardiographic colour flow Doppler mapping and right heart catheterisation. CT scanning demonstrated a leaking aneurysm of the descending thoracic aorta with stenosis of the proximal lumen due to atheroma and thrombus causing a functional coarctation. The findings were confirmed at surgery.