Sarawak River Flow Behaviour after Matang Bypass Channel Construction during Low Tide Using InfoWorks River Simulation (RS)

Flood is occurring more frequently in Kuching nowadays due to the impact of climate change and rapid urbanization. The only discharge outlet for Sarawak River Basin currently is at Kuching Barrage and Shiplock. Sarawak State Government had decided to build Matang Bypass Channel from Sarawak River’s “Oxbow” to Batang Salak River for mitigating the flooding issues within Sarawak River Basin. Matang Bypass Channel had a bottom width of 250 m, 500 m reserve width and 8 Km in length. Flow behaviour with two discharge outlets during low tides are unknown yet. Therefore, this research is carried out to study Sarawak River flow behaviour after construction of Matang Bypass Channel using InfoWorks River Simulation (RS). Rainfall data used is January 2018. Four scenarios investigated are 1) Open two gates at Matang Bypass Channel opens and all gates at Kuching Barrage, 2) Open all gates at Matang Bypass Channel and Kuching Barrage, 3) Open gates at Matang Bypass Channel, but close all gates at Kuching Barrage, 4) Close all gates at Matang Bypass Channel, but open all gates at Kuching Barrage. Results revealed that when water gates are opened, sea water has the potential to backflow into Sarawak River basin through Kuching Barrage since sea level at Kuching Barrage discharge outlet is always 0.5 m higher than Matang Bypass Channel discharge outlet. When the gates at Matang Bypass Channel are fully opened and Kuching Barrage are closed, Kuching Barrage will retain the excess water and the river water will only be discharged into ocean through Matang Bypass Channel. In contrast, as the gates at Matang Bypass Channel are closed and at Kuching Barrage are fully opened, Matang Bypass Channel will store the excess water and river water will be discharged through Kuching Barrage alone.

Myocardial protection with pinacidil induced hyperpolarized arrest during cardiopulmonary bypass

Objective To investigate the myocardial protective effects of pinacidil induced hyperpolarized arrest and compare with those afforded by conventional depolarized hyperkalemic arrestMethods Eighteen dogs were equally divided into three groups: normothermic hyperpolarized group (Group A), hypothermic hyperpolarized group (Group B), and hyperkalemic group (Group C) Pinacidil (50μmol/L) containing 37℃ St Thomas solution (K+5mmol/L, 10ml/kg), pinacidil (50μmol/L, Sigma, USA) containing 4℃ St Thomas solution (K+ 5mmol/L, 10ml/kg) and 4℃ standard St Thomas solution (K+ 16mmol/L, 10ml/kg) were infused respectively through the aortic root after aorticclamping Heart arrest and its recovery, ultrastructure of the myocardium, the level of serum myocardial enzymes, and lipid peroxide and adenine cleotide of the myocardium were measuredHemodynamics during ischemia and after reperfusion were observedResults The percentages of normal mitochondria and glycogen did not change much during ischemia (except at 60 min) and after reperfusion in B Group, but declined markedly in Group C 30 min and 60 min after ischemia and 20 min after reperfusion (P<0.01) In Group A,they were lower than those of Group B before ischemia, but higher than those of Group C The recoveries of CO, SV, CI, LVSW, RVSW and MAP in Group B were significantly better than those in other two groups 15 min and 30 min after reperfusion (P<0.05and0.01, respectively) However, they were still better in Group A than those in Group C(P<0.05 and 0.01, respectively)The onset of heart arrest was faster in Groups C and B than that in Group A Highly elevated serum myocardial enzymes were observed 60 min after ischemia and 20 min after reperfusion in Group C, while they were only mild in the hyperpolarized groups, especially in Group B, and their recoveries were rapid Adenine nucleotides of the myocardium were better preserved in Group B than in other two groups 30 min, 60 min after ischemia, and 20 min after reperfusion (P<0.05 and 0.01, respectively)They were also much better in Group A than in GroupC(P<0.05and0.01,respectively)Lipid peroxide of the myocardium were significantly lower in Group B than in other groups 20 min after reperfusion (P<0.01),and they were lower in Group A than in Group C(P<0.05) Conclusions Myocardial protection for global ischemia during cardiopulmonary bypass (CPB) could be achieved with hyperpolarized heart arrest induced by pinacidil, an ATP sensitive potassium channel opener,especially in the hypothermic state The protection is weaker in normothermia but is still superior to that with traditional depolarized hyperkalemic arrest