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Objective To determine the role of membrane potential and intracellular calcium kinetic changes in producing vascular hyporeactivity during severe hemorrhagic shock Methods Rats were subjected to hemorrhagic shock (HS) for 2 hours The spinotrapezius muscle was prepared for microscopy and the responses of arterioles in the muscle to norepinephrine(NE) were tested The resting membrane potentials of isolated arterial strips were measured with a microelectrode Membrane potential and intracellular Ca 2+ ([Ca 2+ ]i) changes in isolated arteriolar smooth muscle cells (ASMCs) were determined with fluorescent probes and a confocal microscopy Results The arteriolar resting membrane potential was decreased from -36 7±6 3?mV in control to -29 2±5 3?mV concurrent with the increase of vasoreactivity to NE at 20?minutes after HS At 120?minutes post HS, the resting potential hyperpolarized to -51 9±9 1?mV, and NE stimulated [Ca 2+ ]i increase was reduced to 50% of the control values during the appearance of arteriolar hyporeactivity, i e the NE threshold of the arteriolar response increased 15 fold 2?hours after the onset of hemorrhage as compared with normal animals The state of vasoreactivity was closely related to the resting potential of vascular smooth muscle in hemorrhagic shock, with a correlation coefficient of 0 96 Treatment with glybenclamide, a selective blocker of ATP sensitive K + (K ATP ) channels, decreased the resting potential, increased NE stimulated [Ca 2+ ]i increase, and partially restored vasoreactivity in severe hemorrhagic shock Conclusion The results suggested that membrane hyperpolarization and the reduction of NE stimulated [Ca 2+ ]i increase in smooth muscle cells appeared to contribute to the vascular hyporeactivity in hemorrhagic shock The mechanism is likely to involve in K ATP channels
Objective To determine the role of membrane potential and intracellular calcium kinetic changes in producing vascular hyporeactivity during severe hemorrhagic shock Methods HS were for hemorrhagic shock (HS) for 2 hours The spinotrapezius muscle was prepared for microscopy and the responses of arterioles in the muscle to norepinephrine (NE) were tested The resting membrane potentials of isolated arterial strips were measured with a microelectrode Membrane potential and intracellular Ca 2+ ([Ca 2+] i) changes in isolated arteriolar smooth muscle cells (ASMCs) were determined with fluorescent probes and a confocal microscopy Results The arteriolar resting membrane potential was decreased from -36 7 ± 6 3? mV in control to -2 29 2 ± 5 3? mV concurrent with the increase of vasoreactivity to NE at 20? minutes after HS At 120? minutes post HS, the resting potential hyperpolarized to -51 9 ± 9 1? MV, and NE stimulated [Ca 2+] i increase was reduced to 50 % of the control values during the appearance of arteriolar hyporeactivity, ie the NE threshold of the arteriolar response increased 15 fold 2? hours after the onset of hemorrhage as compared with normal animals The state of vasoreactivity was closely related to the resting potential of vascular smooth muscle in hemorrhagic shock, with a correlation coefficient of 0 96 Treatment with glybenclamide, a selective blocker of ATP sensitive K + (K ATP) channels, decreased the resting potential, increased NE stimulated [Ca 2+] i increase, and partially restored vasoreactivity in severe hemorrhagic shock Conclusion The results suggested that membrane hyperpolarization and the reduction of NE stimulated [Ca 2+] i increase in smooth muscle cells Established to suggest to the vascular hyporeactivity in hemorrhagic shock The mechanism is likely to involve in K ATP channels