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The mechanism of local metabolic regulation of coronary blood flow is still unclear. It is still unknown which control system- an \open-loop feedback control\" or a \"close-loop control\" - operates in the coronary circulation and whether common mechanisms exist in this control. To separate the putative chemicals proposed to be physiological regulators in the coronary bed the time courses of coronary resistance change in response to either increased cardiac work or hypoxia have been examined before and after a ‚àövº and adenosine inhibition. An acute open-chest sheep model was used for this investigation. The sheep were anaesthetised with sodium pentobarbitone and instrumented for circumflex coronary artery and pulmonary artery flows left ventricular proximal aortic and coronary sinus pressure. Continuous coronary sinus oxygen saturation was measured by a fibre optic technique. Blood samples from coronary sinus and proximal aorta were analysed for blood gases Na+ and K+. An occluding band was placed around the proximal aorta to produce variable increments of aortic pressure for variable periods. Low oxygen gases (5? 5�2 and 90%N2) were used to produce systemic hypoxia. Phentolamine propranalol and 8-phenyltheophylline were used as a ‚àövº and adenosine blockers respectively and nonadrenaline and isoprenaline (injected into left ventricle) and intra-coronary injection of adenosine were used to test the efficacy of the blockers. Continuous coronary resistance was calculated throughout each intervention. The recovery of coronary resistance to normal after the change of the afterload of the left ventricle had a constant half life of 4.7¬¨¬±0.2 seconds. The half life was not related to either the degree or the duration of increased work. a ‚àövº and adenosine inhibitors did not alter the half life but produced more profound changes in coronary resistance due to increased cardiac work. The half life of exogenous adenosine was about 26 seconds. During the increase of aortic pressure the coronary sinus oxygen saturation varied significantly both above and below the steady state unpredictably but with systemic hypoxia there was vasodilation during which the oxygen level in the coronary sinus was closely linked to coronary resistance with a small \"hysteresis\" when the hypoxia was reversed. After adenosine blockade the coronary resistance and oxygen supply were more closer linked. The results suggest an open loop control system with a short acting mediator whose half life is the same for varying periods and degrees of increased work but very much shorter than that of adenosine. The metabolic control of coronary flow is not dependent on the oxygen requirements of the muscle. Multiple factors may involved in the local coronary vasoregulation. Current data do not support adenosine as the common factor in metabolic vasodilation."

Additional file 5 : Table S5. Repeat number of 24-loci MIRU-VNTR loci in MTB isolates of clades BSP2 and TSL6.

Additional file 3 : Table S3. The 24-loci MIRU-VNTR data of 2161 isolates for MST building.

Additional file 2 : Table S2. The Spoligotype International Type (SIT) information.

Additional file 1 : Table S1. The source of available data in this study.

Additional file 4 : Table S4. Dataset used in the MST of T and Beijing families for the 1742 MTB isolates.

Minimally invasive esophagectomy (MIE) is increasingly accepted in the treatment of locoregional or advanced esophageal cancer. Laparoscopic-thoracoscopic Ivor-Lewis esophagectomy has been proved to be effective in treating middle and distal esophageal cancer, however, intrathoracic esophagogastric anastomosis is technically complex. When using circular stapler for making intrathoracic anastomosis in MIE, both transoral and transthoracic methods are frequently used for delivering the anvil into the esophageal stump. Herein, we report a new method to construct a thoracoscopic esophagogastric anastomosis by using a circular stapler: efficient purse-string stapling technique (EST). This technique is easy to handle and especially good to be used in patients with distal esophageal cancer or expanded esophageal cavity.