Detection of myocardial ischaemia by epicardial accelerometers in the pig.

BACKGROUND: We describe a novel technique for continuous real-time assessment of myocardial ischaemia using a three-axis accelerometer. METHODS: In 14 anaesthetized open-chest pigs, two accelerometers were sutured on the left ventricle (LV) surface in the perfusion areas of the left anterior descending (LAD) and circumflex (CX) arteries. Acceleration was measured in the longitudinal, circumferential, and radial directions, and the corresponding epicardial velocities were calculated. Regional LV dysfunction was induced by LAD occlusion for 60 s. Global LV function was altered by nitroprusside, epinephrine, esmolol, and fluid loading. Epicardial velocities were compared with strain by echocardiography during LAD occlusion and with aortic flow and LV dP/dt(max) during interventions on global LV function. RESULTS: LAD occlusion induced ischaemia, shown by lengthening in systolic strain in the LV apical anterior region (P<0.01) and concurrent changes in LAD accelerometer circumferential velocities during systole (P<0.01) and during the isovolumic relaxation phase (P<0.01). The changes in accelerometer circumferential velocities during LAD occlusion were greater compared with the changes during the interventions on global function (P<0.01). For the LAD accelerometer circumferential velocities, sensitivity was 94-100% and specificity was 92-94% in detecting ischaemia. CONCLUSIONS: Myocardial ischaemia can be detected with epicardial three-axis accelerometers. The accelerometer had the ability to distinguish ischaemia from interventions altering global myocardial function. This novel technique may be used for continuous real-time monitoring of myocardial ischaemia during and after cardiac surgery.

Role of nutrient HCO3(-) in protection of amphibian gastric mucosa.

In in vitro bullfrog fundic mucosa inhibited with 10(-3) M metiamide and exposed to a luminal pH of 2 a progressive slow decline in potential difference (PD) and short-circuit current (Isc) and a rise in resistance (R) were observed when the nutrient solution (N) contained 18 mM HCO3(-), but these changes were restored by an N containing 50 mM HCO3(-). Substitution of PO4(3-) or N-tris(hydroxymethyl)-methyl-2-aminoethanesulfonic acid for NHO3(-) in N caused a rapid drop in PD and Isc in inhibited tissues, changes that could be prevented by 10(-4) M histamine. Ulceration occurred more frequently in metiamide-inhibited gastric sacs exposed to artificial gastric juice with an N of 18 mMHCO3(-) than with 50 mM HCO3(-), but histamine prevented ulceration in the 18 mM HCO3(-) solution. JnetCl approximated Isc under most experimental conditions in inhibited mucosa and was reduced dramatically as were both Jn leads to sCl and Js leads to nCl when HCO3(-) was removed from N. In histamine-stimulated tissues, removal of nutrient HCO3(-) did not influence Cl- transport. Our results are consistent with the proposal that HCO3(-) in N supports normal Cl- flux and that the alkaline tide of actively secreting oxyntic cells can do the same in the absence of ambient HCO3(-).

Effect of 16-16-dimethyl-prostaglandin E2 on ulceration of isolated amphibian gastric mucosa.

In order to investigate the cytoprotective action of 16-16-dimethyl-prostaglandin E2 (16-16D), we studied its effect on sacs of isolated amphibian gastric mucosa known to ulcerate with high frequency in the absence of nutrient HCO3-. The actions of 16-16D, 2.85 X 10(-6) M, were also studied in an in vitro chamber. The incidence of ulceration in HCO3- -free nutrient media containing 10(-4) M histamine was significantly reduced by 16-16D. When artificial gastric juice (AGJ) was instilled into the lumen of the sac, protection occurred only after a pretreatment period of 60 min. Cytoprotection was not observed when active secretion of H+ was inhibited with 10(-3) M metiamide, and AGJ was placed in the lumen of the sac. In open sheets of fundus stimulated with 10(-4) M histamine, 16-16D did not influence H+ secretion. Isc was significantly higher than in control tissues. We conclude that 16-16D is cytoprotective in amphibian gastric mucosa by an action independent of changes in acid secretion or in blood flow. In addition, our studies suggest that 16-16D may increase the availability to the surface cells of nutrient HCO3- produced by actively secreting oxyntic cells.