[Effect of a major trauma and subsequent regeneration on the rate of metamorphosis in Xenopus laevis Daudin tadpoles].
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Biomedical subjects
Publications and source records attributed to J Michalowski.
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Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3-5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance.
Influence of sympathetic stimulation on the relation of ventricular pressure--directly recorded wall tension were investigated in the left ventricle of the opened chested dogs. It was shown, that despite the substantial decrease of the end-diastolic pressure, sympathetic stimulation did not result in decrease in the wall tension per unit pressure. Investigation of the diastolic circumferential segment length-diastolic pressure relation revealed, that diastolic compliance was increased under the sympathetic stimulation. The revelance of these findings to the regulation of the ventricular performance is discussed.
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Tension was measured within the outer layers of the left ventricular wall of the dog heart with the strain-gauge force transducer coupled to the wall at diastole without the distortion of its geometry. The transducer still attached to the wall or its segments was calibrated with the passive forces and with the known active force on the isolated, beating heart. The differences between the readings of the transducer and the calibrating force did not exceed 20% and in most experiments they were much smaller. The transducer was practically insensitive to the force perpendicular to the measured one. The proposed method seems to be more reliable than the formerly used by these and other authors.