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Although previous studies report a reduction in myocardial volume during systole, myocardial volume changes during the cardiac cycle have not been quantitatively analyzed with high spatiotemporal resolution. We studied the time course of myocardial volume in the anterior mid-left ventricular (LV) wall of normal canine heart in vivo (n = 14) during atrial or LV pacing using transmurally implanted markers and biplane cineradiography (8 ms/frame). During atrial pacing, there was a significant transmural gradient in maximum volume decrease (4.1, 6.8, and 10.3% at subepi, midwall, and subendo layer, respectively, P = 0.002). The rate of myocardial volume increase during diastole was 4.7 [+ or -] 5.8, 6.8 [+ or -] 6.1, and 10.8 [+ or -] 7.7 ml*[min.sup.-l]*[g.sup.-l], respectively, which is substantially larger than the average myocardial blood flow in the literature measured by the microsphere method (0.7-1.3 ml*[min.sup.-1]*[g.sup.-1]). In the early activated region during LV pacing, myocardial volume began to decrease before the LV pressure upstroke. We conclude that the volume change is greater than would be estimated from the known average transmural blood flow. This implies the existence of blood-filled spaces within the myocardium, which could communicate with the ventricular lumen. Our data in the early activated region also suggest that myocardial volume change is caused not by the intramyocardial tissue pressure but by direct impingement of the contracting myocytes on the microvasculature. myocardial structure; ventricular pacing; mechanical dyssynchrony

A new regime for silica glass machining for micro-optical fabrication applications, which uses pulsed C[O.sub.2] laser radiation in the 2.5-100-[micro]s pulse width region that has been generated by an acousto-optic modulator, is investigated. A filamentary melt ejection process that generates fibers and significant melt displacement limits machining quality below 30-[micro]s pulse width. Ablation and melt ejection thresholds are quantified relative to pulse width, and the region from 30 to 50 [micro]s is identified for low-threshold, smooth machining without melt displacement and ejection effects.

A quantitative device was developed to analyz the cellular and molecular mechanisms of mechanotransduction in relation to homogeneous equibiaxial strain in cultured cells. The practical experimental device that can produce equibiaxial strains of 0-10% is composed of a plating area and a multiwell device with seven 10-mm. diameter wells. The biocompatible device can be utilized in experiments that are characterized by multiple treatments, small sample sizes and conservation of reagents.

The intervention of hypertrophic response to angiotensin II (ANG II) in the heart of rat is controlled by the cardiac fibroblasts. The ANG II receptors situated on neonatal rat cardiac fibroblasts (NF) excite NF to generate transferable factors which follows in stimulation of hypertrophy of neonatal rat cardiac myocytes (NM). For experimental observations, cultured NF and NM are used.

Gloss, Bernd, Sonia Villegas, Francisco J. Villarreal, Anselmo Moriscot, and Wolfgang H. Dillmann. Thyroid hormone-induced stimulation of the sarcoplasmic reticulum [Ca.sup.2+] ATPase gene is inhibited by LIF and IL-6. Am J Physiol Endocrinol Metab 278: E738-E743, 2000.--We investigated the effects of the leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) on 3,3', 5-triiodo-L-thyronine, or thyroid hormone ([T.sub.3])-stimulated sarcoplasmic reticulum [Ca.sup.2+] ATPase (SERCA2) gene expression on cultured neonatal rat cardiac myocytes. A reduction of [T.sub.3] induced increases in SERCA2 mRNA levels after co-treatment with LIF or IL-6. To investigate for the molecular mechanism(s) responsible for the blunted gene expression, a 3.2-kb SERCA2 promoter construct containing a reporter gene was transfected into cardiac myocytes. [T.sub.3] treatment stimulated transcriptional activity twofold, whereas co-treatment with [T.sub.3] and either of the cytokines caused an inhibition of [T.sub.3]-induced SERCA2 transcriptional activity. A [T.sub.3]-responsive 0.6-kb SERCA2 construct also showed a similar inhibition by cytokines. Cytokine inhibition of SERCA2 transcriptional activity was also evident when a 0.6-kb SERCA2 mutant, [T.sub.3]-unresponsive promoter construct was used. Treatment with [T.sub.3] and cytokines showed a significant decrease in transcription when a reporter construct was used that was comprised of direct repeats of SERCA2 thyroid response element I. These data provide evidence for cytokine-mediated inhibitory effects on the SERCA2 promoter that may be mediated by interfering with [T.sub.3] action. cardiac hypertrophy; heart failure; contraction; relaxation; cytokines