Absence Of Microbubbles Research Articles

Spectral Normalization for Ultrasonic Contrast Microbubble Detection

Ultrasonic contrast agents consisting of microbubbles are used to assess tissue perfusion. The microbubbles are highly reflective and nonlinear and thus produce harmonics that are stronger than those from tissues. However, the magnitude of harmonic signals resulting from a region with microbubbles also depends on the acoustic pressure of incident ultrasound and the attenuation of intervening tissues in the ultrasound path. Therefore, the harmonic magnitude, as used in traditional harmonic imaging, may not be a reliable indicator of the presence or absence of microbubbles, and hence, tissue perfusion. To compensate for these effects, we present two parameters defined as the ratio of the harmonic to the fundamental component (HFR) and the ratio of the harmonic to squared fundamental (HSFR). A simplified model is used to illustrate the usefulness of these two parameters. Experiments show that both parameters improve detection of microbubbles and that HSFR performs better than HFR.

A study on premature ventricular contractions caused byultrasound exposure with microbubbles using cultured ventricular muscle cells

It has been shown that diagnostic ultrasound examination using a contrast agent cancause premature ventricular contractions (PVCs). In this study, we investigated a usefulness ofa new technique using cultured cardiac myocytes to study mechanisms of PVC production.Cardiac myocytes were isolated from neonatal rats and cultured on a cover glass. The coverglass was attached to an observation chamber in which it was possible to observe changes inmyocytes during ultrasound exposure. In the experiments, cardiac myocytes were exposed topulsed ultrasound in the presence and absence of microbubbles. The pressure amplitudes(peak-negative pressures) were set at 5 steps, −0.28, −0.55, −0.73, −0.92 and −1.1 MPa,and threshold pressure to produce a PVC was recorded. The results showed that the presence ofmicrobubbles attached to a cell reduces threshold pressure for producing PVCs, and it wasconcluded that our method is useful for studying the mechanisms of PVC production.

Microbubble-Induced Phospholipase C Activation Does not Correlate with Platelet Aggregation

The effect of nitrogen-(N2-)microbubbles on platelets resembles that of common platelet agonists with respect to aggregation and secretion, but is considerably slower and is poorly inhibited by aspirin. This paper reports the effect of microbubbles on platelet phospholipase C activity in gelfiltered human platelets prelabelled with [32P]Pi ([32P]-GFP). The experiments were run in the presence of an ADP scavenging system in order to rule out effects of ADP. Stimulation of [32P]-GFP for 30 min with microbubbles caused a significant reduction in single platelets (p < 0.0004) and a significant increase in 32P-activity in the phosphatidic acid (PA) fraction (p < 0.02). Epinephrine potentiated the microbubble-induced reduction in single platelets (p < 0.05), but did not enhance the amount of 32P in the platelet [32P]PA fraction. The 32P-radioactivity in the PI-fraction increased with time to a similar extent when [32P]-GFP was stirred for 30 min in absence of microbubbles as it did after 30 min of agonist exposure. There were no significant changes in the [32P]PIP and [32P]PIP2 fractions. Aspirin abolished the microbubble-induced increase in 32P-activity in the PA fraction, but had no significant effect on the reduction in single platelets. Aspirin had a small but significant, reducing effect on platelet aggregation induced by a combination of epinephrine and microbubbles (p < 0.05). With epinephrine, however, aspirin did not completely abolish the increase in [32P]-PA. It is concluded that microbubbles alone cause platelets to aggregate by a novel mechanism that operates independent of cyclooxygenase-dependent arachidonic acid metabolites and phospholipase C activation.