Changes of left ventricular pressure-diameter-velocity relations by alterations of heart rate in conscious dogs

Changes of left ventricular (LV) pressure-diameter-velocity relations by alterations in heart rate (HR) were investigated in 6 conscious dogs, instrumented with a pair of ultrasonic crystal probe, a micromanometer in LV and pacing electrodes on the left atrium. By atrial pacing the following four stages of HR were produced: stage (S)-I 112, S-II 134, S-III 158 and S-IV 179 bpm (mean HR). These alterations in HR were repeated before and during acute pressure loadings by methoxamine infusion. LV pressure-diameter and pressure-velocity relations were evaluated by the slope value of LV peak systolic pressure (LVSP)-end-systolic diameter, E (D) max, and by the ratio of changes in mV cf (mean velocity circumferential fiber shortening) and LVSP before and during pressure loading, delta mVcf/delta LVSP, respectively. The average of E(D) max at each stage of HR was 9.45, 12.63, 12.59, 11.22 mmHg/mm, and delta mVcf/delta LVSP was -0.009, -0.006, -0.007, -0.009 circ./sec.mmHg, respectively. E(D) max increased more at S-II and S-III than at S-I, and reversely, E(D) max decreased more at S-IV than at S-II. Similarly, delta mVcf/delta LVSP increased more at S-II than at S-I and decreased more at S-IV than at S-II, while delta LVSP and delta EDD (end-diastolic diameter) were not different between stages. These changes in E(D) max and delta mVcf/delta LVSP presented the mountainous pattern effected by alterations in HR, whose changes were almost similar to that of LV peak positive dp/dt and mVcf before pressure loading. Thus, E(D) max is augmented by an increase in HR, which suggests the Bowditch-effect. Reversely, a decrease in E(D) max at a higher rate indicates a depressed inotropic state. E(D) max is dependent on HR and is a sensitive indicator of the contractility of LV.     

Abnormal accessory mitral leaflet simulating left ventricular outflow tract tumor

This is a case report of an uncommon form of subaortic stenosis caused by an abnormal accessory mitral leaflet simulating a left ventricular outflow tract tumor. A 5-year-old boy with a systolic heart murmur underwent cardiac catheterization which demonstrated a subaortic stenosis with a 90 mmHg peak systolic pressure gradient. Angiography showed a tumor-like structure in the left ventricular outflow tract. At operation this mass was found to be an abnormal bulky accessory mitral leaflet. Resection of this deformed leaflet was carried out successfully.     

Identification of small subunit of serine palmitoyltransferase a as a lysophosphatidylinositol acyltransferase 1‐interacting protein

Lysophosphatidylinositol acyltransferase 1 (LPIAT1), also known as MBOAT7, is a phospholipid acyltransferase that selectively incorporates arachidonic acid (AA) into the sn‐2 position of phosphatidylinositol (PI). We previously demonstrated that LPIAT1 regulates AA content in PI and plays a crucial role in brain development in mice. However, how LPIAT1 is regulated and which proteins function cooperatively with LPIAT1 are unknown. In this study, using a split‐ubiquitin membrane yeast two‐hybrid system, we identified the small subunit of serine palmitoyltransferase a (ssSPTa) as an LPIAT1‐interacting protein. ssSPTa co‐immunoprecipitated and colocalized with LPIAT1 in cultured mammalian cells. Knockdown of ssSPTa decreased the LPIAT1‐dependent incorporation of exogenous AA into PI but did not affect the in vitro enzyme activity of LPIAT1 in the microsomal fraction. Interestingly, knockdown of ssSPTa decreased the protein level of LPIAT1 in the crude mitochondrial fraction but not in total homogenate or the microsomal fraction. LPIAT1 was localized to the mitochondria‐associated membrane (MAM), where AA‐selective acyl‐CoA synthetase is enriched. These results suggest that ssSPTa plays a role in fatty acid remodeling of PI, probably by facilitating the MAM localization of LPIAT1.     

Interferential Electric Stimulation Applied to the Neck Increases Swallowing Frequency

Swallowing disorders are a common complaint among the elderly. Recently, surface electrical stimulation applied to the neck region has received increased attention as a new modality to treat pharyngeal dysphagia. Previous reports used pulsed current at a frequency range of 1-120 Hz. Kilohertz-frequency alternating currents (ACs) have not been tested for treating dysphagia. Therefore, we evaluated the effects of interferential currents (IFCs), the most popular modality of amplitude-modulated kilohertz-frequency ACs in clinical practice, on the swallowing reflex in healthy subjects. We found that IFC stimulation at the sensory threshold with 50-Hz modulation significantly increased the number of swallows without any discomfort, but pure AC stimulation at the carrier frequency did not have a significant effect. There was no statistically significant difference in the time course of the number of swallows among 1,000-, 2,000-, 4,000-, and 6,000-Hz carrier frequencies. The number of swallows remained increased during the 15-min IFC stimulation, suggesting that IFC stimulation facilitates the swallowing reflex without adaptation, at least during this stimulation period. We suggest that an IFC stimulation or a low-frequency, modulated kilohertz AC stimulation, which would be more comfortable than pulsed currents, is an alternative stimulation mode for treating pharyngeal dysphagia.