Accuracy of the Unipolar Electrogram for Identification of the Site of Origin of Ventricular Activation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73873/1/j.1540-8167.1997.tb00619.x.pd

Site of Accessory Pathway Block After Radiofrequency Catheter Ablation in Patients with the Wolff-Parkinson-White Syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73717/1/j.1540-8167.1994.tb01111.x.pd

Transverse propagation of action potentials between parallel chains of cardiac muscle and smooth muscle cells in PSpice simulations

BACKGROUND: We previously examined transverse propagation of action potentials between 2 and 3 parallel chain of cardiac muscle cells (CMC) simulated using the PSpice program. The present study was done to examine transverse propagation between 5 parallel chains in an expanded model of CMC and smooth muscle cells (SMC). METHODS: Excitation was transmitted from cell to cell along a strand of 5 cells not connected by low-resistance tunnels (gap-junction connexons). The entire surface membrane of each cell fired nearly simultaneously, and nearly all the propagation time was spent at the cell junctions, the junctional delay time being about 0.3 – 0.5 ms (CMC) or 0.8 – 1.6 ms (SMC). A negative cleft potential (V(jc)) develops in the narrow junctional clefts, whose magnitude depends on the radial cleft resistance (R(jc)), which depolarizes the postjunctional membrane (post-JM) to threshold. Propagation velocity (θ) increased with amplitude of V(jc). Therefore, one mechanism for the transfer of excitation from one cell to the next is by the electric field (EF) that is generated in the junctional cleft when the pre-JM fires. In the present study, 5 parallel stands of 5 cells each (5 × 5 model) were used. RESULTS: With electrical stimulation of the first cell of the first strand (cell A1), propagation rapidly spread down that chain and then jumped to the second strand (B chain), followed by jumping to the third, fourth, and fifth strands (C, D, E chains). The rapidity by which the parallel chains became activated depended on the longitudinal resistance of the narrow extracellular cleft between the parallel strands (R(ol2)); the higher the R(ol2 )resistance, the faster the θ. The transverse resistance of the cleft (R(or2)) had almost no effect. Increasing R(jc )decreases the total propagation time (TPT) over the 25-cell network. When the first cell of the third strand (cell C1) was stimulated, propagation spread down the C chain and jumped to the other two strands (B and D) nearly simultaneously. CONCLUSIONS: Transverse propagation of excitation occurred at multiple points along the chain as longitudinal propagation was occurring, causing the APs in the contiguous chains to become bunched up. Transverse propagation was more erratic and labile in SMC compared to CMC. Transverse transmission of excitation did not require low-resistance connections between the chains, but instead depended on the value of R(ol2). The tighter the packing of the chains facilitated transverse propagation

Genetic Background Can Result in a Marked or Minimal Effect of Gene Knockout (GPR55 and CB2 Receptor) in Experimental Autoimmune Encephalomyelitis Models of Multiple Sclerosis

PMCID: PMC379391

Vitamin D in the general population of young adults with autism in the Faroe Islands

Vitamin D deficiency has been proposed as a possible risk factor for developing autism spectrum disorder (ASD). 25-Hydroxyvitamin D3 (25(OH)D3) levels were examined in a cross-sectional population-based study in the Faroe Islands. The case group consisting of a total population cohort of 40 individuals with ASD (aged 15–24 years) had significantly lower 25(OH)D3 than their 62 typically-developing siblings and their 77 parents, and also significantly lower than 40 healthy age and gender matched comparisons. There was a trend for males having lower 25(OH)D3 than females. Effects of age, month/season of birth, IQ, various subcategories of ASD and Autism Diagnostic Observation Schedule score were also investigated, however, no association was found. The very low 25(OH)D3 in the ASD group suggests some underlying pathogenic mechanism

Effect of transverse gap-junction channels on transverse propagation in an enlarged PSpice model of cardiac muscle

BACKGROUND: In previous PSpice modeling studies of simulated action potentials (APs) in parallel chains of cardiac muscle, it was found that transverse propagation could occur between adjacent chains in the absence of gap-junction (gj) channels, presumably by the electric field (EF) generated in the narrow interstitial space between the chains. Transverse propagation was sometimes erratic, the more distal chains firing out of order. METHODS: In the present study, the propagation of complete APs was studied in a 2-dimensional network of 100 cardiac muscle cells (10 × 10 model). Various numbers of gj-channels (assumed to be 100 pS each) were inserted across the junctions between the longitudinal cells of each chain and between adjacent chains (only at the end cells of each chain). The shunt resistance produced by the gj-channels (R(gj)) was varied from 100,000 MΩ (0 gj-channels) to 1,000 MΩ (10 channels), 100 MΩ (100 channels) and 10 MΩ (1,000 channels). Total propagation time (TPT) was measured as the difference between the times when the AP rising phase of the first cell (cell # A1) and the last cell (in the J chain) crossed 0 mV. When there were no gj-channels, the excitation was transmitted between cells by the EF, i.e., the negative potential generated in the narrow junctional clefts (e.g., 100 Å) when the prejunctional membrane fired an AP. For the EF mechanism to work, the prejunctional membrane must fire a fraction of a millisecond before the adjacent surface membrane. When there were many gj-channels (e.g., 100 or 1,000), the excitation was transmitted by local-circuit current flow from one cell to the next through these channels. RESULTS: TPT was measured as a function of four different numbers of transverse gj-channels, namely 0, 10, 100 and 1,000, and four different numbers of longitudinal gj-channels, namely 0, 10, 100 and 1,000. Thus, 16 different measurements were made. It was found that increasing the number of transverse channels had no effect on TPT when the number of longitudinal channels was low (i.e., 0 or 10). In contrast, when the number of longitudinal gj-channels was high (e.g., 100 or 1,000), then increasing the number of transverse channels decreased TPT markedly. CONCLUSION: Thus, complete APs could propagate along a network of 100 cardiac muscle cells even when no gj-channels were present between the cells. Insertion of transverse gj-channels greatly speeded propagation through the 10 × 10 network when there were also many longitudinal gj-channels