Insights into the co-localization of magnitude-based versus direction-based indicators of disturbed shear at the carotid bifurcation.

The observed co-localization of disturbed flow and lesion prevalence at predisposed districts such as the carotid bifurcation has led to the identification of the wall shear stress (WSS) as biomechanical localizing factor of vascular dysfunction. In particular, a proatherogenic role is attributed to low and oscillatory WSS. However, the endothelial cells (ECs) are exposed to a complex hemodynamic milieu that can be only partially described by low/oscillatory WSS. Recently, in the attempt to close this gap, descriptors of the complex multidirectional nature of WSS have been proposed, i.e., the axial component of WSS (aligned with the vessel׳s centerline, to quantify flow reversal), and the transverse WSS (transWSS, quantifying the WSS component orthogonal to the cycle averaged WSS direction). Here we explore the relationship between recently-proposed indicators quantifying WSS multidirectionality and "established" WSS-based hemodynamic descriptors of low/oscillatory WSS, in a representative sample (N=46) of subject-specific computational hemodynamics models of ostensibly normal carotid bifurcations. To do it, we quantitatively assess the co-localization of those descriptors at the luminal surface, aiming at providing connections among the peculiar hemodynamic features captured by the different descriptors. According to our findings: (1) regions of flow reversal are moderately co-localized with low WSS; (2) high WSS oscillations (quantified by the oscillatory shear index, OSI) at the carotid bulb are prevalently aligned with the main flow, where flow reversal is predominant; (3) regions where transWSS is high do not co-localize with the other descriptors. We suggest that the investigated WSS-based descriptors might represent different hemodynamic disturbances with different impact on ECs homeostasis, potentially being part of WSS phenotypes more effective in localizing the map of vascular atherosclerotic lesions.

Nerve communication between the glossopharyngeal nerve, external carotid plexus and the superficial cervical ansa: human autopsy case.

The authors encountered a very rare human autopsy case in which the supernumerary branch of the glossopharyngeal nerve and a nerve branch arising from the external carotid plexus communicated with the superficial cervical ansa. This anomaly was observed on the left side of a 71-year-old male cadaver during the gross anatomical seminar at Niigata University in 2004. The nerve fascicle and fiber analyses indicated that the supernumerary branch of the glossopharyngeal nerve separated cranial to the branches to the pharyngeal constrictor muscles, carotid sinus and stylopharyngeal muscle and sent the nerve fibers to the muscular branches to the platysma and the cutaneous branches to the cervical region. Additionally, it was shown that the branch arising from the external carotid plexus sent the nerve fibers to the cutaneous branch to the cervical region. Although the external carotid plexus is primarily postganglionic sympathetic fibers originating from the superior cervical ganglion, the vagus and glossopharyngeal nerves gave off branches connecting to the plexus, and therefore it was not possible to determine the origins of this branch of the external carotid plexus. The present nerve fascicle analysis demonstrates that the supernumerary branch of the glossopharyngeal nerve, which innervated the platysma, did not share any nerve components with the branches to the pharyngeal constrictor muscles, carotid sinus and stylopharyngeal muscle, suggesting that this supernumerary branch may be categorized into the different group from these well-known branches.

Inhibition of platelet-derived growth factor receptor tyrosine kinase inhibits vascular smooth muscle cell migration and proliferation.

Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) have been linked to vascular smooth muscle cell (SMC) migration and proliferation leading to atherosclerosis, restenosis, and chronic allograft rejection. This study describes the effect of CGP 53716, a specific PDGFR tyrosine kinase inhibitor on SMC proliferation and migration in vitro and in neointimal formation in vivo. CGP 53716 inhibited dose dependently tyrosine phosphorylation of both the known PDGFRs: the PDGFR-alpha and PDGFR-beta. In primary rat SMC cultures, a dose-dependent inhibition of PDGF-AA and PDGF-BB induced migration, and tritiated thymidine incorporation of SMC was seen at nontoxic concentrations. After rat carotid artery ballooning injury in vivo, the migration of alpha-actin-positive cells on the luminal side of internal elastic lamina was decreased with 50 mg x kg(-1) x day(-1) of CGP 53716 from 38 +/- 10 (control group) to 4 +/- 2 (P<0.0001, Mann-Whitney U test, N=18). CGP 53716 did not inhibit the number of replicating bromodeoxyuridine (BrdU)-incorporating cells in the intima, media, or adventitia during BrdU labeling at 0-96 postoperative h, though it inhibited significantly (P<0.01) the replication of medial and intimal cells from 93 h onward. Intima/media ratio was inhibited by 40% after 14 days in the CGP 53716-treated group (P=0.028) after rat aortic denudation. The results indicate that inhibition of the PDGFR tyrosine kinase inhibits SMC migration and proliferation in vitro, SMC migration, and, to a lesser extent, proliferation after ballooning injury in vivo, confirming a causal role for activation of the PDGFR and the formation of neointimal lesions.

Ultrastructural characteristics of glomus cells in the external carotid artery during larval development and metamorphosis in bullfrogs, Rana catesbeiana.

Electron microscopic observations of the external carotid artery in the larvae of the bullfrog, Rana catesbeiana, showed that glomus cells are present in the subendothelial stroma of the septum between the expanded region of the external carotid artery and the carotid arch. There were some differences in the ultrastructure of the glomus cells at each stage of larval development. At the early stages (stages I, III, V, X), most glomus cells were isolated and free from the covering of a supporting cell. The cytoplasm of the glomus cells contained fewer dense-cored vesicles. No synaptic junctions were observed. At the middle stages (stages XV, XX, XXI), some glomus cells showed a tendency to form small clusters. Between adjacent cells in a cluster, gap junctions were often observed. The number of dense-cored vesicles increased remarkably. Intimate apposition of the glomus and smooth muscle cells (g-s connection) was also observed. Nerve terminals containing clear vesicles were observed in synaptic contact with glomus cells at this phase. At the metamorphic climax (stages XXII-XXV), in addition to g-s connections, the glomus cells made intimate apposition to the cells around the glomus cells. The afferent synapses described in other amphibians were not encountered in this study. These findings suggest that the glomus cells at the early stages of development are nonfunctional, the vascular regulation via the g-s connection starts at the middle stages, and the chemoreception starts after metamorphosis.

Distribution of carotid body type I cells and other periadventitial type I cells in the carotid bifurcation regions of the rabbit.

The distribution of carotid body type I and periadventitial type I cells in the carotid bifurcation regions was investigated unilaterally in seven and bilaterally in two New Zealand White rabbits. Carotid body type I cells occurred in close proximity to the wall of the internal carotid artery immediately rostral to the carotid bifurcation, within a division of connective tissue with definable but irregular borders. Caudally, and separate from the main mass of carotid body type I cells, isolated groups of periadventitial type I cells lay freely in the connective tissue around the internal carotid artery and alongside the carotid bifurcation and common carotid artery. A overall picture of the carotid body in the rabbit was reconstructed and the occurrence and significance of periadventitial type I cells discussed.