Establishment of a rabbit model of superior vena cava obstruction.

OBJECTIVE: To explore a method of establishing a rabbit model of superior vena cava obstruction (SVCO) by injecting VX2 tumor cell suspension transcutaneously under ultrasound guidance. METHODS: A suspension of VX2 tumor cells was prepared under sterile conditions. Fifteen adult healthy New Zealand White rabbits were enrolled in the experiment. Under ultrasound guidance, about 0.1 ml of the living tumor cell suspension was transcutaneously injected in front of the anterior wall of the right superior vena cava (SVC). The lumen, wall, blood flow of SVCs and adjacent tissues were examined with gray-scale and color Doppler ultrasonography, every 3 days starting from the 9th day after injection. Meanwhile, CT scanning and digital subtraction angiography (DSA) were also performed. The rabbits were dissected immediately after death and tissue samples were collected for pathologic examination. RESULTS: Fourteen out of 15 rabbits developed tumors that were located close to SVCs and/or SVCs cavity, which was shown by ultrasonography. The diameters of the tumors were 80.7 +/- 4.3 mm. These tumors grew close to SVCs area and resulted in compression and infiltration of SVCs. CT scanning and DSA confirmed the establishment of the SVCO model. The achievement rate of the SVCO model was 93.3%. No rabbit died of complications. CONCLUSION: A method of establishing a rabbit SVCO model by injecting VX2 tumor cell suspension under ultrasonographic guidance was established successfully, and it proved to be simple, effective and repeatable. The imaging characteristics of this model are in good accordance with those of SVCO in patients.     

Left superior vena cava, a remnant of embryological development

A 46-year-old Brugada syndrome patient underwent insertion of a dual-chamber implantable cardioverter- defibrillator (ICD), revealing a left-sided superior vena cava (SVC), (figure 1), running, characteristically, left from the sternum and flowing into the great cardiac vein. Following this course, the atrial lead was placed in the right atrium (RA) (figure 2, arrow, note dorsal position). The ventricular lead was inserted through the connecting anonymous vein between left and right SVC (figure 1, double arrow), into the right SVC and right ventricle (RV). The presence of a left superior vena cava results from the persistence of the embryonic left anterior cardinal vein. This anomaly is present in approximately 0.5% of the general population and in 3 to 5% of persons with other congenital heart defects, as established by autopsy.     

Refractoriness of the sheep superior vena cava myocardial sleeve

The cardiomyocytes in the superior vena cava (SVC) myocardial sleeve have distinct action potentials and ionic current profiles, but the refractoriness of these cells has not been reported. Using standard intracellular microelectrode techniques, we demonstrated in sheep that the effective refractory period (ERP) of the cardiomyocytes in the SVC (114.7 +/- 6.5 ms) is shorter than that in the inferior vena cava (IVC) (166.7 +/- 6.2 ms), right atrial free wall (RAFW) (201.0 +/- 6.0 ms) and right atrial appendage (RAA) (203.1 +/- 5.8 ms) (P < 0.05). The right atrial cardiomyocyte ERP was heterogeneously shortened by acetylcholine, a muscarinic type 2 receptor (M(2)R) agonist. After perfusion with 15 microM acetylcholine, the shortest ERP occurred in the SVC (the ERP in the SVC, IVC, RAFW and RAA was 53.6 +/- 2.7, 98.9 +/- 2.2, 121.8 +/- 6.0 and 109.7 +/- 5.1 ms, respectively; P < 0.05). Carbachol (1 microM), another M(2)R agonist, produced a similar effect as acetylcholine. Furthermore, we used methoctramine, a M(2)R blocker, 4-DAMP, a muscarinic type 3 receptor (M(3)R) blocker, and tropicamide, a muscarinic type 4 receptor (M(4)R) blocker to inhibit the acetylcholine-induced ERP shortening of SVC cardiomyocytes, and found that the 50% inhibitory concentration for methoctramine, 4-DAMP and tropicamide was 5.91, 45.72 and 80.34 nM, respectively. Therefore, we conclude that the sheep SVC myocardial sleeve is a unique electrophysiological region of the right atrium with the shortest ERP both under physiological condition and under cholinergic agonist stimulation. M(2)R might play a major role in the response of the SVC myocardial sleeve to parasympathetic nerve tone. The association between the distinct refractoriness in SVC and atrial fibrillation originating from the region deserves further investigation.     

Venous valves in the large branches of superior vena cava

In 97 human cadavers the valves of the following blood vessels were investigated with regard to their cusps and their sizes and positions: the internal jugular veins, the subclavian veins, the brachiocephalic veins, and the superior vena cava. The cusps of each of the valves, which consist of two or three parts, are neither always of equal size nor obligatorily sufficient. Unipartite valves may be sufficient as well as insufficient. Internal jugular veins: The inferior bulb of the internal jugular vein is provided with valves which in 6% of the cases consist of three parts, in 66% of two parts, and in 15% of only one cusp. The concave margins of most of them go down as far as the venous angle. The convex edges attached to the wall of the vein extend to a higher level on the right side than on the left. In 13% there do not exist any valves. Varieties are described separately in this paper. Subclavian veins: Valves are found along the length of the vessel. Only few of them reach the venous angle. In rare cases there exist two valves: one at the beginning, the other at the end of the subclavian vein. In 4% of the cases the valves consist of three, in 75% of two cusps. In 12% they are unipartite. In 9% there are no valves to be found. The right side is more often without valves than the left. Brachiocephalic veins: Only a minority of these vessels is provided with valves. Most of these consist of one cusp, are insufficient, and are situated in the left innominate vein.(ABSTRACT TRUNCATED AT 250 WORDS)     

A model for passive elastic properties of rat vena cava

A two-dimensional model for the elastic properties of vena cava abdominalis under orthotropic deformation is introduced and tested against the experimental data obtained from six specimen of rat venae cavae by pressurization experiments. The model is based on membrane approximation and suited for vessels where most of the elastic elements are oriented axially, while circumferential contraction is exerted by redirecting axial stress by some network of oblique fibers. For the experimental data considered in this paper, the ratio between axial and circumferential stress depends almost exclusively on the circumferential extension ratio. As a consequence, the mechanical system can be formally decomposed in a kinematic system reacting by axial contraction on circumferential extension without any loss or storage of energy, serially connected to a hyperelastic system acting only in axial direction. Both systems are modeled separately by equations obtained by a purely phenomenological approach with two parameters for each system. This leads to reasonable reproduction of the experimental data. Introducing a correction parameter, which takes into account that the model assumption on the decomposition does not hold exactly, we get better reproduction of data. However, this is paid for by loss of physical rigor and in particular by departing from the assumption of hyperelasticity.     

Discovery of a persistent left superior vena cava during pacemaker implantation

An 83-year-old male was admitted to the coronary care unit because he had developed a total atrioventricular (AV) block after he had undergone a transurethral resection of the prostate for benign prostate gland hypertrophy.     

The relationship between the longitudinal pressure gradient and the blood flow velocity in the canine superior vena cava

In the superior vena cava of anaesthetized open chest dogs the axial pressure gradient (delta P) was measured simultaneously with the blood flow velocity (V) under a variety of preload conditions. Both delta P and V curves showed distinct systolic and diastolic waves. Peak delta P ranged between 26 and 93 P/cm (0.2-0.7 mm Hg/cm) and V varied between 0.095 and 0.19 m/s. Peak systolic delta P, but not peak diastolic delta P was significantly linearly correlated to respectively peak systolic V and peak diastolic V. The shape of delta P and V curves corresponded fairly well but variations of delta P preceded the variations of V. Both the shape correspondence and the phase lag between delta P and V were evaluated by means of the normalized cross-correlation technique. During volume expansion the shape correspondence improved and the phase lag decreased. It is concluded that the transient vena caval blood velocity variations are directly related to the pulsatile axial pressure gradient.     

Neural connections of the heart and superior vena cava in the rabbit and man

Innervational connections of the heart and the superior vena cava wall have been studied in the rabbit and the man. Besides, series of their embryos, impregnated with silver salts after Cajal-Favorsky have been investigated. Methods of Bielschowsky-Gros, Gomori and Karnovsky-Roots have also been applied. Adrenergic nervous elements have been revealed by means of incubation the slices in 2% solution of glyoxylic acid. Abundant cholinergic and adrenergic nervous plexuses are revealed on the wall of the superior vena cava, they are tightly connected with corresponding plexuses of the heart. Developmental of these nervous connections is followed, when embryogenesis of the cardiac nervous plexuses and large major vessels is studied in serial sections of embryos and fetuses of the rabbit and the man.     

A model of embolic chronic pulmonary hypertension in the dog

Despite numerous efforts, a reliable model of chronic embolic pulmonary hypertension has not been established. To develop such a model five conscious mongrel dogs were embolized repeatedly over 16-30 wk with Sephadex microspheres 286 +/- 70 micron in diameter. Hemodynamic and respiratory measurements were obtained just prior to each embolization. Chronic pulmonary hypertension developed in all dogs. Pulmonary hypertension was not accounted for by increased cardiac output, wedge pressure, right atrial pressure, or systemic arterial pressure. Gas exchange was little altered. Lung histological study revealed microspheres clustered within vessels. In three dogs increased pulmonary arterial pressure was sustained despite cessation of embolization for up to 5 mo. Reembolization in one of these caused further pulmonary hypertension. In two dogs acute pulmonary vasodilation by O2 breathing and administration of prostaglandin E1 reduced, but did not abolish, the increased pulmonary vascular resistance, suggesting some vascular tone was present. An embolic model of chronic pulmonary hypertension in awake dogs allows further investigation into the evolution of pulmonary hypertension.