Physiological contractility of cardiomyocytes in the wall of mouse and rat azygos vein.

We recently demonstrated the abundant presence of cardiomyocytes in the wall of thoracic veins of adult mouse and rat. The highly differentiated morphology and myofilament protein contents of the venous cardiomyocytes suggested contractile functions. Here we further investigated the contractility of mouse and rat azygos venous rings compared with that of atrial strips and ventricular papillary muscle. 5-Bromo-4-chloro-indolyl-galactopyranoside (X-gal) staining of transgenic mouse vessels expressing lacZ under a cloned cardiac troponin T promoter demonstrated that the venous cardiomyocytes are discontinuous from atrial myocardium and aligned in the wall of thoracic veins perpendicular to the vessel axis. Histological sections displayed sarcomeric striations in the venous cardiomyocytes, which indicate an encirclement orientation of myofibrils in the vessel wall. Mechanical studies found that the rings of mouse and rat azygos vein produce strong cardiac type twitch contractions when stimulated with electrical pacing in contrast to the weak and slow smooth muscle contractions induced using 90 mM KCl. The twitch contraction and relaxation of mouse azygos veins further exhibited a cardiac type of ß-adrenergic responses. Quantitative comparison showed that the contractions of venous cardiomyocytes are slightly slower than those of atrium muscle but significantly faster than those of ventricular papillary muscle. These novel findings indicate that the cardiomyocytes abundant in the wall of rodent thoracic veins possess fully differentiated cardiac muscle phenotype despite their anatomical and functional segregations from the heart.

Anatomical comparison of a defect in the hepatic segment of the inferior vena cava with the normal azygos system

During anatomical practice between 2001-2002 at the Tokyo Women's Medical University, a defect in the hepatic segment of the inferior vena cava was encountered in a 94-year-old male cadaver. Although this type of defect has often been observed clinically using imaging diagnosis, the topological changes in the small vessels and surrounding structures have not been described previously. Here, the topological changes in small vessels and surrounding structures, in addition to the morphology of a defect in the hepatic segment of the inferior vena cava, are described in detail. Normal variations in the venous system were also examined using 26 human cadavers for comparison. The following results and interpretations were obtained: The thoracic portion of the anomalous vein originated from the azygos system, judging from the topological relationships among the main venous trunk, small vessels, and the autonomic nerves. Although a close relationship between the inferior vena cava and the azygos system was recognized, the development of each venous system should be regarded as independent, based on the normal variations observed in 26 human cadavers and the currently available medical literature. The boundary between the cardinal vein (inferior vena cava) and the azygos system might be the lower border of the renal vein, since the renal vein drained into the ventral aspect of the inferior vena cava and the left renal artery ran superficially across the abdominal portion of the anomalous vein. Examination of topological changes in the surrounding structures may provide important clues regarding the morphogenesis of defects in the hepatic segment of the inferior vena cava and normal venous systems (AU)

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Plasma level of transforming growth factor beta1 measured from the azygos vein predicts prognosis in patients with esophageal cancer.

PURPOSE: Transforming growth factor (TGF)-beta regulates cell growth inhibition. When tumor cells lose their sensitivity to TGF-beta growth inhibition, the excess TGF-beta that results may act on tumor cells to facilitate tumor development. Previously, we have shown that an elevated systemic TGF-beta 1 level is not related to tumor progression in esophageal cancer (Y. Fukai et al., Int J Cancer 2003;104:161-6). We considered that systemic inflammation or chronic disease, in addition to the tumor, may influence the plasma TGF-beta level. Therefore, we examined the hypothesis that the plasma TGF-beta level measured from the azygos vein would independently predict tumor progression and prognosis in patients with esophageal cancer. EXPERIMENTAL DESIGN: Fifty-seven plasma samples were obtained intraoperatively from the azygos vein in patients with esophageal cancer. ELISA was used to quantify the plasma TGF-beta 1 levels, which were correlated with pathological features and patient survival. RESULTS: The mean plasma TGF-beta 1 level measured from the azygos vein of esophageal cancer patients was 5.09 +/- 0.48 ng/ml (mean +/- SE). The survival rates of patients with a high TGF-beta 1 level (defined as a level above the 4.6 ng/ml level of normal controls) in the azygos vein were significantly lower than those of patients with a low TGF-beta 1 level (P = 0.0317). Moreover, the TGF-beta 1 level in the azygos vein was an independent prognostic factor for overall survival (P = 0.0474). CONCLUSIONS: The level of plasma TGF-beta 1 measured from the azygos vein is an independent predictor in patients with esophageal cancer and may reflect tumor progression more specifically because the azygos vein is responsible for venous return from the esophagus.

Stroke-prone SHR vascular muscle Ca2+ current amplitudes correlate with lethal increases in blood pressure.

Studies on the possible causal relationship between the Ca2+ channel current density in the vascular muscle cell (VMC) and increases in blood pressure were extended by a comparison of stroke-prone spontaneously hypertensive rats (SP-SHR) with N/nih outbred normotensive rats. Maximal amplitudes of both L-type and T-type Ca2+ channel currents were significantly increased in SP-SHR without a difference in cell capacitance. SP-SHR peak current amplitudes in 20 mM Ba2+ averaged 446 +/- 64 pA while N/nih averaged 156 +/- 25 pA (clearly separated statistically). Both L-type and T-type Ba2+ currents (IBa) were significantly increased in SP-SHR, shown also by peak current frequency distributions. There was a significant shift to the left of both activation (7 mV) and inactivation (15 mV) current-voltage (I-V) plots. SP-SHR IBa recovery from inactivation was significantly slower (103 versus 61 ms) than in N/nih VMC. The increases in SP-SHR IBa amplitude under maximized conditions correlated with increases in blood pressure. Together with earlier observations of increased vascular muscle Ca2+ current density coexistent with blood pressure elevation in Kyoto-Wistar SHR, these data provide evidence for altered function of Ca2+ channels as a fundamental component of hypertension. Since the Ca2+ channel alterations exist in venous VMCs of newborn SP-SHR rats (in a low pressure blood vessel and at a time when increased Ca2+ current density could not be an effect of increased blood pressure), our results add to the growing evidence of Ca2+ channel abnormalities as a cause of genetic hypertension.