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A technique that measures myocardial elastance directly using minute vibration is developed. First, stress-strain relationship is identified and using the measured displacement and force, the elastance is calculated using an equation of motion for a particular point in the cardiac cycle. The simultaneous solution of the equation at difference frequencies yields an elastance with a unique value. This technique can be applied in the evaluation of regional elastance.

The increases in vagal stimulation was examined to determine whether these increases directly depress ventricular contractility through negative chronotropic effect. The study utilized sympathectomized open-chest rabbits to measure left ventricular contractility through end-systolic elastance. Results of the investigation showed that the negative inotropic effect on vagal stimulation is a result of a negative chronotropic effect.

The role of the neural arc in blood pressure regulation of the baroreflex system was investigated in rabbit hearts. Hemodynamic parameters during the random pressure perturbation into carotid sinuses indicated an increase in neural baroreflex arc. The acceleration in the slow peripheral responses occurred in the low frequency range of 0.1-1 Hz. It is concluded that neural arc regulation is related to the maintenance of baroreflex stability and quickness.

Shishido, Toshiaki, Masaru Sugimachi, Osamu Kawaguchi, Hiroshi Miyano, Toru Kawada, Wataru Matsuura, Yasuhiro Ikeda, and Kenji Sunagawa. Novel method to estimate ventricular contractility using intraventricular pulse wave velocity. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H2409-H2415, 1999.--We developed a novel technique for estimating ventricular contractility using intraventricular pulse wave velocity (PWV). In eight isolated, cross-circulated canine hearts, we used a fast servo pump to inject a volume pulse into the base of the left ventricular chamber at late diastole and at late systole. We measured the transit time of the volume pulse wave as it traversed the distance from base to apex and calculated the intraventricular PWV. The intraventricular PWV increased from diastole (2.3 [+ or -] 0.4 m/s) to systole (11.7 [+ or -] 2.4 m/s, P [is less than] 0.0001 vs. diastole). The square of the intraventricular PWV at late systole correlated linearly with the left ventricular end-systolic elastance (r = 0.939, P [is less than] 0.0001) and with the end-systolic Young's modulus (r = 0.901, P [is less than] 0.0001). Moreover, the intraventricular PWV was insensitive to preload. We conclude that the intraventricular PWV at late systole reflects left ventricular end-systolic elastance reasonably well. The fact that estimation of PWV does not require volume measurement or load manipulation makes this technique an attractive means of assessing ventricular contractility. cardiac mechanics; ventricular elastance; hemodynamics; muscle properties; stress-strain relationship

Central post-stroke pain (CPSP) is one of the most under-recognized consequences of cerebral stroke, but the development of an effective treatment strategy is urgent. High-mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE, one of the receptors of HMGB1) have recently been shown to be critical in the modulation of nociceptive transduction following peripheral neuropathy. The aim of this study was to determine the interactions between CPSP and HMGB1/RAGE signaling. Male ddY mice were subjected to 30 min of bilateral carotid artery occlusion (BCAO). The development of hind paw mechanical allodynia was measured after BCAO using the von Frey test. Neuronal damage was estimated by histological analysis on day 3 after BCAO. The expression levels of the HMGB1 protein in the spinal cord and the sciatic nerve were significantly increased on day 3 after BCAO, although no effects of BCAO were noted on RAGE protein expression. BCAO-induced mechanical allodynia was significantly decreased by the intravenous and intrathecal administration of anti-HMGB1 monoclonal antibody. The BCAO-induced increase of phosphorylation of extracellular signal-regulated kinase (ERK) was canceled by the administration of anti-HMGB1 monoclonal antibody. In addition, BCAO-induced mechanical allodynia was significantly decreased by intrathecal administration of U0126, an inhibitor of ERK. The results showed that BCAO-induced mechanical allodynia can be regulated by the activation of HMGB1/RAGE signaling. [ABSTRACT FROM AUTHOR]

Presents a new technique for evaluation of regional myocardial elastance with the use of minute vibration. Application of minute vibration; Normalization of myocardial elastance; Validity of the mechanical model in representing myocardial properties; Relationship between myocardial and left ventricular chamber time-varying elastance.

Activation of vagus nerve exerts orexin-A (OXA)-mediated suppression of post-ischemic glucose intolerance and cerebral ischemic neuronal damage. Cerebral ischemia induces hepatic inflammatory factors and contributes to the development of hepatic insulin resistance by activating sympathetic nerves. However, it is not enough to understand whether OXA regulates these phenomena through activation of vagus nerve. In this study, we demonstrated that the involvement of OXA-induced activation of vagus nerve in the induction of hepatic inflammatory factors by cerebral ischemia. Focal cerebral ischemic model construction was performed by 2 h of middle cerebral artery occlusion (MCAO) in ddY male mice. OXA-positive neurons were visualized using the retrograde tracer Fluoro-Gold™. Intrahypothalamic OXA (5 pmol/mouse) administration significantly suppressed the MCAO-induced post-ischemic glucose intolerance and neuronal damage. The MCAO-induced decrease in hepatic insulin receptors and increase in hepatic gluconeogenic enzymes were suppressed by OXA administration. These effects were canceled by N -butylscopolamine (a muscarinic receptor antagonist). MCAO-induced increases in hepatic F4/80, tumor necrosis factor-α, and interleukin-1β on day 1 after MCAO were reversed by OXA administration. These effects were abolished by N -butylscopolamine or hepatic vagotomy. These results suggest that OXA-induced activation of vagus nerve regulates the post-ischemic elevation of hepatic inflammatory factors, and which may be contributed to part of OXA-mediated regulation of post-ischemic glucose intolerance. [ABSTRACT FROM AUTHOR]

Central post-stroke pain (CPSP) is one of the complications of cerebral ischemia and neuropathic pain syndrome. At present, there are few studies of pain in regions such as the spinal cord or sciatic nerve in cerebral ischemic animal models. To identify proteomic changes in the spinal cord and sciatic nerve in global cerebral ischemic model mice, in the present study we performed an investigation using proteomic methods. In a comparison between the intensity of protein spots obtained from a sham and that from a bilateral carotid artery occulusion (BCAO) in spinal cord and sciatic nerve, the levels of 10 (spinal cord) and 7 (sciatic nerve) protein spots were altered. The protein levels in the spinal cord were significantly increased in N(G),N(G)-dimethylarginine dimethylaminohydrolase 1 (DDAH1), 6-phosphogluconolactonase isoform 1, and precursor apoprotein A-I and decreased in dihydropyrimidinase-related protein 2 (CRMP-2), enolase 1B, rab guanosine 5'-diphosphate (GDP) dissociation inhibitor beta, septin-2 isoform a, isocitrate dehydrogenase subunit alpha, cytosolic malate dehydrogenase, and adenosine triphosphate synthase. The protein levels in the sciatic nerve were significantly increased in a mimecan precursor, myosin light chain 1/3, and myosin regulatory light chain 2 (MLC2), and decreased in dihydropyrimidinase-related protein 3 (CRMP-4), protein disulfide-isomerase A3, 3-hydroxy-3-methylglutaryl-coenzyme A synthase 1, and B-type creatine kinase. In addition, CRMP-2 and CRMP-4 protein levels were decreased, and DDAH1 and MLC2 protein levels were increased on day 1 after BCAO using Western blotting. These results suggested that changes in these proteins may be involved in the regulation of CPSP.