The effects of pentobarbital and chloralose on cardiac sympathetic nerve activity (CSNA), renal sympathetic nerve activity (RSNA), arterial pressure (AP), and heart rate (HR) were examined using conscious cats. Arterial blood was sampled intermittently to measure plasma epinephrine. Pentobarbital (25-30 mg/kg iv) decreased CSNA, RSNA, AP, and HR. The reduction of CSNA (71 +/- 7%) was larger and lasted longer than that of RSNA (33 +/- 12%). Chloralose (40-50 mg/kg iv) decreased CSNA 66 +/- 9% and HR, increased RSNA 127 +/- 122%, and did not affect AP. The baroreflex relationship between AP and CSNA was examined by increasing AP to 145 mmHg and decreasing AP to 55 mmHg. Both pentobarbital and chloralose shifted the AP-CSNA relationship curve downward and blunted the slope of the curve, indicating that both drugs attenuate tonic and baroreflex cardiac sympathetic outflow. Pentobarbital and chloralose reduced plasma epinephrine, suggesting a decrease in adrenal sympathetic nerve activity. It is concluded that pentobarbital or chloralose affects differentially sympathetic outflows to different organs such as the heart, kidney, and adrenal gland.

Background-Synchrotron radiation has been used to analyze crossbridge dynamics in isolated papillary muscle and excised perfused hearts with the use of x-ray diffraction techniques. We showed that these techniques can detect regional changes in rat left ventricle contractility and myosin lattice spacing in in situ ejecting hearts in real time. Furthermore, we examined the sensitivity of these indexes to regional ischemia. Methods and Results-The left ventricular free wall of spontaneously beating rat hearts (heart rate, 290 to 404 bpm) was directly exposed to brief high-flux, low-emittance x-ray beams provided at SPring-8. Myosin mass transfer to actin filaments was determined as the decrease in reflection intensity ratio (intensity of 1,0 plane over the 1,1 plane) between end-diastole and end-systole. The distance between 1,0 reflections was converted to a lattice spacing between myosin filaments. We found that mass transfer (mean, 1.71Ϯ0.09 SEM, nϭ13 hearts) preceded significant increases in lattice spacing (2 to 5 nm) during systole in nonischemic pericardium. Left coronary occlusion eliminated increases in lattice spacing and severely reduced mass transfer (PϽ0.01) in the ischemic region. Conclusions-Our results suggest that x-ray diffraction techniques permit real-time in situ analysis of regional crossbridge dynamics at molecular and fiber levels that might also facilitate investigations of ventricular output regulation by the Frank-Starling mechanism. Key Words: ischemia Ⅲ myocardial contraction Ⅲ myosin Ⅲ radiography D espite the history of studies on crossbridge dynamics, lower photon counts and poorer quality of diffraction patterns obtained from cardiac muscle than skeletal and insect flight muscles 1-3 have limited progress with cardiac muscle until recently. 4,5 Some of us used third-generation synchrotron radiation (SPring-8, Japan Synchrotron Radiation Research Institute) to determine x-ray diffraction patterns in excised, perfused rat hearts while moving systematically across the left ventricular (LV) equator from the epicardium through to the ventricular cavity. 6 X-ray diffraction patterns of cardiac muscle produce 2 equatorial-position reflections from the lattice-like arrangement of its protein elements. 2 Mass transfer of myosin heads to actin during contraction is inferred from a decrease in the integrated 1,0 reflection intensity (I 1,0 , lattice plane containing only thick myosin filaments) and an increase in 1,1 reflection intensity (I 1,1 , plane with thick myosin and thin actin filaments). 7 The myocardial intensity ratio (defined as I 1,0 /I 1,1 ) is minimal in the rigor state and maximal in a quiescent state. 1,2,6,8 Furthermore, the distance between 1,0 reflection peaks (d 1,0 spacing) represents the myosin lattice spacing, which is inversely related to sarcomere length in isolated fibers 5 as static myocytes maintain a constant cell volume. Whether decreases in myofilament spacing contribute to increasing Ca 2ϩ sensitivity and increased probability of crossbridge formation at longe...

Responses in efferent cardiac sympathetic nerve activity (CSNA) and heart rate (HR) to a 100-s anterior descending coronary artery occlusion were measured in cats under awake, atropinized, anesthetized, or anesthetized and atropinized states. In the conscious state, at 20 and 90 s of occlusion, CSNA increased by 23% and then decreased by 7%, respectively, whereas HR decreased by 5 and 17%, respectively. With atropinization and/or anesthesia, the initial increase in CSNA was inhibited and the later decrease in CSNA was enhanced, whereas the bradycardia was diminished. HR changed in proportion to CSNA responses with high correlations, i.e., r = +0.89, +0.90, +0.96, and +0.91 for the four states, respectively. In the conscious state, the CSNA-HR relation line shifted toward bradycardia, but this shift was blocked by atropinization and anesthesia. This finding suggested that, in the conscious state, cardiac vagal nerve activity (CVNA) increased immediately and did not decrease during occlusion. At the early stage of occlusion, HR response (bradycardia or tachycardia) was determined by the relative contribution of enhanced CSNA and CVNA. At the later stage of occlusion, bradycardia was induced by a combination of decreased CSNA and enhanced CVNA. In anesthesia and/or atropinization it was induced mainly by the decreased CSNA.

We measured simultaneously and continuously the sympathetic nerve activity to the heart (CSNA) and kidney (RNA) together with heart rate (HR) and arterial blood pressure (AP) in conscious cats. The time course and magnitude of their responses to behavioral stimuli and norepinephrine iv administration were analyzed quantitatively. The increases in CSNA and RNA occurred almost simultaneously with the onset of standing, walking or eating behavior. The abrupt increases in CSNA and RNA were not preceded by a decrease in AP so it was unlikely to have been a reflex initiated by baroceptors. Rather, the increases in CSNA and RNA were followed by increases in HR and AP. The lag time ranged from 2 to 10 sec. Relative response magnitude of CSNA differed significantly from that of RNA. Thus, when AP increased spontaneously by behavioral stimuli, there was always preceding nonuniform increases in CSNA and RNA. On the other hand, when AP was elevated by norepinephrine iv administration, CSNA and RNA were inhibited proportionally to a rise in AP due to baroreflexes. At rest, the baroreflex effect on CSNA was greater than that on RNA. Cardiac-related discharges of CSNA and RNA, which were induced reflexly by baroceptor input, occurred dominantly at rest. However, with excitement or at the onset of body movements, they were diminished significantly. Our results suggested that AP adjustment associated with various behavior was made directly by a nonuniform central activation of the sympathetic nerve activity to the heart and blood vessels and partly by a central modulation of the baroceptor input.