The change of state in the central nervous system ofGymnocorymbus ternetzi after detection of hypoxanthine-l(N)-oxide, hypoxanthine-3(N)-oxide, and of the alarm substance from conspecifics was measured quantitatively by means of the fishes' equilibrium behavior. The fish swam freely in a tiny cage, illuminated horizontally from one side. The change of the angle of inclination of the dorsoventral axis of the fish was registered by means of a videorecorder. The recordings were later measured on the monitor in single frames at 0.2-sec intervals where the equilibrium position of the fish could be accurately determined ± 1 °. Various substances were presented to the fish, and their effects upon equilibrium position were recorded. An enhanced optical alertness shown by an increase in the fishes' inclination was generally produced with alarm substance. Without any additional stimulation, the factorU, representing quantitatively the degree of the change of central state, varied slightly within the experimental period of 1 min; however, this factor never exceededU= 1.0 ± 0.15 in control fish. The increase ofU usually exceeded considerably the value 1.15 when skin extract from conspecifics or 7-8 μg of hypoxanthine-3(N)-oxide were given. However, when hypoxanthine-l (N)-oxide was presented,U generally did not exceed 1.15. The difference between hypoxanthine-3(N)-oxide and hypoxanthine-l(N)-oxide was highly significant. This result is in accordance with the findings on fish schools ofDanio malabaricus, where hypoxanthine-3(N)-oxide elicited the fright reaction, but hypoxanthine-1(N)-oxide was ineffective. The results support the hypothesis that the alarm substance from the skin ofPhoxinus phoxinus is identical with hypoxanthine-3(N)-oxide. The results with alarm substance or hypoxanthine-3(N)-oxide did not show any adaptation. This was also true in fish that were stimulated repeatedly at intervals of a couple of minutes only. InGymnocorymbus, which has compensated for removal of the otolith of one utriculus, conspecific skin extract triggers the typical postoperative phenomenon, i.e., rotation around the fishes' long axis towards the operated side. Whereas such a decompensation could be elicited by hypoxanthine-3(N)-oxide as well, hypoxanthine-l(N)-oxide had no effect. This finding is interpreted as an effect of the alarm substance and of hypoxanthine-3(N)-oxide on the centers of equilibrium.
The myocardial interaction between the ventricles was studied using isolated, flow-perfused, paced rabbit hearts beating isovolumically. In general, increasing left ventricular (LV) volume increased right ventricular (RV) diastolic and developed pressures. In particular, with a peak RV volume (RVV), increasing LV volume (LVV) from zero to two-thirds of its peak volume increase RV diastolic pressure by 1.7 mmHg (N=10, P less than 0.001) and RV developed pressure by 1.5 mmHg (N=10,P less than 0.001). For the LV, small RVV caused LV diastolic and developed pressure to increase, while large RVV increased LV diastolic pressure but decreased LV developed pressure. With a LVV held at two-third of peak volume, increasing RVV from zero to its peak volume caused LV diastolic pressure to increase by 2.5 mmHg (N=10,P less than 0.001) and LV developed pressure to decrease by 2.0 mmHg (N=10, P less than 0.001). The position of the interventricular septum correlated with LV diastolic pressure and RV diastolic and developed pressure changes (P less than 0.01). The results demonstrate that the diastolic and developed pressure-volume relationships of either ventricle can be acutely altered by varying the volume of the other ventricle.
The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.
Regional right ventricular (RV) motion was examined in six acutely instrumented dogs by implanting radiopaque markers in three regions of the free wall: the apex, the midventricle, and the outflow tract. These markers were filmed at the paced heart rate of 180 beats/min with a high-speed biplane X-ray system, and their motion was analyzed with a digital computer. Local deformation was separated into percent length changes in the two mutually perpendicular principal directions. The major component exhibited shortening along a path from apex to conus. (apex - 13.6%, midventricle -13.1%, conus -8.7%); the minor component exhibited small amounts of lengthening and some shortening (apex +4.7%, midventricle +1.8%, conus -0.5%). From these two measurements we calculated the peak RV free wall thickening (apex 13.6%, midventricle 14.1%, conus 10.9%). The experimental technique developed for this study was found to be suitable for the repeated analysis of intact ventricular performance in chronic animal studies. The results reveal that in systole the RV free wall undergoes a sequential contraction, which begins at the apex and ends in the conus.
Regional right ventricular (RV) wall motion was analyzed in six closed-chest, anesthetized, paced dogs by measuring distances between chronically implanted radiopaque markers on RV free wall and septum. Normally, contraction started in the sinus region 25 ms before conus region. Highest velocities of shortening occurred in the conus region (2.42 +/- 0.33 lengths/s) and in septum-to-free-wall direction (2.56 +/- 0.40 l/s). Percent shortening for all regions was between 12% and 17%. The data indicate that the RV ejects blood by a uniform reduction in its free wall surface area and septal-to-free-wall distance. Reduced venous return decreased end-diastolic length, percent shortening, maximum velocity of shortening, and time to end-systolic length. RV pressure overload increased end-diastolic length and decreased percent shortening and maximum velocity of shortening. LV pressure overload led to a nonhomogeneous contraction pattern. Percent shortening and maximum velocity of shortening increased in sinal and conal transverse directions and decreased in sinal and conal longitudinal directions; these changes indicate a mechanical interaction between RV and LV.
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