Left ventricular effects on right ventricular developed pressure.

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.     

Altered Na+-K+-ATPase, cell Na+ and lipid profiles in canine arterial wall with chronic cigarette smoking

1. We evaluated the influence of cigarette smoking on arterial wall membranes, using Na+-K+-ATPase activity, free cholesterol (FC) and phospholipid (PL) contents as indices of membrane structural and functional integrity. 2. Segments of aorta, carotid and femoral arteries were obtained from normal dogs (controls) and dogs subjected to chronic cigarette smoking for 2 yr (12 cigarettes a day). 3. Na+-K+-ATPase activity was assessed in segments of carotid and femoral arteries using a ouabain-sensitive 86Rb uptake procedure for intact tissues. 4. Free cholesterol and phospholipids were separated, identified, and quantitated from extracts of aortic samples by means of two dimensional thin-layer chromatography. 5. Na+-K+-ATPase activity was reduced in the smoker group in both carotid and femoral arteries. This reduced enzyme activity was accompanied by a rise in cell Na+ levels at both arterial sites. 6. Aortic FC was elevated and the PL profile was altered in the smoker group; as a result, phosphatidylcholine was reduced, whereas lysophosphatidylcholine, phosphatidic acid, and cardiolipin were elevated. 7. Phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingolipid levels were unchanged. In addition, the FC/PL ratio was increased in the smokers. 8. Taken together, the changes in Na+-K+-ATPase activity, FC/PL ratio and phospholipid profiles observed are consistent with the hypothesis that chronic cigarette smoking causes a reorganization of the phospholipid bilayer in the smooth-muscle cell membrane of the arterial wall.     

The influence of pentoxifylline on skin-flap survival

Experimental studies were performed on rats to demonstrate the effects of pentoxifylline (20 mg/kg per day), administered enterally, on skin-flap viability. This was compared to saline controls and to the alpha-blocking agent (phenoxybenzamine 1 mg/kg per day). Pentoxifylline-treated flaps had a greater than 50 percent increase in tissue survival over controls as compared to 22 percent with phenoxybenzamine. The two drugs in combination appeared to have no additional benefit over the use of pentoxifylline alone. Although a quantitative difference in red-cell flow could not be demonstrated in the experimental flaps utilizing 99mTc pertechnetate-tagged red-cell imaging, the dramatic increase in tissue viability suggests that the rheologic properties of pentoxifylline are important in altering the pathophysiology of skin-flap failure.     

Right and left ventricular pressure-volume response to respiratory maneuvers

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.     

Variable-frequency train stimulation of canine latissimus dorsi muscle during shortening contractions

George, David T., Stuart A. Binder-Macleod, Thomas N. Delosso, and William P. Santamore. Variable-frequency trainstimulation of canine latissimus dorsi muscle during shorteningcontractions. J. Appl. Physiol. 83(3):994-1001, 1997.In cardiomyoplasty, the latissimus dorsi muscle(LDM) is wrapped around the heart ventricles and electrically activatedwith a constant-frequency train (CFT). This study tested the hypothesesthat increased mechanical performance from the LDM could be achieved byactivating the muscle with variable-frequency trains (VFTs) of shorterduration or containing fewer stimulus pulses than the CFT now used. Themechanical performance of the canine LDM (n = 7) during shortening contractionswas measured while the muscle was stimulated with 5- and 6-pulse CFTs(of duration 132 and 165 ms, respectively) and 5- and 6-pulse VFTs (ofduration 104 and 143 ms, respectively) that were designed to takeadvantage of the catchlike property of skeletal muscle. Measurementswere made from fresh and fatigued muscles. For the fresh muscles, the VFTs elicited significantly greater peak power than did the 6-pulse CFT. When the muscles were fatigued, VFT stimulation significantly improved both the peak and mean power produced compared withstimulation by CFTs. These results show that stimulation of the LDMwith shorter duration VFTs is potentially useful for application incardiomyoplasty.

     

Alterations in canine coronary arteries produced by chronic cigarette smoking

Segments of left circumflex coronary artery were obtained from beagles that had been exposed to cigarette smoke for 2 years and from nonsmoking controls. A ring sample from each was used to determine passive (0-Ca2+ and 2 mM EGTA) and active (75 mM K+) force-length relations. Other contiguous samples were used to determine collagen and elastin content, water content and distribution, and total electrolyte content. No significant differences were found in passive mechanical properties or the collagen and elastin content of arteries from the two groups of animals. Maximum values of active force development were found to be increased in arteries from smoking dogs as were values on the ascending part of the active force-length curve. Total water content and the distribution space of an extracellular marker (60Co-EDTA) were not significantly different among arteries from the two groups. This along with the similarity of total electrolyte contents suggests that values of cell volume were not different between the two groups and that the above differences in active force development represent alterations in smooth muscle cells at the subcellular level. These results suggest that the contribution of chronic smoking as one of a group of cardiac risk factors may be due to an effect of augmenting coronary artery smooth muscle contractility.