Myocardial perfusion in compensated and failing hypertrophied left ventricle

1985 ◽  
Vol 249 (3) ◽  
pp. H534-H539 ◽  
Author(s):  
D. G. Parrish ◽  
W. S. Ring ◽  
R. J. Bache

This study examined blood flow in the hypertrophied left ventricle with and without failure. Left ventricular hypertrophy was produced in 20 dogs by banding the ascending aorta at 6-7 wk of age; studies were performed after animals reached adulthood. Sixteen dogs had compensated hypertrophy, while four dogs had cardiac failure manifested by left ventricular dilatation and end-diastolic pressures greater than 18 mmHg. The degree of hypertrophy, assessed by left ventricular-to-body weight ratio, was similar in animals with compensated hypertrophy (7.29 +/- 0.26 g/kg) and failure (8.45 +/- 0.15); both were greater than control (4.50 +/- 0.15, P less than 0.01). Left ventricular systolic pressure was similar in compensated hypertrophy (184 +/- 9 mmHg) and failure (226 +/- 29), as compared with control (130 +/- 4; P less than 0.01). Left ventricular blood flow measured with microspheres was 0.89 +/- 0.07 ml X min-1 X g-1 in control animals, was increased to 1.34 +/- 0.05 with compensated hypertrophy (P less than 0.001), and was further increased with failure to 1.86 +/- 0.40 (P less than 0.05). The left ventricular wall thickness-to-cavity diameter ratio was increased to 0.63 +/- 0.04 with compensated hypertrophy but was only 0.40 +/- 0.05 in dogs with failure (P less than 0.01), suggesting that wall stress was greater in hearts with failure. These data suggest that increased blood flow rates in dogs with failure resulted from increased myocardial O2 requirements due to increased systolic wall stress. Need for increased blood flow during resting conditions in dogs with failure would impair the ability for further coronary vasodilation during periods of cardiac stress.

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.


1975 ◽  
Vol 229 (2) ◽  
pp. 501-505 ◽  
Author(s):  
T Nivatpumin ◽  
T Yipintsoi ◽  
S Penpargkul ◽  
J Scheuer

To study the effects of acute uremia on the inotropic state of the rat heart, we subjected rats to bilateral nephrectomy and studied their hearts in the open chest 24 h later. Uremic rats had significantly higher systolic blood pressure than sham-operated animals. Left ventricular systolic pressure and maximum dP/dt, both during ejection and isovolumic contrations, were higher for any given end-diastolic pressure in hearts of uremic rats than in sham-operated animals. This difference in performance charcteristics was not abolished by doses of propranolol that blocked the heart rate response to isoproterenol. The administration of phenoxybenzamine during the 24 h of uremia abolished the blood pressure rise in uremic rats, but the increased contractile state persisted. Treatment of sham-operated animals with methoxamine to produce the same course of blood pressure as observed in uremic rats was also associated with an increased inotropic state. These results indicate that in the rat, acute uremia is associated with an increased inotropic state that is not mediated by beta-adrenergic mechanisms. The systolic hypertension of acute uremia is not the major cause of the increased contractility, although systolic hypertension without uremia can mimic the performance characteristics found in hearts of uremic rats.


2006 ◽  
Vol 84 (10) ◽  
pp. 985-991 ◽  
Author(s):  
T.V. Kondratiev ◽  
T. Tveita

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n = 7) were cooled to 15 °C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 μg/min Epi, i.v., for 1 h during cooling to 28 °C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 °C. Group 2 served a saline solution control. At 37 °C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 °C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 °C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 °C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.


2016 ◽  
Vol 40 (9) ◽  
pp. 842-855 ◽  
Author(s):  
Anastasios Petrou ◽  
Gregor Ochsner ◽  
Raffael Amacher ◽  
Panagiotis Pergantis ◽  
Mathias Rebholz ◽  
...  

2000 ◽  
Vol 279 (4) ◽  
pp. R1157-R1164 ◽  
Author(s):  
A. Barbera ◽  
G. D. Giraud ◽  
M. D. Reller ◽  
J. Maylie ◽  
M. J. Morton ◽  
...  

The effects of right ventricular (RV) systolic pressure (RVSP) load on fetal myocyte size and maturation were studied. Pulmonary artery (PA) pressure was increased by PA occlusion from mean 47.4 ± 5.0 (±SD) to 71 ± 13.6 mmHg ( P < 0.0001) in eight RVSP-loaded near-term fetal sheep for 10 days. The maximal pressure generated by the RV with acute PA occlusion increased after RVSP load: 78 ± 7 to 101 ± 15 mmHg ( P< 0.005). RVSP-load hearts were heavier (44.7 ± 8.4 g) than five nonloaded hearts (31.8 ± 0.2 g; P < 0.03); heart-to-body weight ratio (10.9 ± 1.1 and 6.5 ± 0.9 g/kg, respectively; P < 0.0001). RVSP-RV myocytes were longer (101.3 ± 10.2 μm) than nonloaded RV myocytes (88.2 ± 8.1 μm; P < 0.02) and were more often binucleated (82 ± 13%) than nonloaded myocytes (63 ± 7%; P < 0.02). RVSP-loaded myocytes had less myofibrillar volume than did nonloaded hearts (44.1 ± 4.4% and 56.1 ± 2.6%; P < 0.002). We conclude that RV systolic load 1) leads to RV myocyte enlargement, 2) has minor effects on left ventricular myocyte size, and 3) stimulates maturation (increased RV myocyte binucleation). Myocyte volume data suggest that RV systolic loading stimulates both hyperplastic and hypertrophic growth.


1996 ◽  
Vol 24 (02) ◽  
pp. 169-176 ◽  
Author(s):  
Xi Huang ◽  
Yiming Zang ◽  
Yuming Wang ◽  
Guobao Niu ◽  
Aidong Wen ◽  
...  

Hemodynamic actions of intravenous (iv) administration of tetramethylpyrazine phosphate (TMPP) and sodium ferulate (SF) alone or in combination were studied in anesthetized dogs. When given alone, TMPP increased left ventricular systolic pressure (LVSP), peak positive first derivative of left ventricular pressure (+LVdp/dt), coronary blood flow (CBF) and heart rate (HR) while decreasing mean aortic pressure (mAoP). SF alone did not produce any significant hemodynamic changes. When the two were administered in combination, SF antagonized dose-dependently the hemodynamic actions of TMPP. Results of this study did not support the efficacy of combined treatment of Ligusticum wallichi and Angelica root, which contain TMPP and SF respectively.


1988 ◽  
Vol 255 (3) ◽  
pp. H679-H684
Author(s):  
J. D. Schipke ◽  
J. Alexander ◽  
Y. Harasawa ◽  
R. Schulz ◽  
D. Burkhoff

We predicted the shape of the end-systolic pressure-thickness relationship (ESPTR) by modeling the left ventricle as thick-walled sphere. To test the validity of the predicted relationships, we then measured the ESPTR over wide volume ranges in seven isolated blood-perfused canine hearts. Both simulation and experiments demonstrated that the ESPTR is curvilinear. However, within a physiological left ventricular systolic pressure range (80–150 mmHg), the ESPTR was described reasonably well by a straight line. Within that pressure range, changes in left ventricular contractile state, assessed by slope changes of the end-systolic pressure-volume relationship, were associated with almost parallel shifts in the ESPTR. In contrast, in a low pressure range (less than 80 mmHg), contractility changes were associated with slope changes of the ESPTR. We conclude that, in general, there are limitations in the application of ESPTR for assessing left ventricular contractility, but if the limitations are recognized and accounted for, then the ESPTR may be useful for assessing contractility changes in vivo.


1981 ◽  
Vol 240 (1) ◽  
pp. H39-H44 ◽  
Author(s):  
H. Suga ◽  
T. Hayashi ◽  
M. Shirahata

We scrutinized the recently reported correlation between the canine left ventricular systolic pressure-volume area (PVA) and cardiac oxygen consumption rate per beat (Vo2) by use of an improved method of Vo2 assessment. PVA is the specific area in the pressure-volume (PV) plane bounded by the end-systolic and end-diastolic PV lines and the systolic segment of the PV loop. Different from the previous study in which Vo2-PVA data from isovolumic and ejecting contractions were pooled for analyses, we analyzed Vo2-PVA data from the two different modes separately to examine whether there was any difference of Vo2-PVA relationship between them. The results indicated that the linear regressions of Vo2 on PVA were virtually the same for isovolumic and ejecting contractions. The regression line was Vo2 (ml O2/beat) = a[PVA (mmHg x ml x beat-1)] + b, where a = 1.64 (+/- 0.12 SE) X 10(-5) (ml O2/beat)/(mmHg x ml x beat-1) and b = 0.015 +/- 0.002 ml O2/beat in 10 hearts. We conclude that PVA serves as a reliable predictor of Vo2 regardless of the mode of contraction in a given left ventricle with a stable inotropic background.


1991 ◽  
Vol 261 (1) ◽  
pp. H212-H219 ◽  
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
G. Guideri ◽  
P. Anversa

To determine whether moderate ingestion of alcohol for protracted periods of time affects normal cardiac performance and produces myocyte damage, male Fischer 344 rats at 4 mo of age were given 30% ethanol in their drinking water every day for a period of 8 mo. Experimental animals and age-matched controls were examined hemodynamically and morphometrically at 12 mo of age. Body and cardiac growth were depressed in alcoholic animals by 15 and 12%, respectively. Although left ventricular (LV) weight was reduced by 14% in alcoholic rats, no difference in right ventricular (RV) weight was noted, and consequently the ratio of RV weight to body weight increased by 12%. Systemic arterial pressures as well as LV peak systolic pressure decreased in alcoholic rats despite an unchanged heart rate. Myocardial contractility in alcoholic rats was further depressed as revealed by a significant decrease in the peak rate of ventricular pressure decay. Importantly, end-diastolic pressure was elevated 5.2-fold in the left ventricle and 2.9-fold in the right ventricle after 8 mo of ethanol consumption. LV diastolic chamber volume increased through myocardial remodeling as the longitudinal axis and transverse diameters from the base to the apex increased in experimental animals while the thickness of the LV diminished. Structural and hemodynamic alterations resulted in a 571% increase in the volume of diastolic circumferential wall stress on the left ventricle. Damage to the myocardium was increased in alcoholic animals with the volume percent of myocardial lesions increasing 342% in the wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)


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