An Improved Technique for Producing Ventricular Hypertrophy with a Subcoronary Valvular Aortic Stenosis Model

Sink, James D.; Attarian, David E.; Chitwood, W. Randolph; Hill, Ronald C.; Pellom, Gary L.; Wechsler, Andrew S.

doi:10.1016/s0003-4975(10)61259-3

Cited by 25 publications

(7 citation statements)

References 2 publications

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“…After 6 months, we found significant increases in both heart weight/body and left ventricular weight/body weight ratios in these animals. Others using this model have also found similar responses (1,2,18). This compensatory cardiac growth is typical of the model.…”

Section: Discussionsupporting

confidence: 72%

“…In 16 animals (Groups I and Ill), we produced left vcntricular hypertrophy by plicating the non-coronary sinus of Valsalva (18). The surgery was performed in puppies at the age of 6-8 weeks, weighing 4-6 kg.…”

Section: Methodsmentioning

confidence: 99%

“…The non-coronary aortic valve cusp was plicated with a single horizontal mattress stitch using a non-absorbable suture reinforced with teflon felt pledgets. All animals had a palpable thrill in the ascending aorta following plication, which is sufficient to produce significant left ventricular hypertrophy (18). No effort was made to measure transvalvular gradients at this point.…”

Section: Methodsmentioning

confidence: 99%

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Regional oxygen supply and consumption balance in experimental left ventricular hypertrophy

Scholz

Grover²,

Mackenzie³

et al. 1990

Basic Res Cardiol

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The aim of the present study was to determine if the relationship between myocardial O2 supply and O2 consumption was preserved after prolonged pressure overload due to aortic valve stenosis. This was examined in anesthetized open-chest dogs in which the aortic valve was plicated 6 months previously. We measured coronary blood flow with radioactive microspheres and regional small vessel O2 saturation with microspectrophotometry, to obtain O2 supply, and O2 consumption. Regional O2 consumption was calculated as the product of flow and O2 extraction. The left ventricular weight/body weight ratio was 81% greater in the dogs with aortic valve stenosis. There were no hemodynamic differences between the groups except that left ventricular systolic pressure was 38 +/- 22 mm Hg greater than aortic in the hypertrophied group. Coronary blood flow did not differ between the control and hypertrophied groups nor were there subepicardial vs subendocardial differences. When maximal coronary flow was determined with chromonar (10 mg/kg), the flow increase was significantly attenuated in the hypertrophied subendocardium (242.1 +/- 82.3 (hypertrophy) vs 512.4 +/- 204.1 ml.min-1.100 g-1 (control). There were no significant differences in O2 extraction or O2 consumption/g between control and hypertrophied animals. There was a significantly lower O2 supply/consumption ratio in the subendocardium compared to the subepicardium of both groups. However, the O2 supply/consumption ratio was not decreased by hypertrophy. Thus, despite significant hypertrophy, a loss of flow reserve and a high left ventricular pressure, O2 supply/consumption balance is preserved in valvular aortic stenosis at rest.

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Section: Discussionsupporting

confidence: 72%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Regional oxygen supply and consumption balance in experimental left ventricular hypertrophy

Scholz

Grover²,

Mackenzie³

et al. 1990

Basic Res Cardiol

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“…All animals had a palpable thrill in the ascending aorta following plication. No direct valve gradients were measured since the presence of a thrill in the aorta has been shown to represent a pressure gradient of at least 15 mm Hg, which is sufficient to produce significant left ventricular hypertrophy at 6 months [2,18]. The pericardium was repaired and the thoracotomy was closed over a temporary chest tube.…”

Section: Methodsmentioning

confidence: 99%

Pacing-Induced Cardiac Failure of Hypertrophic Hearts: Effects of Cyclic GMP Reduction

Huang¹,

Weiss²,

Tse³

et al. 1999

Journal of Surgical Research

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“…In eight mongrel puppies, pressure-overload left ventricular hypertophy was created using aortic valve plication (Scholz et al 1993;Sink et al 1980). The animals were 6-8 weeks old and weighed 4-6 kg.…”

Section: Experimental Preparationmentioning

confidence: 99%

Positive inotropy due to lowering cyclic GMP is also mediated by increases in cyclic AMP in control and hypertrophic hearts

Naim¹,

Rabindranauth²,

Weiss³

et al. 1998

Can. J. Physiol. Pharmacol.

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The aim of the current study was to determine if lowering myocardial cyclic GMP by guanylate cyclase inhibition would add independently to the positive inotropic effects caused by raising cyclic AMP and if these effects are modified in left ventricular hypertrophy (LVH) produced by aortic valve plication. Isoproterenol (ISO) (0.1 mg x kg(-1) x min(-1)) was infused into a branch of the left anterior descending coronary artery of seven control and eight hypertrophy open-chest anesthetized dogs. After 10 min, simultaneous infusion of methylene blue (MB) (2 mg x kg(-1) x min(-1)) was initiated at the same site. Hypertrophy increased heart weight and heart weight/body weight ratio. While both drugs increased left ventricular dP/dt(max), no additional global effects were observed in either group. Changes in regional variables followed the same pattern in both groups, i.e., ISO produced an increase that was enhanced by the addition of MB. ISO increased segment shortening, with a significant change in the control group. ISO increased regional force in both groups. The addition of MB increased force above ISO levels, with a significant change in the LVH group. ISO increased regional minute work (g x mm x min(-1)) (control, 1779 +/- 428 to 2541 +/- 500; LVH, 1157 +/- 253 to 1839 +/- 404) and O2 consumption. MB further increased regional work (control, 2993 +/- 952; LVH, 2416 +/- 853) and O2 consumption. ISO raised cyclic AMP (pmoles x g(-1)) (control, 468 +/- 41 to 580 +/- 84; LVH, 445 +/- 43 to 562 +/- 71) and had no effect on cyclic GMP (pmoles x g(-1)) (control, baseline 3.27 +/- 0.22, ISO 2.87 +/- 0.23; LVH, baseline 6.84 +/- 1.12, ISO 5.66 +/- 0.54). The addition of MB lowered cyclic GMP (control, 2.41 +/- 0.26; LVH, 3.68 +/- 0.35), but also increased cyclic AMP (control, 1021 +/- 121; LVH, 1107 +/- 134). Similar results were observed in control hearts using a specific soluble guanylate cyclase inhibitor (ODQ) in terms of changes in local work, O2 consumption, and cyclic nucleotides. Thus, at least part of the positive inotropic response to lowering cyclic GMP was mediated by changes in cyclic AMP in the current model. This was true in both control and LVH animals, although baseline cyclic GMP levels were higher, and a larger reduction in cyclic GMP was observed with MB in the LVH group.

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An Improved Technique for Producing Ventricular Hypertrophy with a Subcoronary Valvular Aortic Stenosis Model

Cited by 25 publications

References 2 publications

Regional oxygen supply and consumption balance in experimental left ventricular hypertrophy

Regional oxygen supply and consumption balance in experimental left ventricular hypertrophy

Pacing-Induced Cardiac Failure of Hypertrophic Hearts: Effects of Cyclic GMP Reduction

Positive inotropy due to lowering cyclic GMP is also mediated by increases in cyclic AMP in control and hypertrophic hearts

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