Normalization of impaired coronary circulation in hypertrophied rat hearts.

Sato, Fumitoshi; Isoyama, Shogen; Takishima, Tamotsu

doi:10.1161/01.hyp.16.1.26

Cited by 39 publications

(12 citation statements)

References 29 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, the characteristics of the perfusate modify the coronary hemodynamics measured in isolated hearts. 6 or in our previous ex vivo hearts perfused with crystalloid solution containing red blood cells and albumin 27 (less than 2.0 versus near 3.0 of peak/resting flow in control group young hearts described in our previous study 27 ). Therefore, in this study we added bovine red blood cells and serum albumin to estimate coronary perfusion pressureflow relations under resting conditions and during maximal vasodilation in pressure-overloaded and sham-operated control hearts.…”

Section: Discussionmentioning

confidence: 76%

“…The perfusate was equilibrated with a 20% O^ 3% COfc and 77% N 2 gas mixture by bubbling. 27 ' 28 The perfusate pH, POj, Pco^ and hematocrit were measured and ranged from 7.32 to 7.45, from 114 to 149 mm Hg, from 20 to 42 mm Hg, and from 31% to 34%, respectively. We prepared approximately 1,000 ml perfusate for use on the same day and studied one or two pairs of hearts of sham-operated and banded rats in each age group as far as possible, using the same perfusate to eliminate the effects of slight variation in pH, PO2, Pcc^, and hematocrit on coronary circulation.…”

Section: Perfusion Techniquementioning

confidence: 99%

“…' 27 In the present study, the purpose was to examine the effects of pressure overload on abnormalities of the coronary circulation and myocardial hypertrophy in young adult and aged rats. It was impossible to examine the response of the myocardium and coronary vasculature to more severe pressure overload because more severe loading might have produced an extremely high mortality in old rats, as mentioned in the previous study of Isoyama et al 10 The data in this study show myocardial hypertrophic response and coronary hemodynamic response to relatively mild pressure overload in the two age groups.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Effect of age on coronary circulation after imposition of pressure-overload in rats.

1991

Self Cite

View full text Add to dashboard Cite

We examined the effects of pressure overload on coronary circulation in young adult (7 months old) and old rats (18 months old). Four weeks after the ascending aorta was banded, in vivo left ventricular pressure was measured to estimate the degree of pressure load. In the two age groups, similar increases in peak left ventricular pressure were observed (113 ±7 mm Hg in sham-operated rats versus 160 ±11 mm Hg in banded rats of the young adult group; 103 ±7 mm Hg in sham-operated rats versus 156±11 mm Hg in banded rats of the old group). After isolating the hearts, they were perfused with Tyrode's solution containing bovine red blood cells and albumin. Resting coronary perfusion pressure-flow relations and reactive hyperemic response after a 40-second ischemia were obtained under beating but nonworking conditions. In young adult banded rats, significant myocardial hypertrophy was observed at the organ level (124% of controls in left ventricular dry weight/body weight ratio; 119% in left ventricular dry weight/tibial length ratio) and at the cell level. Minimal coronary vascular resistance obtained by the perfusion pressure-peak flow relation during reactive hyperemia increased to 150% of controls, and coronary flow reserve decreased significantly. In contrast, myocardial hypertrophy was not observed at the organ or cell level in old banded rats. However, minimal coronary vascular resistance increased, and flow reserve decreased significantly. Thus, pressure overload with coronary arterial hypertension caused abnormalities of the coronary circulation in old subjects even in the absence of myocardial hypertrophy. These coronary vascular changes as well as diminished hypertrophic response may explain the high incidence of heart failure or ischemic episodes during chronic hemodynamic stress in aged patients. Address for reprints: Tamotsu Takishima, MD, First Department of Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai 980, Japan.Received February 19, 1990; accepted in revised form November 6, 1990. creases in shortening velocity have been reported at organ and muscle levels.413 -17 Furthermore, the capacity for myocardial hypertrophy to develop in response to chronic pressure-or volume-overload is diminished in aged subjects compared with younger adults. 10-11 -18 -19 At present, however, there is no information concerning the coronary vascular response to stress from chronic pressure overload in aged subjects.Abnormalities of the coronary circulation in pressure-overloaded hearts are caused by hypertensive vascular changes 20 -21 as well as by the presence of myocardial hypertrophy. 22-24 Therefore, even if a similar pressure-overload stress is applied to young adult and old subjects, the stress may produce different effects on coronary circulation between young and old subjects directly through underlying agerelated changes in coronary vasculature or indirectly through the diminished myocardial hypertrophic response. To test this hypothesis, we examined the effects of pr...

show abstract

Section: Discussionmentioning

confidence: 76%

Section: Perfusion Techniquementioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Effect of age on coronary circulation after imposition of pressure-overload in rats.

1991

Self Cite

View full text Add to dashboard Cite

show abstract

“…16 In our previous study, 18 " 20 the abnormalities of the coronary circulation in cardiac hypertrophy were not fixed but were fully reversible in short-term pressure overload (4 weeks). 18 " 20 However, decreased vasodilator reserve in long-term pressure-overloaded hearts (10 weeks) did not reverse after relief of the overload. 19 Thus, the duration of pressure overload and coronary hypertension, and the time after its relief may be important factors that modulate collagen metabolism in the heart.…”

Section: Methodological Considerationsmentioning

confidence: 94%

“…The preparation of bovine red blood cells has been described elsewhere. 20 Whole bovine blood was centrifuged, and the red blood cells were washed twice with the Tyrode's solution at 4°C. The washed red blood cells and serum albumin were added to the Tyrode's solution.…”

mentioning

confidence: 99%

Collagen deposition and the reversal of coronary reserve in cardiac hypertrophy.

et al. 1992

Self Cite

View full text Add to dashboard Cite

The aim of this study was to clarify how collagen deposition or medial hypertrophy of the vascular wall affects the coronary dilator reserve in pressure-overloaded hearts and whether inhibition of collagen deposition reverses the abnormalities after relief of pressure overload. We used ascending aortic banding and debanding methods and superimposed /J-amlnopropionitrile in some of the banded rats (50 mg/kg i.p., twice a day). Ten weeks of banding increased in vivo peak systolic left ventricular pressure and produced medial hypertrophy, an increase in collagen deposition in the myocardial and pertvascular tissues, and myocardial hypertrophy in the banded group without /3-aminopropionltrile treatment Superimposition of /J-aminopropionitrile treatment on banding inhibited the increase in collagen deposition. In the groups debanded after the 10-week banding period, both with and without 0-amlnopropionitrile treatment, medial and myocardial hypertrophy regressed 4 weeks after debanding. We estimated coronary dilator reserve in Langendorff preparations perfused with modified Tyrode's solution containing oxygenated bovine red blood cells and serum albumin. The ratio of reactive peak flow after brief ischemia-to-resting flow decreased in both of the banded groups. After debanding, the ratio remained lower in the banded group without 0-aminopropionitrile treatment than in the control group. However, debanding in the group with 0-aminopropionitrile treatment increased the ratio to a level similar to that of the control group. Thus, in pressure-overloaded cardiac hypertrophy with coronary hypertension, coronary reserve seems to be determined by medial hypertrophy independently of collagen deposition, but collagen deposition plays an important role in the reversal of vasodilator reserve after relief of the overload. 6 -81112 However, it is not clear how the collagen deposition in hypertrophied hearts affects the coronary circulation.In the present study, we attempted to clarify how the collagen deposition or medial hypertrophy of the vascular wall affects the coronary dilator reserve in pressureoverloaded hearts and whether the inhibition of collagen deposition reverses the abnormalities after relief of the overload. To inhibit collagen deposition in the vascular and extravascular myocardial tissue, we superimposed

show abstract