Effect of angiotensin inhibition on the coronary artery lower pressure limit in anesthetized dogs

Rouleau, Jacques R.; Simard, Denis; Kingma, Jonh G

doi:10.1139/y00-071

Cited by 4 publications

(1 citation statement)

References 32 publications

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“…After return to baseline, coronary PFR were constructed by incremental (5-to 10-mmHg increments) lowering of arterial pressure; the autoregulatory break point (LPL) for each curve was determined as described previously (23). Coronary pressures were not allowed to fall below the LPL to avoid potential preconditioning effects.…”

Section: Coronary Pfr and Distribution Of Myocardial Blood Flowmentioning

confidence: 99%

Influence of Acute Renal Failure on Coronary Vasoregulation in Dogs

Kingma

Vincent

Rouleau

et al. 2006

Journal of the American Society of Nephrology

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Impaired renal function is associated with an increased risk for cardiovascular events and death, but the pathophysiology is poorly defined. The hypothesis that coronary blood flow regulation and distribution of ventricular blood flow could be compromised during acute renal failure (ARF) was tested. In two separate groups (n ‫؍‬ 14 each) of dogs with ARF, (1) coronary autoregulation (pressure-flow relations), vascular reserve (reactive hyperemia), and myocardial blood flow distribution (microspheres) and (2) coronary vessel responses to intracoronary infusion of select endothelium-dependent and -independent vasodilators were evaluated. In addition, coronary pressure-flow relations and vascular reserve after inhibition of nitric oxide and prostaglandin release were evaluated. Under resting conditions, myocardial oxygen consumption increased in dogs with ARF compared with no renal failure (NRF; 11.8 ؎ 9.2 versus 5.0 ؎ 1.5 ml O 2 /min per 100 g; P ‫؍‬ 0.01), and the autoregulatory break point of the coronary pressure-flow relation was shifted to higher diastolic coronary pressures (60 ؎ 17 versus 52 ؎ 8 mmHg in NRF; P ‫؍‬ 0.003); the latter was shifted further rightward after inhibition of both nitric oxide and prostaglandin release. The endocardial/epicardial blood flow ratio was comparable for both groups, suggesting preserved ventricular distribution of blood flow. In dogs with ARF, coronary vascular conductance also was reduced (P ‫؍‬ 0.001 versus NRF), but coronary zero-flow pressure was unchanged. Vessel reactivity to each endothelium-dependent/independent compound also was blunted significantly. In conclusion, under resting conditions, coronary vascular tone, reserve, and vessel reactivity are markedly diminished with ARF, suggesting impaired vascular function. Consequently, during ARF, small increases in myocardial oxygen demand would induce subendocardial ischemia as a result of a limited capacity to increase oxygen supply and thereby contribute to higher risk for adverse coronary events and mortality. Several major clinical trials have documented that reduced renal function is associated with increased risk for cardiovascular events and death (2,3) in patients with acute or chronic renal disease (4). Renal disease also is an important risk factor for cardiovascular complications after myocardial infarction and cardiogenic shock (5). Renal failure modifies most factors that regulate cardiovascular function via direct hemodynamic effects, neurogenic reflexes, and circulating hormones (6). The loss of cardiovascular reserve as a result of renal disease may explain the high morbidity and mortality in patients with end-stage renal failure (4,7,8). Coronary autoregulation is an important homeostatic mechanism for maintenance of nutrient and oxygen delivery to the myocardium (9 -11). Intrinsic autoregulatory mechanisms adjust tone within the microvasculature to maintain distribution of myocardial blood flow over a range of oxygen supply and demand requirements (9). Factors that are involved include intra-and ext...

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Section: Coronary Pfr and Distribution Of Myocardial Blood Flowmentioning

confidence: 99%

Influence of Acute Renal Failure on Coronary Vasoregulation in Dogs

Kingma

Vincent

Rouleau

et al. 2006

Journal of the American Society of Nephrology

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Angiotensin inhibition and coronary autoregulation in a canine model of LV hypertrophy

Rouleau¹,

Simard²,

Blouin³

et al. 2002

Basic Research in Cardiology

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In humans with hypertension and LV hypertrophy, beneficial effects of angiotensin inhibition may be associated with preserved autoregulatory capacity. We studied the effect of acute angiotensin converting enzyme (ACE) inhibition on coronary autoregulatory pressure-flow relations and transmural distribution of blood flow in sham and LV hypertrophy dogs. Heart/body weight ratio increased (p = 0.001) from 5.5 +/- 0.7 in sham to 6.9 +/- 0.5 in LV hypertrophy dogs. The lower coronary pressure limit (LPL) on the pressure-flow relation was 47 +/- 2 mmHg in sham and 57 +/- 6 mmHg (p = 0.001) in LV hypertrophy dogs; after acute ACE-inhibition the LPL was reduced to 40 +/- 5 mmHg and 49 +/- 6 mmHg (p = 0.001), respectively. Transmural distribution of blood flow was preserved at the LPL in both groups before and after acute ACE-inhibition. Concomitant blockade of prostaglandin and nitric oxide release and bradykinin catabolism had no additional effects on the LPL and distribution of blood flow. After acute ACE-inhibition in LV hypertrophy dogs, distribution of blood flow across the LV wall was preserved and subendocardial vascular reserve was maintained even though the LPL was significantly lower. Preservation of autoregulatory capacity by ACE inhibitors contributes to beneficial outcome in patients with hypertension and LV hypertrophy.

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