Stenosis Resistance Research Articles

Fixed vs nonfixed coronary stenosis: The response to a fall in coronary pressure in a canine model

The resistance of a coronary stenosis capable of passive vasomotion may change in response to alterations in intraluminal pressure. We studied the effects of a fall in perfusion pressure on the hemodynamics of two types of coronary stenosis in 12 open chest dogs: 1) a stenosis produced by placing a soft wire snare around the artery, and 2) a stenosis that was fixed in severity, produced by introducing and tying a short section of hollow plastic tubing into the coronary artery. Aortic pressure, coronary pressure proximal and distal to the stenosis, and coronary flow were measured. Pressure in the stenotic artery was lowered by tightening a snare placed very proximally on the artery. In arteries with a snare stenosis, lowering proximal coronary pressure by a mean of 31 mm Hg caused a rise in stenosis resistance from 0.86 +/- 0.06 to 1.38 +/- 0.14 units (p less than 0.001). However, in arteries with a fixed plastic stenosis, lowering the proximal coronary pressure by a mean of 30 mm Hg caused a fall in stenosis resistance from 0.36 +/- 0.04 to 0.21 +/- 0.03 units ( p less than 0.001). The increase in resistance of the snare stenoses as pressure was lowered may be attributed to passive narrowing of the stenotic segment, suggesting that these stenoses were not fixed in severity. However, the fixed plastic stenoses did not show an increase in resistance as pressure fell because the tubing was not capable of passively narrowing. Therefore, the hemodynamics of a coronary stenosis depend importantly on the type of stenosis that is present and whether it is capable of vasomotion.

Contribution of stenosis resistance to the rise in total peripheral resistance during experimental renal hypertension in conscious dogs.

1. Mild, moderate and severe renal artery stenosis was induced by uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, following by a return to control values 24 h after deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. In moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. In these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. In mild stenosis the changes in both cardiac output and total peripheral resistance was variable and not statistically significant. In this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. In all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of non-renal beds.

Changes in ischemic blood flow distribution and dynamic severity of a coronary stenosis induced by beta blockade in the canine heart.

The effects of equipotent beta 1-receptor-blocking doses of propranolol, metoprolol and sotalol on distal coronary pressure, stenosis resistance and regional myocardial blood flow (endo/epi) were studied in anesthetized dogs with a severe noncircumferential stenosis of the left circumflex coronary artery. No significant differences between the three beta blockers were observed for overall hemodynamics and regional myocardial blood flow. After drug treatment, subendocardial blood flow (0.47 +/- 0.05 to 0.78 +/- 0.05 ml/min/g) and endo/epi (0.67 +/-0.04 to 1.18 +/- 0.04) increased significantly (p less than 0.05) in the ischemic region. These changes were associated with a marked increase in distal coronary perfusion pressure and a decrease in heart rate. Resistance across the stenosis decreased significantly (p less than 0.05) after beta-receptor blockade (3.2 +/- 0.3 to 1.4 +/- 0.2 units). Atrial pacing to control heart rate only partially attenuated these changes. These results suggest that a favorable redistribution of ischemic blood flow after beta blockade is the result of an increase in distal diastolic pressure-time index and an autoregulation-induced increase in distal bed vascular resistance due to a decrease in myocardial oxygen demand associated with beta blockade. The latter effect also resulted in a decrease in the dynamic severity of a proximal coronary stenosis.

Redistribution of myocardial blood flow distal to a dynamic coronary arterial stenosis by sympathomimetic amines: Comparison of dopamine, dobutamine and isoproterenol

The effects of dopamine, dobutamine and isoproterenol on coronary hemodynamics, severity of stenosis, distal bed resistance and transmural myocardial perfusion gradients with radioactive microspheres were studied in dogs with a mild obstruction of the left circumflex coronary artery anesthetized with morphine-chloralose. Changes in transmural blood flow were related to the ratio of the diastolic aortic pressure-time Index to tension-time index (DPTI/TTI) and the ratio of the distal diastolic coronary pressure-time index to tension-time index (DDPT1/TTI). At doses of 5 gmg/kg per min, dopamine had no significant effect on DPTI/TTI, DDPTI/TTI or endocardial/epicardial flow ratio; however, dobutamine produced a slight decrease in this flow ratio and in DDPTI/TTI. At doses of 10 gmg/kg per min, both drugs produced a significant (p <0.05) reduction in diastolic coronary pressure distal to the stenosis, DDPTI/TTI and endocardial/epicardial flow ratio without change in DPTI/TTI. In comparison, isoproterenol (0.01 and 0.05 gmg/kg per min) produced dose-related decreases in endocardial/epicardial flow ratio, DDPTI/TTI and DPTI/TTI. During infusion of each sympathomimetic agent, there was a corresponding reduction in distal bed vascular resistance but a concomitant increase in stenosis resistance. The results also show that dopamine and dobutamine, as well as isoproterenol, are capable of producing a maldistribution of coronary blood flow distal to a mild coronary arterial stenosis and that such a redistribution of flow is dependent on dose, reduction of the distal diastolic coronary pressure-time index and decrease in DDPTI/TTI. It Is further concluded that hemodynamic changes distal to a coronary arterial stenosis seriously jeopardize the usefulness of DPTI/TTI; however, DDPTI/TTI can be used to predict drug effects on the endocardial/epicardial flow ratio in an ischemie area. This study demonstrates that “fixed” stenoses can undergo dynamic processes and sympathomlmetic amines increase the resistance to flow through a stenotic coronary artery in the nonfailing heart.

The importance of renal vascular tone in determining the severity of renal artery stenosis in dogs.

1. The effects of the state of renal vascular tone during induction of renal artery stenosis on the subsequent systemic blood pressure and renin responses have been studied in chronically instrumented, conscious dogs. 2. In one group of dogs, renal vascular tone was altered by brief (2-3 min) renal artery infusions of ACh, saline, methoxamine or angiotensin II during narrowing of the renal artery to reduce distal pressure to 40 mmHg. The infusions were turned off 1 min later. 3. The more vasoconstricted the kidney at the time of stenosis, the slower was the restoration of distal renal artery pressure and the greater the rises in systemic blood pressure, plasma renin activity (PRA) and effective stenosis resistance. At the end of 1 hr of stenosis, the rises in systemic blood pressure were 4.3 +/- 3.3, 11.3 +/- 3.3, 28.9 +/- 3.3 and 26.3 +/- 2.8 mmHg for the ACh, saline, methoxamine and angiotensin II-infused dogs respectively; rises in PRA were 0.3 +/- 0.24, 1.18 +/- 0.42, 5.09 +/- 1.38 and 4.02 +/- 0.74 ng/ml. per hr respectively. 4. In another group of dogs a given aortic-renal artery pressure gradient was produced on two occasions: (i) with the animal conscious; (ii) under brief sodium pentobarbitone anaesthesia and preparation for surgery. After 24 hr systemic blood pressure had risen by 15.7 +/- 3.6 mmHg above initial values when stenosis was induced under anaesthesia (P < 0.05) and only by 1.2 +/- 3.6 mmHg (N.S.) when it was induced with the animal conscious. Corresponding rises in PRA were 1.29 +/- 0.42 (P < 0.05) and 0.25 +/- 0.11 (N.S.) ng/ml. per hr. Establishment of a given gradient in the high vascular resistance kidney of the anaesthetized dog thus requires greater narrowing of the renal artery than in the lower resistance renal bed of the conscious animal. 5. The tone of the renal vascular bed is a major determinant of the severity of renal artery stenosis.

Effect of coronary arterial pressure on coronary stenosis resistance.

Effect of coronary arterial pressure on coronary stenosis resistance.