Coronary Vessel Diameter Research Articles

Nonischemic myocardial damage induced by nonocclusive constriction of coronary artery in rats

To determine whether reduction in coronary vessel diameter leads to alterations in cardiac function, coronary perfusion, and tissue integrity, the left coronary artery of rats was narrowed and ventricular hemodynamics measured at 3 and 5 days after surgery. Coronary artery narrowing averaged 62% and end-diastolic pressure was increased, whereas peak systolic pressure, positive change in pressure over time, stroke volume, and total peripheral resistance were decreased. However, this impairment of function was accompanied by a preservation of resting coronary blood flow (CBF), although a 43% decrease in maximal CBF was detected. Foci of reparative fibrosis and myocytolytic necrosis were found primarily in the endomyocardium and midmyocardium. These lesions were temporally distinct, corresponding to 5 days and 12- to 24-h-old forms of myocardial damage, respectively. The changes in maximal CBF correlated with the degree of stenosis, whereas the volume fraction, average cross-sectional area, and number of foci of reparative fibrosis lesions per unit area of myocardium correlated exclusively with end-diastolic pressure. In conclusion, reductions in luminal diameter of a major coronary artery not affecting resting coronary perfusion have a profound detrimental impact on cardiac performance and initiate immediate myocyte cell loss that is ongoing. Thus tissue and cellular damage may not be ischemic in nature but rather mediated by other mechanisms such as unbearable mechanical stress.

Small coronary vessel pressure and diameter in an intact beating rabbit heart using fixed-position and free-motion techniques.

Small coronary vessel pressure and diameter in an intact beating rabbit heart using fixed-position and free-motion techniques.

Factors Influencing Patency of Saphenous Vein Grafts

To determine factors affecting saphenous vein graft patency, 218 grafts in 66 unselected patients were studied angiographically 1 year after operation. Fourteen variables were extracted from the angiograms, electrocardiograms, and intraoperative flow measurements to assess their predictive value. Preoperative coronary vessel diameter and degree of proximal stenosis measured angiographically correlated significantly with graft patency. Graft patency for vessels > 1.5 mm in diameter with > 70% stenosis was 93% (98 out of 105). Vessel size at operation and the presence of reactive hyperemia > 20 ml per minute also correlated significantly with graft patency. Reactive hyperemia increased significantly as the severity of the vessel stenosis proximal to the graft increased, thus suggesting a mechanism for the improved patency rate of grafts to more stenotic vessels. The patency rate of the end-to-side component of a continuity graft (left anterior descending coronary artery and diagonal or marginal artery in 1 graft) was 100% and of the side-to-side component, 77%. This study shows that the patency rate for saphenous vein grafts compares favorably with the reported patency for internal mammary grafts when critical factors such as vessel size (> 1.5 mm) and degree of stenosis (> 70%) are considered in bypass selection.

Sympathetic control of major coronary artery diameter in the dog.

The diameter of a major coronary artery, the ramus interventricularis ventralis (RIV), was measured in dogs with arrested hearts perfused by an extracorporeal circulation. The resting diastolic diameter was 1.78 +/- 0.07 mm (mean +/- SE) at a diastolic pressure of 74.2 +/- 3.4 mm Hg. Bilateral supramaximal stimulation of fibers leaving the cranial pole of the stellate ganglion decreased the diameter by 71.2 +/- 8.9 micrometer, i.e., 4.0 +/- 0.5% of the resting diameter. Stimulation of the left stellate ganglion contributed 59.8 +/- 5.7% of the maximum response; that of the right contributed 40.3 +/- 5.5%. Stimulation of the thoracic ganglia (T2-4) resulted in a 1.2 +/- 0.4% decrease in coronary vessel diameter. RIV failed to respond to bilateral caudal cervical ganglion stimulation. After iv administration of phentolamine, 1-2 mg/kg, no response to sympathetic stimulation could be elicited. Therefore, it appears that alpha-receptors are activated by the release of the sympathetic neurotransmitter to sympathetic stimulation and that beta-receptors are not involved in the response of RIV to sympathetic stimulation.

Comparative study of coronary vessel diameters in intravital and postmortal angiograms (author's transl)

In a total of 21 mongrel dogs a comparison between intravital and postmortal coronary arteriograms was made so as to establish the difference in vessel diameter. Fresh postmortal hearts injected in situ showed an average increase in coronary vessel diameter of approx. 6 per cent. Examinations of 24 hour postmortal hearts which were removed from the animals showed a vessel diameter increase of barely 20 per cent in the mean. These 20 per cent correspond fairly well with literature information about the maximal widening of coronary vessels with nitroglycerin. Nerves which are still functioning, and humoral substances which may influence the still living muscle in vessel walls are supposed to be the reason for the smaller increase in fresh postmortal in situ illustrated coronary arteries. It must be stressed, that the measured differences between intravital and postmortal coronary artery diameters can only be representative of wall sections free of arterioslcerosis.

Cellular protection during myocardial ischemia: the development and characterization of a procedure for the induction of reversible ischemic arrest.

An isolated perfused working rat heart model was used to investigate the extent to which various protective agents, used either singly or in combination, were able to increase the resistance of the heart to periods of transient ischemia. The aim of the studies was to develop a solution which, if infused into the coronary vessels just prior to the onset of ischemia, would rapidly induce arrest and would also counteract several of the deleterious cellular changes known to occur during myocardial ischemia. Agents with induce cardiac arrest, modify cellular ion loss, affect substrate utilization, energy production and energy stores, affect coronary vessel diameter and cell swelling, prevent dysrhythmias, and affect metabolic rate were investigated. The additive effects of these agents were evaluated. An aqueous solution was formulated which contained high concentrations of potassium and magnesium, in combination with adenosine triphosphate, creatine phosphate and procaine. This solution increased the recovery of the ischemic (37 degrees C for 30 min) rat heart from 0% to 93%. The safe period of ischemia could be further increased by the use of hypothermia.

Dynamic pressures in the pial arterial microcirculation.

Dynamic pressures in the pial arterial microcirculation.

Evaluation of dipyridamole (Persantin)

Cardiovascular effects of a newly synthesized benzoxadiazol derivative K+ channel opener, YM099, 2-(7,8-dihydro-6,6-dimethyl-6H-[1,4]oxazino[2,3-ƒ][2,1,3]benzoxadiazol-8-yl) pyridine N-oxide, were evaluated in dogs. In pentobarbital-anesthetized dogs, YM099 (1–10 μg/kg i.v.), similarly to levcromakalim (1–10 μg/kg i.v.), dose dependently increased coronary artery blood flow, max.dp/dt and cardiac output, and decreased total peripheral resistance and mean blood pressure, with a small increase in heart rate. These vasodilator effects were antagonized by glibenclamide (3 mg/kg i.v.). Interestingly, YM099 selectively increased coronary artery blood flow, although it increased carotid, coronary, mesenteric and renal artery blood flows and cardiac output. In addition, YM099 (1–10 μg/kg i.v.) increased large conductive coronary artery vessel diameter as well as coronary artery blood flow. In conscious dogs, YM099 (100 μg/kg i.v.) also increased the diameter of large conductive and small resistive coronary arteries. In conclusion, YM099 is a potent vasodilator agent, with particularly pronounced effects on the coronary artery. These effects of YM099 may be mediated by the opening of ATP-sensitive K+ channels.