[Evaluation of non-circular orbit in thallium-201 myocardial SPECT].
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Heart↗
Biomedical subjects
H Tomoike
Publications and source records attributed to H Tomoike.
Smooth muscles from spastic coronary artery segments show hypercontractility to histamine.
An animal model of coronary spasm was produced in Göttingen miniature pigs by a selective endothelial denudation of the coronary artery. Five months after the denudation, intracoronary bolus administration of 10 micrograms/kg histamine reduced the luminal diameter angiographically by 57 +/- 16 and 17 +/- 10% (P less than 0.01) in the previously denuded and contralateral control coronary arteries. Muscle fibers of 0.08-0.1 mm wide were prepared from circumferential bundles of the medial smooth muscle in the spastic and nonspastic coronary arteries. Upward shifts of either dose-tonic contraction relationships in Ca2(+)-containing solution or dose-monophasic contraction relationships in Ca2(+)-free solution were noted in muscle fibers taken from the spastic site compared with those from the nonspastic site with no difference between the mean effective dose values. After skinning the muscle fibers with saponin, there was no significant difference in the Ca2+ concentration-tension relationships between the two fibers. These findings suggest that an increased number of histaminergic receptors and/or augmentation of signal transduction, but not Ca2+ sensitivity of the contractile proteins in the medial smooth muscle cells, cause histamine-induced coronary hypercontraction.
Animals↗
Quantitative and autoradiographic analyses of alpha-adrenergic and serotonergic receptors on aorta and coronary artery.
Norepinephrine, epinephrine, and 5-hydroxytryptamine (5-HT) modulate the vascular tone via specific receptors on the vascular wall. Binding characteristics and localization of alpha-adrenergic and serotonergic receptors were determined in porcine aortas and coronary arteries. Radioligand binding studies were done using frozen sections of vascular tissue (10 microns thick), and the obtained data were compared with findings on microsomal fractions prepared from smooth muscle cells. Affinities [dissociation constant (Kd)] of 125I-labeled 2-[beta-(4-hydroxyphenyl)-ethylaminomethyl]-tetralone (BE 2254), an alpha 1-antagonist, for alpha-adrenergic receptors on aortic and coronary microsomal fractions were 190 and 224 pM, respectively. The Kd of 125I-labeled lysergic acid diethylamide (LSD), a serotonergic antagonist, to serotonergic receptors on the aorta was 403 pM, a value less than that obtained for the coronary artery (873 pM, p less than 0.01). The Kd of 125I-BE 2254 on tissue sections from the aorta was 164 pM and did not significantly differ from that obtained for microsomal fractions. Inhibition constants of adrenergic agonists and antagonists for specific 125I-BE 2254 binding on aortic sections were identical with those obtained for microsomal fractions. Receptor densities examined by 125I-BE 2254 and 125I-LSD were higher in the aorta than in the coronary artery. 125I-BE 2254 bound specifically to alpha 1-adrenergic and 125I-LSD to 5-HT1-like receptors. Radiodensities of 125I-BE 2254 and 125I-LSD were homogeneous macroscopically across the aortic media. Silver grains distributed homogeneously over the smooth muscle cells across the media. There was no accumulation of silver grains to the intima.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic alpha-Antagonists↗
Heterogeneous distribution of a diffusional tracer in the aortic wall of normal and atherosclerotic rabbits.
Tracer distribution as an index of nutritional support across the thoracic and abdominal aortas in rabbits in the presence or absence of atherosclerotic lesions was evaluated using [14C]antipyrine, a metabolically inert, diffusible indicator. Intimal plaques were produced by endothelial balloon denudation of the thoracic aorta and a 1% cholesterol diet. After a steady intravenous infusion of 200 microCi of [14C]antipyrine for 60 seconds, thoracic and abdominal aortas and the heart were excised, and autoradiograms of 20-microns-thick sections were quantified, using microcomputer-aided densitometry. Regional radioactivity and regional diffusional support, as an index of nutritional flow estimated from the timed collections of arterial blood, was 367 and 421 nCi.g-1 (82 and 106 ml.min-1.100 g-1) in thoracic aortic media of the normal and atherosclerotic rabbits, respectively. Radioactivity at the thickened intima was 179 nCi.g-1 (p less than 0.01 versus media). The gruel was noted at a deeper site within the thickened intima, and diffusional support here was 110 nCi.g-1 (p less than 0.01 versus an average radioactivity at the thickened intima). After ligating the intercostal arteries, regional tracer distribution in the media beneath the fibrofatty lesion, but not the plaque-free intima, was reduced to 46%. Thus, in the presence of advanced intimal thickening, the heterogeneous distribution of diffusional flow is prominent across the vessel wall, and abluminal routes are crucial to meet the increased demands of nutritional requirements.
Animals↗
Actions of Ca2+ antagonists on two types of Ca2+ channels in rat aorta smooth muscle cells in primary culture.
Mechanisms of blockade of two types of Ca2+ channels by the organic Ca2+ antagonists, nicardipine, diltiazem, verapamil, and flunarizine, were examined in rat aorta smooth muscle cells in primary culture by using the whole-cell voltage-clamp method. T-type Ca2+ current (T-type ICa) was isolated by an internal perfusion of 5 mM F-, which irreversibly suppressed the L-type ICa, without affecting T-type ICa. L-type ICa was isolated by setting a holding potential at -60 mV, at which most of the T-type Ca2+ channels were inactivated. L-type ICa is halved by 0.1 microM nicardipine, 3.0 microM diltiazem, 0.6 microM verapamil, and 0.1 microM flunarizine, whereas T-type ICa is halved by the same drugs at 0.6, 30, 30, and 0.1 microM, respectively. Diltiazem and verapamil accelerated the decay of L-type ICa and cumulatively blocked L-type ICa during repetitive step depolarizations elicited every 30 seconds ("use-dependent block"). Diltiazem and verapamil neither changed the decay of T-type ICa nor showed a use-dependent block of T-type ICa. Nicardipine and flunarizine blocked both L- and T-type ICa from the first depolarization step after drug treatment ("tonic block") and shifted their steady-state inactivation curves to the left. The estimated binding constants of nicardipine and flunarizine for the inactivated state of T-type Ca2+ channels (48 and 19 nM, respectively) were smaller than those for the resting state of L-type Ca2+ channels (160 and 90 nM, respectively). A low concentration (0.1 microM) of nicardipine initially potentiated T-type ICa and then reduced it. We conclude from these results that 1) nicardipine and flunarizine block not only the resting state but, more preferentially, the inactivated state of both the L- and T-type Ca2+ channels; 2) verapamil and diltiazem preferentially act on the open state of the L-type Ca2+ channel and on the resting and inactivated state of the T-type Ca2+ channel; and 3) the T-type Ca2+ channel of the rat aorta smooth muscle cells appears to be more sensitive to nicardipine and flunarizine than does the L-type Ca2+ channel at around the resting membrane potential.
Animals↗
[Coronary circulation in physiological and pathological states].
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Animals↗
Enhanced responsiveness of smooth muscle, impaired endothelium-dependent relaxation and the genesis of coronary spasm.
Pathophysiology and genesis of coronary artery spasm were examined in vivo and in vitro in Göttingen miniature pigs. Five of 36 consecutive pigs before endothelial denudation showed evidence of regional hyperconstriction after intracoronary administration of histamine (group 1). Histologic examination revealed intimal thickening along the spastic site. Because 5 pigs died during endothelial denudation, cholesterol feeding was randomly assigned to 13 of the remaining 26 pigs (group 2) and others were fed a regular low cholesterol diet (group 3) for 3 months. Regional coronary hyperconstriction was also evident after intracoronary administration of histamine at the site of denudation, and the degree of constriction was 78 +/- 3 and 74 +/- 4% in groups 2 and 3, respectively. Because the intimal thickening was confirmed at the site of spasm in groups 2 and 3, spontaneous as well as denudation-induced intimal thickening accompanied the enhanced responsiveness to histamine, irrespective of the level of serum cholesterol. However, the role of geometry on histamine-induced luminal narrowing was only 6% and was not physiologically significant. Augmented responses of the coronary artery to histamine, but not to phenylephrine or potassium chloride were reproduced in the nonbeating isolated heart preparations perfused at 90 mm Hg with oxygenated Krebs-Henseleit solution, and the degree and location of in vitro hyperconstriction were similar to that in vivo and were not attenuated after pretreatment with the nerve transmitter blockers, guanethidine (3 X 10(-6) M), atropine (10(-6) M) and tetrodotoxin (3 X 10(-7) M). Accordingly, spasm can be provoked without the influence of blood constituents and neural factors.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Sustained dilatation of large coronary artery by alpha-human atrial natriuretic peptide in conscious dogs: a comparison with nitroglycerin.
The effects of alpha-human atrial natriuretic peptide (alpha-hANP) on the coronary circulation were compared with those of nitroglycerin in 16 conscious dogs chronically instrumented with a pair of miniature sonomicrometers and an electromagnetic flow probe placed on the left circumflex coronary artery. alpha-hANP (1 and 10 micrograms) and nitroglycerin (0.1, 1 and 10 micrograms) were administered intracoronarily via a cannula implanted in the proximal left circumflex coronary artery. Both alpha-hANP and nitroglycerin dose dependently increased the coronary diameter and coronary blood flow. Although alpha-hANP (10 micrograms) and nitroglycerin (1 microgram) dilated the large coronary artery to almost the same extent (92 +/- 10 vs. 98 +/- 8 microns), the time course of the dilating action differed; the peak dilatation occurred at 5.6 +/- 0.8 and 0.9 +/- 0.07 min (P less than 0.01), and full recovery occurred at 31.5 +/- 3.8 and 5.5 +/- 1.3 min (P less than 0.01) after alpha-hANP and nitroglycerin, respectively. Topical application of alpha-hANP (50 micrograms) to the epicardial coronary artery of three anesthetized open-chest dogs did not affect the coronary diameter and coronary blood flow, while nitroglycerin (50 micrograms) increased both variables. Thus, intracoronary alpha-hANP dilates the large coronary artery more gradually and more sustainedly than nitroglycerin does.
Animals↗
Effects of ionic and nonionic contrast media on coronary diameter and blood flow in chronically instrumented dogs.
The effects of intracoronary administration of ionic and nonionic contrast media on coronary circulation were studied in 14 chronically instrumented dogs. A pair of 10 MHz piezoelectric crystals and an electromagnetic flow probe were placed on the left circumflex coronary artery, under sterile conditions, to measure the epicardial coronary diameter and coronary blood flow, respectively. A polyethylene tube for drug infusion was inserted into the circumflex coronary artery proximal to the sonomicrometers. In the conscious dogs (n = 8), iopamidol, 2 ml and 5 ml increased the coronary diameter by 64 +/- 19 microns and 66 +/- 19 microns and coronary blood flow by 35 +/- 10% and 61 +/- 18%, respectively (p less than 0.01 vs control level). Meglumine diatrizoate, 2 ml and 5 ml, increased coronary diameter by 102 +/- 20 microns and 114 +/- 18 microns and coronary blood flow by 87 +/- 32% and 107 +/- 26%, respectively (p less than 0.01 vs control level). In the anesthetized dogs (n = 6), a bolus intracoronary injection of 5 ml iopamidol and meglumine diatrizoate within few seconds increased the coronary diameter by 103 +/- 23 microns and 164 +/- 39 microns (p less than 0.05) and increased the coronary blood flow by 126 +/- 33% and 180 +/- 40% (p less than 0.05), respectively. Balloon denudation of the endothelium was performed in six anesthetized dogs. The increases in coronary diameter and coronary blood flow after a bolus injection of contrast medium remained the same after the denudation. Thus application of iopamidol seems to be more suitable than meglumine diatrizoate for quantitative coronary angiography because of the milder and more transient effects on coronary circulation.
Acetylcholine↗
Amelioration by beta-adrenergic blockade of regional myocardial dysfunction induced by coronary artery occlusion after, but not before collateral development in conscious dogs.
Effects of beta-adrenergic blockade on regional myocardial dysfunction induced by coronary artery occlusion were studied in chronically instrumented, conscious dogs before (n = 8) and after (n = 7) collateral development. Intravenous atenolol or propranolol produced no beneficial effects on systolic shortening in the area rendered ischemic during 2 minutes of circumflex occlusion, before collateral development. After the collateral development by repetitive 2-minute coronary occlusions, regional asynergy recovered to the preocclusive level during 2 minutes of occlusion. Both atenolol and propranolol significantly improved the peak reductions of regional shortening by 19 +/- 9% and 18 +/- 9%, respectively (p less than 0.05 versus without beta-blockade). These beneficial actions of beta-blockade were again noted during atrial tachypacing at matched heart rates of 160 +/- 11 beats/min. Thus the beneficial effects of beta-blockade on regional asynergy during coronary occlusion depend on the level of functional state of the collaterals and cannot be totally accounted for by the reduction in heart rate or by the cardioselectivity.
Animals↗
Voltage-dependent anion-selective channels in cultured smooth muscle cells of the rat aorta.
1. Properties of the voltage-dependent anion-selective channel in cultured smooth muscle cells of the rat aorta were studied using the patch-clamp technique. 2. The channel had a single channel conductance of 346 +/- 4 pS (n = 43, mean +/- SEM) with symmetrical 142 mM-Cl- solution in inside-out patch configurations. 3. The channel was activated spontaneously at a potential range -20 approximately +20 mV and inactivated more rapidly with increases to more positive or negative potentials. 4. The channel was selective for anions and the permeability ratio for monovalent anion was Br-:Cl-:HCOO-:CH3COO-:propionate-:aspartate- = 1.1:1:0.7:0.4: less than 0.02: less than 0.02. 5. The openings of the channels were observed more frequently in inside-out membrane patches than in cell-attached ones, and were independent of intracellular free Ca concentrations. 6. The density of this channel was estimated to be 1.3/micron2. 7. Physiological roles of the channel were discussed.
Animals↗
Homogeneous distribution and pressure dependent reduction of coronary blood flow in right ventricular free wall during coronary hypoperfusion in anaesthetised open chest dogs.
Relationship of coronary perfusion pressure with total and regional myocardial blood flow in right ventricular free wall was studied in 10 anaesthetised open chest dogs. The right coronary artery was perfused by an autoperfusion system from the carotid artery. Total coronary blood flow into the perfused area was measured by an extracorporeal electromagnetic flow probe. Critical perfusion pressure of the right coronary artery, defined as the lowest pressure level below which the regional wall motion deteriorated, was 39(SEM1) mm Hg. Reactive hyperaemia was noted at 60(2) mm Hg, a level well above the critical perfusion pressure. There was an inverse linear relation between the level of reactive hyperaemia and perfusion pressure. Regional myocardial blood flow was measured by a tracer microsphere technique at control condition, just above and below the critical perfusion pressures and during coronary occlusion. This correlated closely with values obtained by an electromagnetic flow probe (r = 0.94, p less than 0.001) and both values were dependent on the level of perfusion pressure. Endocardial to epicardial flow ratio remained at unity at any level of coronary perfusion pressure. Thus the level of coronary perfusion pressure was a major determinant of the regional myocardial blood flow into the right coronary artery, and autoregulation of the regional myocardial blood flow was not apparent across the wall, despite the presence of a reactive hyperaemia.
Anesthesia, General↗
Low-voltage-activated calcium current in rat aorta smooth muscle cells in primary culture.
1. Electrical and pharmacological properties of the low-voltage-activated Ca2+ current (ICa, LVA) in rat aorta smooth muscle cells (SMC) in primary culture were examined, particularly in comparison with the high-voltage-activated Ca2+ current (ICa, HVA). Both types of Ca2+ currents were recorded in external solution containing 20 mM-Ca2+, using the whole-cell voltage-clamp technique. 2. ICa, LVA was evoked by step depolarizations to potentials more positive than -60 mV from a holding potential of -100 mV, and reached a peak in the current-voltage (I-V) relationship around -30 mV. ICa, HVA was activated at -20 mV, and reached a peak at +20 mV. 3. The intracellular dialysis of 5 mM-F- irreversibly suppressed ICa, HVA, with time, while it has little effect on the ICa, LVA. The ICa, LVA could be separated from the ICa, HVA by either selecting the holding and test potential levels or by perfusing intracellularly with F-. 4. The ratio of peak amplitude of Ba2+, Sr2+ and Ca2+ currents in the respective I-V relationship was 1.6:1.2:1.0 for high-voltage-activated Ca2+ channels and was 1.0:1.4:1.0 for low-voltage-activated ones. 5. The inactivation phase of ICa, HVA was fitted by a sum of double-exponential functions, the time constants of which were larger when the current was carried by Ba2+ than by Ca2+. The inactivation time course of ICa, LVA was fitted by a single-exponential function, and the time constant was practically the same when the current was carried by Ba2+ or by Ca2+. Activation and inactivation processes of ICa, LVA were potential-dependent. 6. The steady-state inactivation curve of ICa, LVA was fitted by the Boltzmann equation, having a mid-potential of -80 mV and a slope factor of 5.0. The recovery time course from steady-state inactivation was fitted by a sum of two exponential functions. The time constants of the faster phase were 230 and 380 ms, and those of slower phase were 2.8 and 1.8 s at the repolarization potentials of -120 and -100 mV, respectively. 7. The amplitude of ICa, LVA depended on the external Ca2+ concentration ([Ca2+]o), approaching saturation at 95 mM [Ca2+]o. 8. Various polyvalent cations blocked both types of Ca2+ current reversibly in the order (IC50 in M): La3+ (8 x 10(-8)) greater than Cd2+ (6 x 10(-6)) greater than Ni2+ (1 x 10(-5)) greater than Zn2+ (2 x 10(-5)) for ICa, HVA, and La3+ (6 x 10(-7)) greater than Zn2+ (3 x 10(-5)) greater than Cd2+ (4 x 10(-4)) greater than Ni2+ (6 x 10(-4)) for ICa, LVA.(ABSTRACT TRUNCATED AT 400 WORDS)
4-Aminopyridine↗
Duration of ischemia is vital for collateral development: repeated brief coronary artery occlusions in conscious dogs.
The effects of two types of repeated transient coronary artery occlusions on collateral development were examined in chronically instrumented, conscious dogs. A 2-minute coronary occlusion at 32-minute intervals (group 1, n = 11) or a 15-second occlusion at 4-minute intervals (group 2, n = 7) were repeated day and night without interruption. In both groups, the total duration of coronary occlusions each day was the same (90 minutes). Before and after repetitive occlusions of either group, effects of transient 2-minute coronary occlusion on regional segment shortening in the ischemic area were examined to assess the functional state of the collateral vessels. In group 1, systolic segment shortening in the area rendered ischemic was reduced to -97.8 +/- 17.7% of the preocclusive control value during 2 minutes of coronary occlusion. After 125-478 repetitive occlusions (3-11 days), the degree of hypokinesia during the 2-minute occlusion was significantly improved to -0.6 +/- 4.6% of the preocclusive value (p less than 0.001 vs. before the repetition). In group 2, it remained unchanged even after 3,500-5,450 repetitive occlusions (11-16 days): -111.8 +/- 8.2% before and -111.4 +/- 13.8% after the repetition of 15-second occlusions (NS). The ratio of peripheral coronary arterial pressure to aortic pressure during transient-coronary occlusion, measured by selective catheterization, was significantly higher in group 1 than in group 2 (64.4 +/- 5.3% vs. 20.7 +/- 1.3%, p less than 0.001). These findings suggest that myocardial ischemia of 2 minutes but not 15 seconds is vital to provide effective stimuli for angiogenesis.
Angiography↗
Intramural hemorrhage and endothelial changes in atherosclerotic coronary artery after repetitive episodes of spasm in x-ray-irradiated hypercholesterolemic pigs.
To assess whether coronary spasm affects the progression of atherosclerosis and results in evolution of myocardial infarction, the role of coronary spasm on the fine structure of conduit coronary arteries was studied morphologically. Göttingen miniature pigs were fed a semisynthetic diet containing 2% cholesterol and 1.1% sodium cholate. One month after being on this diet, the pigs were anesthetized and the endothelium of a branch of the left coronary artery was denuded using a balloon catheter. X-ray irradiation in a dose of 1,500 rad was given twice selectively to the area denuded, after 4 and 5 months of cholesterol feeding. Five months after endothelial denudation, transient (group A) and repetitive episodes (group B) of coronary spasm were provoked by single and periodic (five times every 5 minutes) intracoronary injections of serotonin (10 micrograms/kg/injection), respectively. The extent of spasm by serotonin at the previously denuded site was 84 +/- 4% (n = 4) and 90 +/- 5% (n = 6) narrowing in groups A and B (p = NS between groups), respectively. Forty minutes after the final administration of serotonin, the left coronary artery was relaxed by nitroglycerin, and the heart was isolated and perfuse-fixed under physiological pressure. Intramural hemorrhage was noted at the spastic site in six pigs of group B but not in group A. The average percent luminal narrowing, on cross sections at the spastic site in group B, was significantly greater than in group A (56 +/- 7% vs. 23 +/- 5%, p less than 0.01). Scanning electron micrographs revealed that the endothelial lining was intact at the nonspastic site in both groups. In addition to the appearance of intercellular bridges at the spastic site in both groups, squeezing of endothelial cells and adhesion of white blood cells were present at the spastic site exclusively in group B. These findings are consistent with the hypothesis that repetitive spasm may have an important role in the progression of atherosclerosis and/or myocardial infarction.
Angiography↗
Isosorbide dinitrate ameliorates myocardial ischemia after development of collateral function in a canine model.
The effects of i.v. administered isosorbide dinitrate (ISDN) on the reduced level of regional myocardial function during coronary occlusion were studied in conscious dogs before and after collateral development and in the absence of persistent coronary stenosis. The animals were instrumented during sterile surgery with a miniature pressure gauge for measuring left ventricular pressure and a cannula for aortic pressure. Two pairs of piezoelectric crystals were placed in normal and ischemic areas to determine regional circumferential length. A hydraulic cuff occluder and a Doppler flow probe were placed around the left circumflex coronary artery. Collaterals were induced to develop by 2 min of coronary occlusion applied repetitively at an interval of 32 min for 2 to 9 days, until the regional dysfunction produced by coronary occlusion had disappeared. Collateral development was estimated according to percentage of systolic shortening and endsystolic length area (ESL area) during the occlusion. Before collateral development, ISDN in a dose of 100 micrograms/kg did not affect the level of regional dysfunction. The ESL area was 250 +/- 54 and 248 +/- 52 mm.sec before and after ISDN, respectively. After collateral development, the ESL area was 51 +/- 13 mm.sec and it decreased by 35% after the i.v. administration of ISDN. The improvement by ISDN of transient myocardial dysfunction was achieved even during electrical tachypacing. Accordingly, the beneficial effects of ISDN on regional wall motion rendered ischemic during transient coronary occlusion were appreciable after coronary collateral development.
Animals↗
Endothelium determines flow-dependent dilation of the epicardial coronary artery in dogs.
The mechanisms of epicardial coronary artery dilation after reactive hyperemia were studied in instrumented conscious dogs. A pair of ultrasonic crystals, an electromagnetic flow probe and a cuff occluder were placed on the left circumflex coronary artery in 12 mongrel dogs under sterile conditions. Reactive hyperemia after 20 s of coronary occlusion dilated the epicardial coronary artery by 120 +/- 14 micron (3.8 +/- 0.6%, p less than 0.01) from 3.167 +/- 0.345 mm. This reactive dilation was abolished by flow-limiting coronary stenosis. However, vasodilation after nitroglycerin was 168 +/- 26 micron (5.1 +/- 0.5%) and 162 +/- 27 micron (4.9 +/- 0.6%), respectively, before and after flow limitation. After removal of the endothelium by a balloon catheter, dilation of the epicardial coronary artery after reactive hyperemia was markedly attenuated to 7 +/- 4 micron (p less than 0.01 versus before denudation), despite the presence of a similar degree of reactive hyperemia. The extent of coronary dilation after nitroglycerin was unchanged before and after de-endothelialization. Thus, the endothelium contributed to reactive dilation but not to the nitroglycerin-induced dilation. The negative feedback control of coronary diameter to changes in flow velocity may relate to the regulation of coronary artery tone.
Animals↗
Functional and anatomical recovery of endothelium after denudation of coronary artery.
Endothelium-related coronary dilation after balloon denudation was compared with the extent of luminal lining of the regenerated endothelial cells. Under conditions of asepsis, a pair of 10-MHz piezoelectric crystals, an electromagnetic flow probe, and a cuff occluder were placed on the left circumflex coronary artery. Seven to 10 days after this instrumentation, the dogs were anesthetized and the endothelium was removed with the use of a balloon catheter. Immediately after balloon denudation, coronary dilations following reactive hyperemia (reactive dilation) and acetylcholine 3 micrograms/kg iv were reduced to 19 +/- 5 (P less than 0.01) and 10 +/- 4% (P less than 0.01) of control, respectively. In 2, 5, and 7-10 days after denudation, reactive dilation in the conscious dogs was 24 +/- 7 (n = 16), 71 +/- 10 (n = 11), and 75 +/- 9% (n = 5) of control, respectively. Acetylcholine-induced coronary dilation in conscious state was 52 +/- 12 (n = 9), 116 +/- 17 (n = 7), and 94 +/- 24% (n = 2) of control in 2, 5, and 7-10 days after denudation, respectively. There was a positive linear relation between the extent of reactive dilation and acetylcholine-induced dilation from 2 to 10 days after denudation (r = 0.734). The amount of reactive hyperemia, nitroglycerin-induced coronary dilation, and ergonovine-induced coronary constriction remained constant during the experimental period. The area covered by the endothelial cells at the denuded site was 8 +/- 3 (n = 5), 18 +/- 9 (n = 6), 64 +/- 9 (n = 6), and 81 +/- 11% (n = 3) of the denuded area in 0, 2, 5, and 7-10 days after denudation, respectively, which linearly related to the percent recovery of reactive dilation (r = 0.912). Thus reactive dilation or acetylcholine-induced coronary dilation depended on the presence of endothelium, irrespective of the shape or alignment of the regenerated tissues. These findings may be clinically relevant because anatomical integrity of the endothelium might be assessed in vivo by reactive dilation or acetylcholine-induced coronary dilation.
Animals↗