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Biomedical subjects

H Tomoike

Publications and source records attributed to H Tomoike.

At least 199 records · Page 11Linked to original sources
PubMed1985

End-systolic pressure-volume, pressure-length, and stress-strain relations in canine hearts.

End-systolic pressure-volume relationship (ESPVR) of the in situ heart in the dog was measured during changes in contractile state and was compared with end-systolic pressure-length (ESPLR) or stress-strain relationship (ESSSR). Circumferential segmental length and wall thickness at the equator and external long and short axis diameters of the left ventricle (LV) were determined sonomicrometrically, and LV volume was calculated by an ellipsoidal model. Circumferential wall stress at the equator was calculated by a very thin shell model. Contractile state was enhanced by an intravenous infusion of dobutamine and was suppressed by propranolol. ESPVR, ESPLR, and ESSSR were determined during a reduction of arterial pressure by occluding temporarily the inferior caval vein (IVC). ESPVR, ESPLR, and ESSSR during changes in end-systolic pressure from 108 +/- 3 to 71 +/- 2 mmHg were linear, irrespective of inotropic states (r greater than 0.92). Slopes of these relationships increased similarly in case of dobutamine and were reduced after propranolol, yet the extrapolated X-axis intercept of ESPVR, ESPLR, and ESSSR remained unchanged. Thus the slope of ESPVR is unique to the inotropic state, and both ESPLR and ESSSR are useful as a substitute for ESPVR when there is no regional wall motion abnormality.

Animals↗
PubMed1985

Role of afterload in determining regional right ventricular performance during coronary underperfusion in dogs.

The relationship between coronary perfusion pressure and regional myocardial performance of the right ventricular free wall was studied, in the presence or absence of right ventricular hypertension in 13 open-chest dogs. The right coronary artery was perfused through a shunt from a carotid artery. Regional systolic shortening of the right ventricular free wall was measured by means of a sonomicrometric technique at various levels of coronary perfusion pressure. Regional shortening was insensitive to coronary perfusion pressure or flow when it was above 31 mm Hg or 0.27 ml/min per g. Once coronary perfusion was below this critical level, regional shortening in both base to apex and circumferential orientations decreased linearly, depending on the degree of perfusion pressure. Despite the presence of a monoexponential relationship between coronary perfusion pressure or flow and regional shortening, a direct linear relation between perfusion pressure and flow was consistently noted, with or without pulmonary artery banding, suggesting that there is limited autoregulation of right coronary flow. The critical perfusion pressure for maintaining regional myocardial function of the right ventricle was highly dependent on the level of right ventricular systolic pressure (r = 0.64 - 0.72, P less than 0.05). Thus, right ventricular systolic pressure was one of the important determinants of regional wall motion during coronary underperfusion.

Animals↗
PubMed1985

Animal models of coronary spasm and the pathophysiological events in regional vascular hypercontraction.

An animal model of coronary spasm was designed 1) to reproduce coronary spasm similar to that seen in patients with variant angina, 2) to determine whether hypercontraction of the vascular smooth muscle occurs at the site of the spasm, 3) to document the relationship between functional and structural changes of the vascular wall and 4) to characterize the pathophysiological features of coronary spasm. After balloon de-endothelialization and feeding of a high cholesterol diet in mongrel dogs and Göttingen miniature pigs, there was evidence of vascular hypercontraction associated with arteriosclerotic changes. Coronary spasm of more than 75% narrowing of the artery was provoked with ischemic signs in miniature swine. These events could be repeatedly provoked by an intracoronary injection of histamine following pretreatment with cimetidine. The site of hypercontraction corresponded well with the site of the de-endothelialization, an area where the basal vascular tone was increased and was related to histamine activity. Thus, the present animal model will shed light on mechanism involved in vasoactive angina pectoris and aid in clarifying the pathophysiology of vascular smooth muscle.

Animals↗
PubMed1985

Coronary spasm and allergy. Retrospective study of the incidence of allergic history in patients with variant angina.

Despite a large number of papers concerning coronary spasm, its mechanism still remains unsolved. Several cases have been reported in which coronary spasm was triggered by allergy. Since histamine is one of the causative substances released in allergic reactions, we speculated on some involvement of an allergic mechanism in the pathogenesis of coronary spasm. We retrospectively examined by questionnaire the incidence of allergic history in patients with variant angina (n = 47) and compared it with that in patients with non-ischemic heart diseases (n = 83). We could not find any relationship between coronary spasm and allergy. Furthermore, we have not experienced any case in which myocardial ischemia was provoked by an allergic reaction. Accordingly, allergy could not be a major cause of coronary spasm in our present experience.

Adult↗
PubMed1985

Chronic instrumentation and its lack of effect on the hemodynamics and regional myocardial blood flow of conscious dogs.

The effects of chronic instrumentation on regional myocardial performance and regional myocardial blood flow were studied in 8 mongrel dogs. Regional segment lengths were measured by an ultrasonic dimension gauge technique at two areas of the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX). Regional myocardial blood flow was measured by a tracer microsphere technique. These measurements were repeated while the animals were conscious on the 4th, 11th, 21st and 28th days after instrumentation. On the 4th day, the heart rate was rather high and regional shortening at both the LAD and LCX areas remained suppressed. After the 11th day, hemodynamic variables such as heart rate, left ventricular pressure and regional wall motion were fairly constant. Regional myocardial blood flow and its distribution were also constant throughout the experimental period. Fibrosis of the epicardium invariably induced by surgical procedures did not affect the distribution of regional blood flow as compared with that of the interventricular septum. Thus, a stable hemodynamic state was recorded after the 11th day following surgical manipulation and the implantation of sensors and catheters did not affect the level of regional myocardial blood flow or its distribution at rest. Such long term reproducible measurements of regional wall motion and regional myocardial blood flow may facilitate chronic studies of cardiovascular physiology.

Animals↗
PubMed1984

End-systolic pressure-length relations during changes in regional contractile state.

End-systolic pressure-length relationship (ESPLR) was examined in the heterogenously contracting heart in open-chest dogs. Regional length was measured sonomicrometrically in the areas of both the left circumflex coronary artery (LCX) and left anterior descending coronary artery (LAD). ESPLR was linear during a transient reduction in arterial pressure following occlusion of the inferior caval vein (IVC). In group 1 (12 dogs), saline as a control condition (Cont) and isoproterenol (Iso, 0.05 microgram/min) to enhance the regional contractile state were infused into the LCX. Percent shortening in the LCX area increased from 13 to 16% (P less than 0.01) in Iso. The slope (Ees) of ESPLR increased from 57 to 71 mmHg/mm (P less than 0.01) in Iso. The extrapolated X-axis intercept (Lo) of ESPLR was unchanged. In the LAD area, Ees and Lo remained constant. In group 2 (13 dogs), lidocaine (1 mg/min, Lid 1; 5 mg/min, Lid 5) was infused into the LCX to induce mild and severe hypokinesis, respectively. Percent shortening in the LCX area was reduced from 14 to 8% (P less than 0.01 vs. Cont) in Lid 1 and 5% (P less than 0.01 vs. Cont, P less than 0.05 vs. Lid 1) in Lid 5. Ees tended to decrease in Lid 1 but to increase in Lid 5 (statistically not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Selective hypercontraction caused by ergonovine in the canine coronary artery under conditions of induced atherosclerosis.

The relationship between the hypercontractile response of the regional coronary artery to ergonovine and induced vascular change after endothelial denudation and a high-cholesterol diet was examined in dogs by arteriographic (in situ) and mechanographic (in vitro) methods. In 15 mongrel dogs, selective endothelial denudation of either the left circumflex coronary artery (LCX) or left anterior descending coronary artery (LAD) was repeated twice 1 month apart by means of coronary arterial catheterization. A high-cholesterol diet (20 g/day) was given thereafter for 3 (n = 15) and 6 (n = 8) months. Although there was no difference in the extent of coronary vasoconstriction between the LAD and LCX before or immediately after endothelial denudation, after intravenous administration of ergonovine a significant augmentation of coronary constriction along the denuded portion was noted arteriographically in the long-term phase (1 to 6 months). At the end of the study in vivo, isometric tension of the strips of the denuded and contralateral intact coronary arteries was measured during the cumulative addition of ergonovine, serotonin, or phenylephrine to the organ bath; agonist responses were standardized by the response to 35 mM KCl. Although the concentration-response relations for phenylephrine (10(-9) M to 10(-5) M) were not significantly different between intact and denuded arteries, responses of the denuded portion to cumulative addition of ergonovine (10(-10) M) or serotonin 10(-9) M to 10(-5) M) exhibited markedly depressed threshold concentrations along with a significantly lowered negative logarithm (pD2) of the dose producing 50% of the maximum effect. The tension developed in the denuded portion was also enhanced over that noted in the contralateral coronary artery during the cumulative addition of ergonovine but not during application of phenylephrine. Thus enhanced constriction documented arteriographically may be derived from the localized hypersensitivity to ergonovine. Microscopically, the endothelial denudation and a long-term high-cholesterol diet resulted in a regional intimal thickening with fibrous proliferation but little lipid deposition. Therefore smooth muscle in atherosclerotic arteries may be hypersensitive to specific agonists such as ergonovine and serotonin in a canine preparation. These results suggest that coronary spasm induced by ergonovine in humans is relevant to the presence of atherosclerotic changes in the vascular wall.

Animals↗
PubMed1984

Development of collateral function with repetitive coronary occlusion in a canine model reduces myocardial reactive hyperemia in the absence of significant coronary stenosis.

The present study was designed to elucidate the role of collateral development, per se, on reactive hyperemia without persistent coronary stenosis in instrumented conscious dogs. Functional states of coronary collaterals were augmented by repetitive 2 minutes of coronary occlusion every 30 minutes for 2-9 days. Regional shortening measured sonomicrometrically recovered from -1.2 +/- 6.5% of the preocclusive state at the end of the first coronary occlusion to 100.5 +/- 1.2% (n = 8, P less than 0.01) after repeated coronary occlusions. Before and after collateral development, transient coronary occlusions of 5, 10, 20, 30, 60, 90, and 120 seconds were randomly performed. The degree of regional dysfunction and the following reactive hyperemic response were measured. Up to 20 seconds of coronary occlusion, the flow ratio and duration of coronary reactive hyperemia increased similarly, both before and after collateral development. However, when the duration of coronary occlusion was over 30 seconds, flow ratio and debt repayment ratio were reduced progressively after the collateral development. Among the indices exhibiting reactive hyperemia, debt repayment ratio decreased initially and correlated well with the recovery of regional dysfunction during coronary occlusion. Thus, the augmentation of collateral function after repetitive coronary occlusion reduces reactive hyperemia even in the absence of significant coronary stenosis.

Animals↗
PubMed1984

Alpha adrenergic receptor activity of epicardial coronary artery in the anesthetized dog.

The epicardial coronary artery plays an important role not only as a conduit artery but also as a locus of coronary spasm. Accordingly, diameter change of the large epicardial coronary artery of the in situ canine heart was continuously measured by ultrasonic dimension gauge technique and the effects of alpha adrenergic stimulation on the caliber were studied. After the intravenous administration of phenylephrine the aortic pressure increased by 28 mmHg, however, the left circumflex coronary artery diameter decreased by 3.4% (p less than 0.01). Norepinephrine and sciatic nerve stimulation after propranolol (1 mg/kg) induced coronary vasoconstriction by 1.3 (p less than 0.025) and 2.5% (p less than 0.05) against the obvious increases of aortic pressure by 16 and 19 mmHg, respectively. Thus alpha adrenergic stimulation, in situ in dogs, was shown to directly constrict the large epicardial coronary artery.

Adrenergic alpha-Agonists↗
PubMed1984

Effects of trapidil and nitroglycerin on coronary circulation in conscious dogs.

Effects of trapidil and nitroglycerin (glyceryl trinitrate) on coronary blood flow or epicardial coronary diameter were studied in conscious dogs, instrumented with a Doppler flow probe or a pair of ultrasonic dimension crystals on the left circumflex coronary artery. Bolus intravenous injections of trapidil (0.5, 1.0 and 2.0 mg/kg i.v.) increased coronary blood flow, dose-dependently, such being comparable at the peak value seen with nitroglycerin (5, 10 and 20 micrograms/kg i.v.). Coronary blood flow following the intravenous administration of trapidil or nitroglycerin increased biphasically and returned to pre-drug levels in 1.4 +/- 0.2 min (trapidil 1 mg/kg i.v.) or 1.0 +/- 0.1 min (nitroglycerin 10 micrograms/kg i.v.), while the mean coronary diameter increased monophasically and approached the control level 5 min after drug administration. The first peak was observed before the maximal decrease in aortic pressure and the second peak was associated with concomitant increases in heart rate and myocardial contractility induced by a sudden hypotension. Propranolol, a beta-blocker, did not modify the initial peak but attenuated markedly the second peak (P less than 0.05) in case of trapidil (1.0 mg/kg i.v.) or nitroglycerin (10 micrograms/kg i.v.), which corresponded with reduced changes in reflex tachycardia and positive inotropism. Therefore, the direct effects of trapidil and nitroglycerin on coronary circulation of conscious dogs are an initial transient dilatation of the resistance vessels followed by a continuation of the dilatation of the conductance coronary vessels.

Animals↗
PubMed1983

Coronary artery spasm induced in atherosclerotic miniature swine.

Angiographically demonstrable coronary artery spasm could be provoked repeatedly by giving intracoronary or intravenous injections of histamine to miniature swine with experimentally induced atherosclerotic lesions of the coronary artery. The spasm induced in this way subsided either spontaneously or after the administration of nitroglycerin and was prevented by a calcium antagonist or an agent that blocks histamine H1 receptors. This model, which suggests that atherosclerotic changes may be one of the primary factors in the occurrence of coronary artery spasm, should facilitate studies on the pathogenesis of this condition.

Animals↗
PubMed1983

Functional significance of collaterals during ameroid-induced coronary stenosis in conscious dogs. Interrelationships among regional shortening, regional flow and grade of coronary stenosis.

We studied the relationships among collateral flow, regional myocardial shortening and the grade of coronary stenosis during ameroid-induced chronic coronary constriction in 22 conscious dogs. A radiolucent ameroid, a Doppler flow probe and a cuff occluder were placed on the left circumflex coronary artery (LCx). Regional myocardial shortening and regional myocardial blood flow were assessed simultaneously using ultrasonic dimension gauges and the tracer microsphere technique, respectively, during temporary occlusion of the LCx. Regional hypokinesia and ischemia were attenuated as a function of time during progressive coronary stenosis. Fifty percent recovery and full recovery of regional shortening during occlusion were observed 19 +/- 3 and 25 +/- 4 days after instrumentation, respectively, when the endocardial blood flow recovered from 0.42 +/- 0.07 ml/min/g at 7 days to 0.56 +/- 0.07 and 0.80 +/- 0.05 ml/min/g, respectively. Greater than 75% coronary stenosis coincided with collateral development, as estimated from regional shortening rate and the appearance of angiographically opacified collaterals. Our study confirms that the development of collateral vessels reduces regional ischemia and hypokinesia induced during abrupt coronary occlusion in a canine model.

Animals↗
PubMed1983

Differential registration of two types of radionuclides on macroautoradiograms for studying coronary circulation: concise communication.

Double-radionuclide autoradiography proved to be feasible using combinations of Tc-99m and I-125, or Tc-99m and C-14. Because of the short half-life of Tc-99m (6 hr), we first registered Tc-99m on x-ray film. Given an adequate Tc-99m:I-125 activity ratio of 20:1, the exposure duration for Tc-99m was still too short for I-125 to blacken the x-ray film. The pure emission from C-14 is completely absorbed by a thin aluminum sheet--hence no problem there. After the decay of Tc-99m, therefore, it was entirely feasible to continue autoradiography with I-125 (T1/2 = 60.2 days) or C-14 (T1/2 = 5730 yr). Based on these conditions, we applied (a) tracer microspheres labeled with I-125 and Tc-99m to define the respective perfusion areas of the left anterior descending, septal, and left circumflex coronary arteries of the beating heart, and (b) Tc-99m pyrophosphate and C-14 antipyrine to demarcate respectively the localization of the infarct-avid substance and the regional blood flow. We verified the first procedure with postmortem angiography and the second with histochemistry.

Angiography↗
PubMed1982

Preocclusive perfusion area as a determinant of infarct size in a canine model.

The extent of myocardial infarction related to the pre-occlusive perfusion are was quantitatively evaluated in a canine model. The perfusion area was determined preocclusively by selective injection of tracer microspheres into the coronary artery in question, then the main trunk and a small lateral branch of the left circumflex coronary artery was occluded in group 1 (10 dogs) and group 2 (10 dogs), respectively. Rapid freezing was used to prepare autoradiographic samples for determination of the perfusion are along with samples for dehydrogenase staining in order to delineate the extent of myocardial infarction. The relationship between perfusion area and infarct size was examined in 50 micrometers thick samples from base, middle and apex of the ventricle and a direct linear correlation between the perfused (P) and infarcted area (I) in the left ventricle (LV) was noted regardless of the perfusion size or the location in the ventricle. The linear relationship I = 0.93P - 4.9 (r = 0.95, P less than 0.001) was obtained in all 20 dogs. Transmural extent of necrosis was larger in the endocardium than in the epicardium, thereby representing a more salvageable myocardium in the epicardium. It is concluded that the preocclusive determination of perfusion are by high resolution autoradiography is a useful method of obtaining physiological perfusion not affected by ischaemia. Also the infarct size when standardized by the perfusion area is mainly influenced by transmural location but not by the spacial geometry or the size of the occluded area.

Animals↗