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Biomedical subjects

H Tomoike

Publications and source records attributed to H Tomoike.

At least 109 records · Page 6Linked to original sources

Clinical significance of decreased myocardial uptake of 123I-BMIPP in patients with stable effort angina pectoris.

The aim of this study was to assess the feasibility of resting myocardial fatty acid metabolic imaging with 123I-beta-methyliodophenyl-pentadecanoic acid (123I-BMIPP) for the detection of patients with stable effort angina pectoris and to clarify the clinical significance of abnormal 123I-BMIPP images. Myocardial imaging with 123I-BMIPP at rest and 99Tcm-methoxyisobutyl isonitrile (99Tcm-MIBI) at rest and during treadmill exercise was performed in 46 patients with suspected effort angina pectoris. Resting 123I-BMIPP imaging detected 43% (17/40) of patients with significant (> or = 50%) coronary artery stenosis and 59% (17/29) of patients with exercise-induced myocardial ischaemia. The patients with abnormal 123I-BMIPP images terminated exercise after a shorter period (4.5 +/- 2.6 vs 6.7 +/- 4.1 min; P < 0.01) and at a lower rate pressure product (16,124 +/- 5211 vs 20,246 +/- 6564 mmHg x beats min-1; P < 0.01) than those with normal 123I-BMIPP images. The presence of ST depression during the exercise test (77 vs 52%; P < 0.05), severe coronary stenosis exceeding 90% (88 vs 43%; P < 0.01), collateral vessels (35 vs 9%; P < 0.01) and a wall motion abnormality of hypokinesis/akinesis (53 vs 30%; P < 0.05) were more frequently seen in patients with abnormal 123I-BMIPP images than in those with normal images. Resting 123I-BMIPP imaging was able to detect the presence of coronary artery stenosis and exercise-induced myocardial ischaemia with moderate sensitivity, and to determine the functional severity of coronary artery disease.

Angina Pectoris↗

Structural and functional characteristics of peripheral pulmonary parenchyma in golden hamsters.

Mechanical properties of the peripheral pulmonary parenchyma of freshly excised hamster lung tissue were examined to evaluate determinants of displacement-tension relationships with regard to structural constituents of the alveolar wall. A tissue segment measuring 50 x 50 x 400-600 microns and consisting mostly of the alveolar wall was prepared from the lung parenchyma adjacent to the pleura. By use of a constant speed maneuver for extension and relaxation of this minute preparation, displacement-tension relationships of peripheral pulmonary parenchyma were examined in a bath filled with 37 degrees C physiological buffer solution. The specimen was repeatedly extended up to 20-40 mg, a little above a point resembling "yield" in displacement-tension relationships. Analyses of displacement-tension relationships constantly showed double exponential relations. The first component at the lower strain was approximated by sigma 1 = A1(e alpha 1 epsilon - 1) and the second component beyond the inflection (yield) point was sigma = s1 + s2 = A1(e alpha 1 epsilon - 1) + A2(e alpha 2 epsilon - 1), where sigma, A, alpha, and epsilon represent stress, constant determined by tissue quantity, elasticity constant, and strain, respectively. Immersion of the lung specimen into elastase resulted in decreases of only alpha 1, and collagenase reduced alpha 2 but not alpha 1. Hyaluronidase, acetylcholine, ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, and norepinephrine did not alter alpha 1 or alpha 2. These observations suggest that alpha 1 and alpha 2 of the peripheral pulmonary parenchyma are mechanical indexes of elastin and collagen characters, respectively.

Acetylcholine↗

Association of ACE gene polymorphisms with coronary artery disease in a northern area of Japan.

The insertion/deletion DNA polymorphism of the gene coding human angiotensin converting enzyme (ACE) was examined in 109 patients with coronary artery disease (CAD) and 93 non-coronary subjects (NCS) living in a northern part of Japan. The presence of risk factors including age, hypertension, hypercholesterolemia, tobacco use, diabetes mellitus and hyperuricemia were also examined. An insertion (I) / deletion (D) polymorphism of the ACE gene was determined by the polymerase chain reaction with oligonucleotide primers encompassing the polymorphic region in intron 16. The template DNA was isolated from peripheral blood leukocytes of patients. The frequency of the D-allele in NCS was 0.27, significantly lower than that reported in Caucasians or in Japanese living in the Osaka area. The frequency of the D-allele in patients with myocardial infarction (MI) and angina pectoris was 0.39 and was higher than that in NCS. The frequencies of genotypes DD, ID, and II were 17.8, 43.3 and 38.9%, respectively, in CAD except in young patients (below 40 years of age) with MI and AP groups, and 6.5, 40.9 and 52.7%, respectively in NCS (p < 0.05 between CAD and NCS). Young MI showed similar frequencies in ACE gene polymorphisms to those in NCS, a pattern which differed from that seen in subjects with CAD (p < 0.05). The numbers of risk factors did not alter the frequency of ACE gene genotype among patients with CAD, however, in normotensives, the odds ratio of DD-genotype was significantly increased to 3.4. Accordingly, ACE gene polymorphism may be associated with morbidity from CAD in Japanese living in northern Japan as has been noted in Caucasians, despite the lower frequencies of the D-allele in the Japanese population.

Adult↗

Simultaneous measurement of pulmonary diffusing capacity for CO and cardiac output by a rebreathing method in patients with pulmonary diseases.

Pulmonary diffusing capacity for CO (DLCO) and cardiac output (Q) were simultaneously measured by a noninvasive rebreathing method (RB) in 15 normal subjects and in 60 patients, including cardiac diseases (CD), bronchial asthma (BA), chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (PF). DLCO and Q were tested by the single breath method (SB) and the dye-dilution method (Dye), respectively. DLCO (RB) correlated well with DLCO (SB) (r = 0.890, p < 0.001). Q(RB) also correlated well with Q(Dye) (r = 0.909, p < 0.001). Factors affecting DLCO (RB) were age, height, body surface area, O2 consumption, Q, hematocrit (Het) and Q.Hct, among which Q.Hct was the prominent influential determinant. DLCO per lung volume was smaller in COPD and PF than in BA or healthy subjects, while, the ratio of DLCO/(Q.Hct) was significantly higher in COPD than in PF. Simultaneous measurements of DLCO and Q offer comprehensive characterization for functional changes in lung parenchyma.

Adult↗

Ca2+ increase and pH decrease induced by hypochlorous acid in single quiescent myocytes isolated from rat ventricles.

Cytosolic free calcium concentration ([Ca2+]i) and intracellular pH (pHi) were simultaneously measured with a fluorescence technique using fura-2 and BCECF. Hypochlorous acid (HOC1) increased [Ca2+]i and decreased pHi of single quiescent myocytes isolated from rat ventricles. The HOC1-induced changes in [Ca2+]i and pHi (delta [Ca2+]i and delta pHi) were 129 +/- 18nM and 0.18 +/- 0.02 (mean +/- SD), respectively, with 200 microM HOC1. A positive linear correlation was obtained between delta [Ca2+]i and delta pHi under various extracellular Ca2+, pH, and Na+ conditions. Chelation of extracellular Ca2+ depressed only one-fourth of delta [Ca2+]i, and Ca2+ antagonists (verapamil and nifedipine) did not reduce delta [Ca2+]i, indicating that delta [Ca2+]i originates mainly from intracellular Ca2+ stores. A disulfide-reducing reagent, 1,4-dithiothreitol (DTT), recovered the increased [Ca2+]i and decreased pHi to the control levels. The simultaneous changes in [Ca2+]i and pHi induced by HOC1 and the simultaneous restoration of the normal [Ca2+]i and pHi in cardiac myocytes.

Animals↗

Vasoreactivity and restenosis after coronary angioplasty in the atherosclerotic pig model.

BACKGROUND: The effect of coronary angioplasty on coronary spasm remains unknown. We examined the effects of balloon angioplasty, using an oversized balloon, on coronary hypercontraction and eventual restenosis in a pig model of coronary spasm. METHODS: We performed balloon angioplasty, using an oversized balloon at the site of coronary spasm superimposed on atherosclerosis with 6 (group A, n = 14) or 1 (group B, n = 14) atmospheres of inflation pressure in miniature pigs. Using coronary angiography we assessed the coronary basal diameter and diameter change in response to histamine and serotonin before, immediately after, and 4 weeks after angioplasty. Histological examinations were performed immediately after and 4 weeks after the angioplasty. RESULTS: Before angioplasty, histamine- and serotonin-induced hypercontraction was reproducibly noted at the atherosclerotic site. Immediately after angioplasty, the coronary diameter became larger (P < 0.01) than before angioplasty in group A, but there was no significant difference in group B. The hypercontraction in group A was abolished immediately after and 4 weeks after angioplasty, whereas the hypercontraction in group B was unchanged. Histological examination revealed medial necrosis immediately after and medial fibrosis 4 weeks after angioplasty, which were more prominent in group A. Four weeks after angioplasty, the magnitude of restenosis was greater in group A than in group B. CONCLUSIONS: Angioplasty using an oversized balloon with the higher atmosphere of inflation pressure abolished coronary hypercontraction immediately after and 4 weeks after angioplasty, which probably resulted from the irreversible damage to medial smooth muscles; however, this did not prevent restenosis.

Angioplasty, Balloon, Coronary↗

Augmentation of coronary responsiveness to serotonin at the site of X-ray-induced intimal thickening in miniature pigs.

OBJECTIVE: X-irradiation is known to enhance atherosclerotic change. We tested whether coronary vasoconstrictor responses are augmented at the sites of X-ray-induced intimal thickening in Göttingen miniature pigs. METHODS: In 17 pigs, a major branch of the left coronary artery was denuded with a balloon catheter. In 10 pigs, the denuded portion of the left coronary artery was selectively irradiated with 15 Gy of X-rays twice at 3 and 4 months after denudation (group 1). The remaining 7 pigs were not irradiated (group 2). The effects of intracoronary administration of serotonin, histamine and phenylephrine on the coronary diameter were studied 3 (3M) and 5 months (5M) after denudation. After the angiographical study at 5M, the vessels were isolated and isometric tension was measured in an organ chamber. RESULTS: The percent reduction in coronary diameter evoked with 10 micrograms.kg-1 of serotonin increased from 39(s.e.m. 4)% before X-irradiation (3M) to 75(6)% after X-irradiation (5M) in group 1 (P < 0.01), while it did not differ in group 2 [39(6)% at 3M vs. 33(8)% at 5M[ [39(6)% at 3M vs. 33(8)% at 5M]. In group 1, serotonin-induced coronary constriction was frequently accompanied by ischemic ECG changes. Histamine (10 micrograms.kg-1)-induced vasoconstriction was also augmented but to a smaller degree [47(6)% at 3M vs. 62(4)% at 5M; P < 0.05] in group 1, while it remained unchanged in group 2[52(5)% at 3M vs. 44(7)% at 5M]. Phenylephrine did not cause detectable contraction in either group at 3M or 5M. Methysergide and ketanserin attenuated serotonin-induced hypercontraction in a dose-dependent fashion. In the in vitro studies, endothelium-dependent relaxation to serotonin was impaired at the denuded site with (group 1) and without (group 2) X-irradiation to a similar extent. Isometric tension of medial smooth muscle developed by serotonin was significantly greater at the denuded site with X-irradiation (group 1) than the control site and the denuded site without X-irradiation (group 2) (P < 0.05). Intimal thickening was significantly greater at the denuded sites with X-irradiation [group 1, 238(45) microns] than at the denuded sites without X-irradiation [group 2, 58(5) microns] (P < 0.05). CONCLUSIONS: These results indicate that X-irradiation augments the coronary vasoconstrictor responses to autacoids, predominantly to serotonin, and that this augmentation is accompanied by enhanced intimal thickening. Serotonin-induced hypercontraction after X-irradiation resulted mainly from the hyperreactivity of medial smooth muscle.

Animals↗

[Coronary angiography (including PTCA)].

Coronary arteriography (CAG) is one of the gold standards for diagnosing the severity of ischemic heart disease (IHD). Characterization of the angiographic findings of the focal coronary lesion was discussed on the basis of Rosch's and American Heart Association (AHA) classification. Recently, progression and regression of coronary atherosclerotic lesions have been assessed by serial CAG. Regression was believed to result from the dissolution or remodeling of thrombus or from the removal of plaque lipid and cellular elements. Accordingly, we also discussed the pitfalls in the evaluation of coronary stenosis. Recent modalities including intravascular ultrasound (IVUS) and angioscopy have been applied to assess the maternal characteristics of coronary atherosclerotic lesions, such as soft plaque, hard plaque, and calcification along with the extent of intimal thickening.

Angioplasty, Balloon, Coronary↗

[Ultrasonographic diagnosis of athero- and arterio-sclerosis].

Modalities to depict atherosclerotic lesion, have recently been rich in approaches, such as angiography, computed tomography, ultrasonography, radionuclide imaging and magnetic resonance imaging. Although the angiography is still one of the gold standards for diagnosing athero- and arteriosclerotic changes, recent developments in interventional catheterization and medical treatments necessitate the detailed characterization of the vascular wall. High-frequency ultrasonography now expands the observation toward the structure and composition of the vascular wall which can not be obtained in angiography. The higher the frequency of ultrasound is, the better the resolution of the echo imaging improves. However, the adequate depth for echo observation from the probe becomes narrower with the increase of the probe frequency. Accordingly, we have to choose an adequate approach for the vessel of interest. For example, transesophageal echocardiography is useful to evaluate the atherosclerotic changes of the descending aorta. Peripheral ultrasonography is useful for the superficial arteries, including carotid arteries, femoral arteries and branchial arteries. The advantages of the peripheral body surface approach are non-invasiveness and repeatability. Intravascular ultrasonography requires invasive technique, but it provides novel information regarding the presence and the extent of atherosclerosis and its characterization such as calcification. Intravascular ultrasonography is a necessary modality for evaluating the effect of the directional coronary atherectomy.

Arteriosclerosis↗

Noninvasive identification of left main and three-vessel coronary artery disease by thallium-201 single photon emission computed tomography during adenosine infusion.

Advanced coronary artery disease, defined as left main or three-vessel coronary disease, was identifiable noninvasively by means of adenosine Tl-201 single photon emission tomography. Among 75 consecutive patients with angiographically documented coronary artery disease, there were 11 patients with the presence (group 1) and 64 patients with the absence (group 2) of advanced coronary artery disease. The lung-to-heart ratio (L/H ratio) of Tl-201 uptake was calculated as the fraction of average Tl-201 counts per pixel in the lung divided by those in the myocardium. The left ventricular dilation ratio (LVDR) was determined as a ratio of left ventricular cavity size in the early image to that in the delayed image. The patients in group 1 had more defects (2.3 +/- 0.6 seg. vs. 0.9 +/- 0.7 seg., p < 0.001), a higher L/H ratio (35 +/- 4% vs. 28 +/- 5%, p < 0.001) and a higher LVDR (1.13 +/- 0.04 vs. 1.06 +/- 0.04, p < 0.001) than those in group 2. The diagnostic accuracy of the identification of advanced coronary artery disease was 89% by perfusion defects, 68% by L/H ratio and 81% by LVDR. Stepwise discriminant analysis revealed that LVDR (F = 36.2, p < 0.0001) and perfusion defects (F = 8.9, p < 0.004) were the significant and independent discriminators of advanced coronary disease. Identification of patients with left main or three-vessel coronary disease was enhanced by additional analysis of cavity dilation of the left ventricle and increased Tl-201 activity in the lung.

Adenosine↗

Noninvasive identification of anthracycline cardiotoxicity: comparison of 123I-MIBG and 123I-BMIPP imaging.

To test the feasibility of myocardial 123I-MIBG and 123I-BMIPP imaging for the early detection of anthracycline cardiotoxicity, 13 patients who had received anthracycline anticancer chemotherapeutic agents were studied. Two-dimensional echocardiography and myocardial imaging with both 123I-MIBG and 123I-BMIPP were performed in 13 patients treated with anthracycline (group A) and 10 normal control subjects (group C). Anterior myocardial images were obtained 15 minutes and 3 hours after the injection of isotopes. The heart-to-mediastinum ratio (H/M ratio) was used to quantify cardiac 123I-MIBG and 123I-BMIPP uptake. The left ventricular shortening fraction (%SF) and the ratio of peak mitral flow velocity in early diastole to that at the time of atrial systole (E/A ratio) were measured by echocardiography. The H/M ratio of 123I-MIBG was lower in group A than in group C (1.5 +/- 0.2 vs. 1.9 +/- 0.2, p < 0.01). The patients in group A had faster clearance of 123I-MIBG from the myocardium than those in group C (27 +/- 10% vs. 22 +/- 4%, p < 0.05). However, the H/M ratio and clearance of 123I-BMIPP were similar between the two groups (H/M ratio: 2.1 +/- 0.2 vs. 2.0 +/- 0.2, clearance: 24 +/- 6% vs. 26 +/- 6%). The %SF (37 +/- 8% vs. 36 +/- 7%) and E/A ratio (1.4 +/- 0.4 vs. 1.6 +/- 0.3) were comparable in groups A and C. The present findings indicated that myocardial imaging with 123I-MIBG could detect myocardial damage in patients treated with anthracycline in the early stage when cardiac systolic and diastolic function was still preserved. Early detection of anthracycline cardiotoxicity by 123I-MIBG would reduce the incidence and severity of heart failure.

3-Iodobenzylguanidine↗

Adenosine-induced heterogeneous perfusion accompanies myocardial ischemia in the presence of advanced coronary artery disease.

The aim of the present study was to elucidate the characteristics of patients in whom transient myocardial ischemia was evoked during adenosine infusion. Thallium-201 (Tl-201) myocardial imaging and two-dimensional echocardiography during adenosine infusion were performed simultaneously in 61 consecutive patients enrolled for the diagnosis of coronary artery disease. Transient reduction of systolic wall motion after adenosine infusion was considered evidence of myocardial ischemia. Tl-201 redistribution was noted in 38 patients, and 23 of them showed a wall motion abnormality during adenosine infusion. Stepwise discriminant analysis was applied to eight variables that showed significant differences by the univariate analysis between patients with the presence and the absence of adenosine-induced wall motion abnormality: myocardial infarction, anginal pain, ST depression, collateral vessels, Tl-201 redistribution, number of diseased vessels of > or = 75% or 90% stenosis and number of segments with Tl-201 redistribution. The number of diseased vessels with > or = 75% stenosis (F = 43.5, p < 0.0001), ST depression (F = 16.0, p < 0.0002), collateral vessels (F = 11.7, p < 0.001) and Tl-201 redistribution (F = 5.6, p < 0.02) were the statistically significant discriminators relating to adenosine-induced wall motion abnormality. Adenosine-induced myocardial ischemia was related to the number of coronary stenoses, reflecting the presence of severe coronary artery disease, and well-developed collaterals that might be integral factors in a coronary steal phenomenon.

Adenosine↗

Organ distribution of thallium-201 during intravenous adenosine infusion: comparison with exercise.

Thallium-201 (Tl-201) distribution during adenosine infusion was assessed quantitatively and compared with that of exercise imaging. Adenosine and exercise Tl-201 single-photon emission computed tomography (SPECT) were performed in 40 patients with suspected coronary artery disease. In the whole-body images (n = 5) and the unprocessed anterior projection images acquired as part of the initial imaging (n = 35), Tl-201 counts in the myocardium were normalized for the injected dose. Total heart counts were higher during adenosine infusion than during exercise (190 +/- 43 counts/MBq vs 145 +/- 31 counts/MBq, p < 0.01). A heart-to-lung count ratio between adenosine infusion and exercise was not different. A heart-to-liver count ratio was lower during adenosine infusion than during exercise (1.3 +/- 0.3 vs 2.3 +/- 0.5, p < 0.01). Regional Tl-201 uptakes at the inferior wall of the left ventricle during adenosine infusion were closely correlated with those uptakes during exercise (r = 0.94, p < 0.01, slope = 0.96). The sensitivity, specificity, and accuracy of adenosine Tl-201 SPECT for the detection of right coronary artery stenosis were comparable with those of exercise imaging. These results indicated that higher Tl-201 uptake in the liver during adenosine than during exercise did not interfere with the interpretation of myocardial images. Tl-201 counts in the myocardium that were larger during adenosine infusion than during exercise reflected a larger increase in coronary blood flow and thus resulted in better image quality.

Adenosine↗

Effects of a new calcium antagonist, CD-832, on coronary and systemic hemodynamics in conscious dogs.

The effects of a new calcium antagonist, CD-832, on coronary and systemic hemodynamics were compared with those of nifedipine in conscious dogs. A pair of 10-MHz piezoelectric crystals and an electromagnetic flow probe were placed on the left circumflex coronary artery (LCX) under sterile conditions to measure epicardial coronary artery diameter (CoD) and coronary blood flow (CBF), respectively. CD-832 (30, 100, and 300 micrograms/kg) and nifedipine (3, 10, and 30 micrograms/kg) produced dose-related increases in large epicardial CoD and in CBF. At doses of CD-832 (100 micrograms/kg) and nifedipine (30 micrograms/kg), producing the same increases in CoD and CBF, the duration of increases in CoD and in CBF was markedly longer after CD-832 than after nifedipine. CD-832 and nifedipine produced dose-related decreases in aortic blood pressure (AoP) and reflex increases in heart rate (HR). However, nifedipine produced significantly (p < 0.01) greater tachycardia than CD-832 in equieffective hypotensive doses. These results demonstrate that CD-832 produces sustained dilation of both large epicardial coronary arteries and small resistance vessels and that the degree of tachycardia after CD-832 is significantly less than that after nifedipine.

Animals↗

Relation of principal components of ECG maps to loci of wall motion abnormality in old myocardial infarction.

The purpose of this study was to examine the correlation between body surface potential distribution and the extent of abnormally contracting segments (ACS) of the left ventricle in patients with old myocardial infarction (MI). Body surface potential distribution was quantitatively analyzed using principal component analysis. The first six principal components were extracted from data set obtained from both 25 normal subjects and 100 patients. The z scores (principal component weights) were calculated in a time domain at every 4 or 8 ms in another 81 patients with previous MI. In anterior MI, the second z scores on T wave and the fourth z scores on QRS complex were significantly lower in the presence than in the absence of ACS at the lateral wall. In inferior MI, the first z scores on QRS complex, the second on T wave, and the third on both Q and T represented significant differences between the presence and the absence of ACS at the posterior wall. Minute differences in the extent of ACS were sensitively and noninvasively detected on z scores of principal components.

Adolescent↗

Pulmonary haemodynamics in awake rats following treatment with endotracheal pancreatic elastase.

The purpose of this paper was to study pulmonary haemodynamics in an elastase-induced emphysema model in awake rats (Group-EL, n = 9) in comparison with saline-treated controls (Group-C, n = 12). Four weeks before haemodynamic study, porcine pancreatic elastase and normal saline were intratracheally instilled in Group-EL and Group-C, respectively. Indwelling pulmonary artery and abdominal aortic catheters were positioned two days before the haemodynamic study. Breathing room air, mean pulmonary artery pressure (Ppa) tended to be higher in Group-EL than in Group-C, although the difference was not statistically significant. Systemic pressure, total systemic vascular resistance and cardiac index did not differ between groups. When exposed to 10% O2, Ppa and pulmonary vascular resistance (PVR) of both groups rose significantly. The increase of Ppa, (but not PVR) in Group-EL during hypoxia was significantly higher than that in Group-C. The magnitude of hypoxic pulmonary vasoconstriction (HPV) tended to be larger in Group-EL than in Group-C. Right ventricles of Group-EL were more hypertrophic than those of Group-C, suggesting a period of higher pulmonary artery pressure than for Group-C. The present results imply that the pressor response of pulmonary vasculature to acute alveolar hypoxia is possibly enhanced in awake rats upon examination four weeks after elastase treatment.

Animals↗

Collateral development induced by repetitive brief coronary occlusion relates to the functional state of pre-existing collaterals.

The effects of pre-existing collaterals (PC) and the perfusion size (PS) on the ischemia-induced collateral development were studied in a canine model. Under aseptic conditions, the dogs were instrumented with pairs of ultrasonic crystals to measure regional wall motion in the territory of the left circumflex (LCX) and left anterior descending coronary artery. A micromanometer was used to measure left ventricular (LV) pressure. Two to 3 weeks after surgery, 2 min coronary occlusion (CO) of LCX was repeated every 32 min consecutively day and night using a remote control, motor-driven hydraulic cuff occluder. Regional wall motion and LV pressure were monitored via a telemetry system in 23 dogs. The functional state of PC was estimated by the level of % reduction of regional wall motion at the end of the first 2 min CO, which ranged from -11 to -141%. PS of LCX area at risk determined by the post mortem angiograms ranged from 35 to 54% (mean +/- SEM; 44 +/- 1%) of LV. Number of CO needed for collateral development ranged from 8 to 628, and was exponentially related to the functional state of PC (r = -0.77, n = 23, p < 0.01), but not to PS (r = 0.43, n = 19, p = 0.07). These results suggest that the functional maturity of pre-existing collaterals is one of the major determinants of collateral development related to ischemic stimuli.

Animals↗

Orally administered beraprost sodium inhibits pulmonary hypertension induced by monocrotaline in rats.

Rats were fed on distilled water (DW) or DW containing beraprost sodium (BPS). BPS concentration was 1.5 or 3.0 mu/ml in DW for the low BPS groups and 6.0 or 10.0 mu/ml in DW for the high BPS group. Monocrotaline (MCT) was subcutaneously given (60 mg/kg), and saline was injected as control. Data were analyzed among the following groups; Groups (Saline + DW), (Saline + Low BPS), (MCT + DW), (MCT + Low BPS) and (MCT + High BPS). Three weeks later, pulmonary (Ppa) and systemic (Psa) arterial pressure were measured under anesthesia. MCT caused significant elevation of Ppa [18.3 +/- 0.6 cmH2O for Group (Saline + DW) vs. 27.2 +/- 1.2 cmH2O for Group (MCT + DW), p < 0.001, mean +/- S.E.] and Ppa was significantly and dose-dependently suppressed by BPS; Group (MCT + DW) vs. Groups (MCT + Low BPS), 23.4 +/- 0.7 cmH2O and (MCT + High BPS), 22.5 +/- 0.5 cmH2O, p < 0.05, mean +/- S.E.). Psa was not lowered dose-dependently by BPS. We conclude that oral beraprost sodium suppresses pulmonary hypertension produced by monocrotaline in rat.

Administration, Oral↗