Biomedical subjects

K Maehara

Publications and source records attributed to K Maehara.

At least 37 records · Page 2Linked to original sources

PubMed1999

Detection of abnormal high-frequency components in the QRS complex by the wavelet transform in patients with idiopathic dilated cardiomyopathy.

In order to investigate whether increased fine, fractionated signals within the QRS complex can detect arrhythmogenic substrates and how these fine signals link with ventricular mechanical dysfunction, wavelet analysis was performed on averaged QRS complexes obtained from the left precordial lead in 26 patients with idiopatic dilated cardiomyopathy (IDCM) and in 12 normal subjects. The number of local maxima and the duration of the wavelet transform were significantly greater in patients with IDCM than in normal subjects; the number at 100 Hz was 8.8+/-3.1 vs 6.0+/-1.1 (p<0.01), and the duration at 100Hz was 93+/-15 vs 75+/-7ms (p<0.01). Both of these indices were greater in the patients with than in those without late potentials, repetitive ventricular premature beats or cardiac death. In addition, significant inverse curvilinear relationships were observed between the left ventricular ejection fraction and both the number of local maxima and the duration of the wavelet transform. In conclusion, fine fragmented signals in the QRS complex detected by wavelet analysis would be an important marker for potentially arrhythmogenic substrates and seemed to progress in parallel with left ventricular mechanical dysfunction in IDCM.

Adolescent↗

PubMed1999

Dissociation of chronotropic and inotropic responses in the rat heart during sympathetic stimulation.

It is not fully resolved how the chronotropic and inotropic responses alter depending on the strength or duration of stimulation, and how the alpha-vasoconstrictor effect competes with metabolic vasodilation during sympathetic stimulation. The present study investigated the effects of differential frequency stimuli on these responses in rat hearts during sympathetic stimulation while keeping the left ventricular end-diastolic volume constant. The heart was perfused at a constant flow or pressure with a modified Krebs-Henseleit solution. Electrical stimulation of sympathetic nerves (SNS) was performed at 4 frequencies (0.2, 0.5, 1 and 3 Hz) for 90 s in pithed rats without or with an a or alpha2 adrenergic receptor antagonist. The heart rate progressively increased during 3-Hz SNS (33+/-10% at 30s, 38+/-14% at 90s), whereas the inotropic action peaked at about 30s and then decreased (left ventricular systolic pressure +23+/-8% at 30s, -1+/-13% at 90s). This phenomenon indicates a negative staircase, in spite of a gradual increase in norepinephrine release. The reduction of contractility did not differ from that shown by constant atrial pacing with an equivalent rate. The coronary alpha1-vasoconstrictor response was competitive with metabolic vasodilation only in the early phase of stimulation and the alpha2-vasoconstrictor action had little contribution to the regulation of coronary circulation. The fact that these results differ from previous findings suggests that sympathetic regulation of the heart should be reconsidered, although direct application of the present results to humans is not clear because of species differences.

Animals↗

PubMed1999

Effects of cardiac contraction and increased coronary sinus pressure on the coronary arterial pressure-flow relationship.

Increased coronary sinus (CS) pressure and cardiac contraction impair coronary inflow independently. However, it has not been determined how the coronary pressure-flow relationship is strongly affected by changes in CS pressure in the beating heart compared to the non-beating heart. The purpose of this study was to evaluate the combined mechanical effects of cardiac contraction and increased CS pressure. Using isolated, perfused canine hearts, coronary perfusion pressure in the left anterior descending coronary artery (LAD) was gradually reduced in beating and non-beating conditions. Measurements were obtained with and without elevation of CS pressure to determine the mean LAD pressure-flow relationships. At normal and elevated CS pressures, the corresponding zero-flow pressures were not significantly different between the beating and non-beating hearts. A rightward shift of the mean coronary perfusion pressure-coronary flow curve for the beating heart compared to the non-beating heart was observed when CS pressure was not elevated. In contrast, the slopes for both beating and non-beating hearts were similar if the CS pressure was increased. There was a smaller increase in the mean intramyocardial pressure (IMP) at elevated CS pressures in the beating heart as compared to the non-beating heart. Moreover, the increase in diastolic IMP with increased CS pressures in the beating heart was significantly less than that in the non-beating heart. These results indicate that cardiac contraction attenuates the inhibitory effects of increased CS pressure on coronary inflow.

Animals↗

PubMed1999

Augmented basal nitric oxide production contributes to maintenance of coronary blood flow in dogs with pacing-induced heart failure.

It remains controversial whether basal nitric oxide (NO) production in coronary resistance vessels in heart failure is enhanced or not. A transonic Doppler flow probe was placed around the left anterior descending coronary artery, and complete atrioventricular block was produced in fifteen dogs. The coronary pressure-flow relationships during long diastole were analyzed without and with pacing-induced heart failure. Three weeks after pacing at 240/min, plasma norepinephrine and renin activity significantly rose. Right atrial pressure and left ventricular end-diastolic pressure increased, and cardiac output and coronary perfusion pressure decreased; however, mean coronary blood flow did not change after pacing (55 +/- 5 to 52 +/- 5 ml/min/100 g, mean +/- SEM). The slope of the diastolic coronary pressure-flow relationship became steeper (1.22 +/- 0.13 to 1.62 +/- 0.09 ml/min/100 g/mmHg, p < 0.05) with a slight increase in the measured zero-flow pressure (29.5 +/- 1.1 to 32.8 +/- 1.5 mmHg, p < 0.05) after pacing. After pretreatment with indomethacin, administration of NG-nitro-L-arginine methyl ester caused an equal increase in the zero-flow pressure before (31.4 +/- 1.7 to 39.2 +/- 2.2 mmHg, p < 0.05) and after heart failure (33.9 +/- 2.5 to 41.6 +/- 2.2 mmHg, p < 0.05), and more decline of the slope of the coronary pressure-flow relationship in heart failure (1.86 +/- 0.22 to 1.20 +/- 0.05 ml/min/100 g/mmHg, p < 0.05) than before heart failure (1.11 +/- 0.12 to 1.05 +/- 0.11 ml/min/100 g/mmHg, N.S.). This indicates that in failing hearts the vasodilatory action of NO in small vessels predominates despite the presence of several vasoconstricting factors. These results suggest that coronary blood flow is maintained despite detrimental hemodynamic and activated neurohumoral factors in the initial stage of heart failure, and that increased basal NO production plays a central role in the maintenance of basal coronary blood flow.

Animals↗

PubMed1999

[Changes in diameter size and F-actin expression in the myocytes of patients with diabetes and streptozotocin-induced diabetes model rats].

Diabetes mellitus may be an independent risk factor for disturbance of cardiac function, but the detailed mechanism remains unclear. In the present study, histological examinations were carried out on 25 hearts from diabetes model rats as well as myocardial biopsy materials from patients with diabetes (n = 25). The mean diameter of the cardiac myocytes in humans was 12.2 +/- 0.5 microns in the control group of patients without diabetes mellitus or hypertension (n = 6), 13.7 +/- 0.8 microns in the hypertension group (n = 3), 9.0 +/- 1.7 microns in the diabetes group (n = 8), and 11.9 +/- 2.0 microns in the diabetes with hypertension group (n = 8). The cardiac myocytes of diabetic patients appeared to be atrophic. Comparison of the size of myocytes in the control rats vs streptozotocin-induced diabetes model rats (n = 7, each) was 5.4 +/- 0.2 vs 5.2 +/- 0.3 microns at 2 weeks; 5.9 +/- 0.1 vs 4.9 +/- 0.9 microns at 12 weeks, and 5.7 +/- 0.1 vs 4.0 +/- 0.2 microns at 24 weeks, respectively, and gradually decreased in streptozotocin rats with aging. Immuno-histochemistry with phaloidin was used to assess F-actin in the cardiac myocytes. The relative cross-sectional area of F-actin in the cardiac myocytes of streptozotocin rats was compared to that in non-streptozotocin rat myocytes. F-actin fluorescence in streptozotocin rats was 89.9 +/- 3.9% at 2 weeks, 77.9 +/- 6.4% at 12 weeks, and 56.8 +/- 5.7% at 24 weeks, indicating a decrease in F-actin. These results suggest that the smaller myocytes observed in patients with diabetes and streptozotocin rats are related to the decrease in F-actin in myocytes.

Actins↗

PubMed1998

Urinary trypsin inhibitor suppresses vascular smooth muscle contraction by inhibition of Ca2+ influx.

Urinary trypsin inhibitor (UTI) and its precursor form inter-alpha trypsin inhibitor (ITI) are present in plasma. To determine the action of UTI on blood vessels, we performed isometric vascular muscle contraction tests, microcirculation studies and measurement of cytosolic free Ca2+ in vascular smooth muscle cells. An isometric vascular muscle contraction test showed that the contractions stimulated by endothelin-1 or norepinephrine were suppressed in the presence of UTI, and that the contractions were not inhibited in the presence of ITI. The microcirculation study showed that the contraction of mesenteric arterioles of WKY rats induced by norepinephrine were inhibited by treatment of UTI, and that they did not alter by treatment of ITI. Pre-incubation of UTI, but not ITI, with vascular smooth muscle cells inhibited the increase of cytosolic free Ca2+ induced by endothelin-1 or norepinephrine. Cell-binding study by biotinylated UTI showed that vascular smooth muscle cells have specific binding site for UTI, but not for ITI. We propose that circulating UTI converted from ITI has a regulatory effect on local vascular tone by regulation of Ca2+ influx into smooth muscle cells.

Animals↗

PubMed1998

Attenuation of ischemia/reperfusion injury in rats by a caspase inhibitor.

BACKGROUND: Z-Val-Ala-Asp(OMe)-CH2F (ZVAD-fmk), a tripeptide inhibitor of the caspase interleukin-1beta-converting enzyme family of cysteine proteases, may reduce myocardial reperfusion injury in vivo by attenuating cardiomyocyte apoptosis within the ischemic area at risk. METHODS AND RESULTS: Sprague-Dawley rats were subjected to a 30-minute coronary occlusion followed by a 24-hour reperfusion. An inert vehicle (dimethylsulfoxide; group 1, n=8) or ZVAD-fmk, at a total dose of 3.3 mg/kg (group 2, n=8), was administered intravenously every 6 hours starting at 30 minutes before coronary occlusion until 24 hours of reperfusion. At this 24-hour point, hemodynamics were assessed by means of cardiac catheterization; then, the rats were killed, and the left ventricle was excised and sliced. The myocardial infarct size/ischemic area at risk and the count of presumed apoptotic cardiomyocytes (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling [TUNEL]-positive cells) within the ischemic area at risk were assessed through triphenyltetrazolium chloride staining and TUNEL methods, respectively. Peak positive left ventricular dP/dt was higher (P=.02) and left ventricular end-diastolic pressure was lower (P=.04) in group 2 than in group 1. The infarct size/ischemic area at risk of group 2 (52.4+/-4.0%) was smaller (P=.02) than that of group 1 (66.6+/-3.7%), and TUNEL-positive cells were fewer (P=.0002) (group 2, 3.1+/-0.9%; group 1, 11.1+/-1.0%). Agarose gel electrophoresis revealed DNA laddering in the border zone myocardium of group 1, but DNA ladder formation was attenuated in group 2. CONCLUSIONS: ZVAD-fmk was effective in reducing myocardial reperfusion injury, which could at least be partially attributed to the attenuation of cardiomyocyte apoptosis.

Amino Acid Chloromethyl Ketones↗

PubMed1998

Morphological and functional changes in coronary vessel evoked by repeated endothelial injury in pigs.

OBJECTIVE: We examined the morphological changes induced by repeated endothelial denudation in coronary artery (CA), as well as functional changes in the endothelium-dependent and smooth muscle responses to various vasoactive agents during the process of intimal thickening. METHODS: We observed vascular responses in denuded and non-denuded portions of pig CA while being fed a normal diet (n = 11, N group) or 2% cholesterol diet (n = 25, C group) to intracoronary acetylcholine (ACh), 5-hydroxytryptamine (5-HT), substance P (SP), and isosorbide dinitrate (ISDN) with and without the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v.) over a period of 8 weeks. Balloon endothelial denudation of the left anterior descending CA was carried out every 2 weeks. RESULTS: In N group, maximum vasoconstriction was obtained with ACh 2 weeks after the first denudation [26 +/- 5% vs. 1 +/- 1% pre-denudation, p < 0.05]. L-NAME did not affect ACh-induced CA diameter changes. Thereafter, the response to ACh was attenuated by repeated denudation in N groups. However, the degree of 5-HT-induced CA narrowing at the denuded portion increased from 7 +/- 4% (0 week) to 88 +/- 8% (8 weeks) (p < 0.05). The changes resulted in severe myocardial ischaemia, and suggested that endothelium-dependent vasodilation was progressively attenuated while hyperreactivity of vascular smooth muscle simultaneously increased. Vasodilation induced by SP was attenuated somewhat, but ISDN-induced vasodilation was preserved. Although mild hypercholesterolaemia was induced in C group, the vascular responses to these vasoactive agents did not differ from those of N group. CONCLUSIONS: Repeated CA endothelial injury and regeneration induce the change of morphology and vascular reactivity in the denuded portion regardless of atherogenic diet. This study strongly suggests that intimal thickening caused by repeated endothelial injury and regeneration induces specific vascular responses to vasoactive agents. Moreover, it is also suggested that during the progression of intimal thickening, increased vascular smooth muscle contraction and decreased endothelium-dependent dilation appear in a stimulus-dependent manner, often leading to severe coronary vasoconstriction accompanied with definitive ECG ST change.

Acetylcholine↗

PubMed1998

Exercise tolerance in asymptomatic elderly men with fluoroscopically detected coronary artery calcification.

STUDY OBJECTIVE: The value of detecting coronary artery calcification (CAC), by cardiac imaging, for the diagnosis of coronary artery disease (CAD) in asymptomatic middle-aged men has been demonstrated. However, the incidence of CAC increases with age. The functional significance of CAC remains unknown in asymptomatic elderly men. The purpose of this study is to explore whether CAC in asymptomatic aging men signifies the presence of cardiovascular dysfunction during exercise. DESIGN: This study was designed to address whether elderly asymptomatic men, selected because they have CAC, have reduced exercise tolerance due to functionally significant CAD. PARTICIPANTS AND SETTING: Thirty-eight asymptomatic male volunteers (ages 50 to 75 years, mean [+/-SD] 64+/-7 years) with a normal resting ECG and at least one coronary risk factor, in a population study. Nineteen subjects had CAC detected by digital subtraction fluoroscopy in at least two major coronary arteries, and 19 subjects had no identifiable CAC. METHODS AND RESULTS: Each subject underwent a symptom-limited incremental exercise test with 12-lead ECG monitoring and respiratory gas analysis. Four indexes of exercise oxygen transport were evaluated: peak oxygen uptake (VO2), lactic acidosis threshold, peak VO2/heart rate ratio, and VO2 relative to a work rate increase. Eleven of 38 subjects (28%) were found to have reduced oxygen transport, which was defined as an abnormal reduction in more than two of the above four indexes of oxygen transport. Five of the 11 subjects with reduced oxygen transport had CAC, and 6 subjects did not (not significant). Only one subject with CAC had exercise ST depression. CONCLUSION: Significant CAC in asymptomatic men over age 50 does not signify exercise limitation due to CAD.

Aged↗

PubMed1997

The role of chondroitin sulfate chains of urinary trypsin inhibitor in inhibition of LPS-induced increase of cytosolic free Ca2+ in HL60 cells and HUVEC cells.

Preincubation of HL60 cells and HUVEC cells with urinary trypsin inhibitor (UTI) inhibited increase of cytosolic free Ca2+ induced by LPS. In contrast, an increase of cytosolic free Ca2+ induced by LPS was not inhibited by deglycosylated UTI, UTI treated with monoclonal antibody of chondroitin sulfate. 45Ca2+ binding showed that UTI binds 45Ca2+ dose-dependently. Scatchard plot analysis showed that UTI has two binding sites for Ca2+, a high affinity binding site (Kd=15 microM) and a low affinity site (Kd=150 microM), and that UTI has more than 70 Ca2+ binding sites per molecule. The Ca2+ binding capacity of deglycosylated UTI and UTI treated with monoclonal antibody of chondroitin sulfate was markedly depressed. Furthermore, UTI forms multi-polymers in the presence of Ca2+ as demonstrated by gel filtration and agarose gel electrophoresis. These results suggest that UTI is a physiological Ca2+ chelator on the cells and that the action is due to chondroitin sulfate chains of UTI.

Binding Sites↗

PubMed1997

A comparison of ultrastructural changes on endomyocardial biopsy specimens obtained from patients with diabetes mellitus with and without hypertension.

The pathogenesis of diabetic cardiomyopathy is unknown. The synergistic, or enhanced, effect of hypertension on pathological changes in the heart of diabetic patients has been highly suspected. The purpose of this study was to evaluate the myocardial changes related to diabetes mellitus with and without hypertension, using biopsy specimens. We examined the ultrastructural changes in biopsy specimens of the endomyocardium obtained from 25 patients. They were divided into four groups: controls without hypertension or diabetes mellitus (n = 6), and patient with hypertension (n = 3), diabetes mellitus (n = 8), and diabetes with hypertension (n = 8). The diabetic patients showed nearly normal or mildly depressed systolic left ventricular function. Ultrastructural pictures were analyzed for thickening of the capillary basement membrane, presence of toluidine blue-positive materials (i.e., materials showing metachromasia) in the myocytes, size of myocytes, and interstitial fibrosis. The thickening of the capillary basement membrane, the accumulation of toluidine blue-positive materials, and interstitial fibrosis were all significantly greater in the patients with diabetes mellitus compared to the control subjects. The myocytes tended to be small (cell atrophy) in the diabetes group. Although these pathological changes in the heart were characteristic of diabetic patients, irrespective of the presence or absence of hypertension, the presence of hypertension increased the pathological changes of myocardial cells as well as abnormality in the capillary vessels in patients with diabetes mellitus. Alterations in the myocardial cells and capillaries, caused by diabetes mellitus, may lead to myocardial cell injury and interstitial fibrosis and, ultimately, to ventricular systolic and diastolic dysfunction, especially when the diabetes is accompanied by hypertension.

Adult↗

PubMed1997

Syncope at sleep onset in a patient with nasopharyngeal carcinoma.

A patient with nasopharyngeal carcinoma developed atypical parapharyngeal-lesion syncope syndrome associated with stereotypical cycles of heart rate variation, which occurred only when he was drowsy before falling asleep. Vagal tone fluctuation is implicated.

Carcinoma, Squamous Cell↗

PubMed1997

Association between the anaerobic threshold and the break-point in the double product/work rate relationship.

A break point in the double product versus work rate relationship (DPBP) during incremental exercise has previously been reported. The aim of the current study was to investigate the frequency and degree of inter-observer agreement with which a DPBP could be detected. We also wished to determine its relationship, if any, to the lactic acidosis threshold (LATla). Ten normal volunteers performed continuous incremental bicycle ergometer exercise under three different concentrations of inspired oxygen (FiO2 = 0.21, 0.15 and 0.12). In addition, a group of patients with diseases expected to result in impaired exercise tolerance performed exercise under room air conditions. Gas exchange was measured continuously and double product was measured at 15-s intervals throughout exercise using an automated sphygmomanometer. Four observers, unaware of subject identity and test condition, analysed a total of 39 tests. All four observers detected a DPBP in 29 cases (74%) and an LAT in 35 cases (90%). The intra-class correlation coefficient was 0.76 for the DPBP and 0.93 for the LATla, indicating a reasonable level of agreement among observers for both break points. The DPBP was closely related to the LATla (r = 0.865, P < 0.0001), although it occurred at a slightly higher oxygen consumption (VO2, bias 0.137 1.min-1, 95% confidence intervals 0.041-0.233). We conclude that the DPBP is a common occurrence during incremental exercise. The close relationship between the DPBP and the LATla suggests that both may reflect similar events at the level of the skeletal muscle cell.

Acidosis, Lactic↗

PubMed1997

Hypolumbarlordosis: a predisposing factor for preeclampsia.

OBJECTIVE: The aim of this research was to study the relationship between lumbar lordosis and preeclampsia. STUDY DESIGN: We studied lumbar lordosis of 52 primipara patients with pregnancy-induced hypertension and 59 normal primipara pregnant women. We determined the lumbar lordotic deviation (LLD) from lumbar lordosis measurement device in the lateral recumbent position and standing position. Roll-over test was performed for both groups. Resistance index (RI) of internal iliac artery was also measured by color Doppler sonography. RESULTS: The LLD was 33 +/- 6.1 degrees week 20-29 and 34 +/- 6.9 degrees week 30-40, respectively. In patients with preeclampsia, the LLD was 19.8 +/- 6.3 degrees week 20-29, 21.3 +/- 7.9 degrees week 30-40. The LLD in patients with preeclampsia was significantly lower than in the normal pregnant women. The LLD correlated to the increase diastolic pressure after roll-over test significantly. Hypolumbarlordosis was frequently associated with high resistance of peripheral vessel. CONCLUSIONS: We conclude that hypolumbarlordosis is frequently associated with preeclampsia. It is also closely related to the mechanism for positive roll-over test and increase of resistance of vessels. As lumbar lordosis does not change greatly in individuals before pregnancy, hypolumbarlordosis may be a predisposing factor for preeclampsia.

Adult↗

PubMed1997

Cold-induced stress stimulates the sympathetic nervous system, causing hypertension and proteinuria in rats.

OBJECTIVE: To determine whether cold-stress stimulation of the soles of the paws would produce a preeclampsia-like syndrome in rats. METHODS: Pregnant or nonpregnant rats were kept in 0 degree C floor and 23 degrees C room temperature cages (the cold-stressed group) or in 23 degrees C floor and 23 degrees C room temperature cages (the control group) for 2 weeks. Their blood pressure, proteinuria, and plasma catecholamines were measured, and histologic studies were performed on all groups. RESULTS: There were no significant differences in systolic blood pressure between the two groups during the first week of the experimental period; however, during the last week of gestation the blood pressure of the cold-stressed group did not fall and was significantly higher than that of the control group. A significant increase in urinary protein excretion was observed in the cold-stimulated pregnant rats, in contrast to the control rats. The concentrations of norepinephrine and epinephrine in the cold-stressed pregnant rats were markedly higher than those in the control rats. A decrease in trophoblast invasion, congestion, and fibrinoid deposits of the labyrinth were observed in the cold-stressed rats. A marked increase in subendothelial fibrinoid deposits in the glomerular capillary was found only in the cold-stressed pregnant rats. The blood pressure, biochemical parameters, and histologic findings in the nonpregnant rats were almost the same as those in the pregnant rats. CONCLUSION: Chronic local cold stimulation of the soles of the paws induces preeclampsia-like phenomena in pregnant and nonpregnant rats, and this model suggests that the cause of preeclampsia is involved in chronic stimulation of the sympathetic nerve.

Animals↗

PubMed1997

Effect of hypoxia and carbon monoxide on muscle oxygenation during exercise.

We used near-infrared spectroscopy (NIRS) to test the hypothesis that reducing oxygen availability during exercise would affect the rate of muscle oxyhemoglobin (O2Hb) desaturation when performing work above the lactic acidosis threshold (LAT), but not below it. Seven healthy men each performed two constant work intensities (60%LAT and the LAT plus 40% of the difference between the LAT and VO2max [40%delta]) four times under the following conditions: (1) 10 min air; (2) 5 min 15%O2 + 5 min air; (3) 5 min air + 5 min 15%O2; (4) 5 min after carbon monoxide (CO) loading to increase the carboxyhemoglobin (COHb) saturation to 15%. During each test, cardiorespiratory parameters and muscle oxygenation measured with NIRS were continuously monitored. Forearm venous blood lactate was measured every 2 to 3 min. Hypoxia and CO accelerated muscle deoxygenation only for exercise above the LAT; for exercise below the LAT, neither progressive deoxygenation nor lactate accumulation occurred after initital, rapid muscle deoxygenation. The rate of decrease in muscle oxygenation between 3 to 5 min of exercise correlated with the increase in VO2 (r = 0.61, p < 0.01) and blood lactate (r = 0.70, p < 0.01) over the same period. These results support the hypothesis that progressive muscle deoxygenation occurs above the LAT and that the rate of deoxygenation is sensitive to oxygen delivery.

Adult↗

PubMed1997

Coronary circulation in the failing heart.

In congestive heart failure, vascular resistance increases because of vasoconstriction caused by activation of the neurohumoral system. On the other hand, vasodilatory responses can partially compensate for vasoconstriction by increasing vasodilatory substances. Although vasoconstrictive forces predominate as a whole, there is heterogeneity in the responses of different vascular beds to vasoactive agents. Especially, as for coronary circulation in the setting of heart failure, many factors may cause disturbances in coronary circulation. Thus, in this review, we discuss from the point of view of neurohumoral modification of coronary flow, coronary flow reserve, endothelial dependent and independent control of vasomotor tone, vascular responses in relation to vessel size or the severity of heart disease, and mechanical factors that determine coronary circulation. Throughout these discussions, the mechanism responsible for the reduction in coronary dilatory capacity is also described. Depressed myocardial blood flow and a blunted flow response to cardiovascular stimulation together may be one important mechanism responsible for the progression of disease in patients with cardiac dysfunction. Accordingly, even though it is not known whether abnormal coronary circulation is a cause or effect of heart failure, the treatment of impaired coronary flow reserve seems to be essential in the care of patients with cardiac dysfunction.

Cardiac Volume↗

PubMed1996

Mechanical stretching induces interleukin-8 gene expression in fetal membranes: a possible role for the initiation of human parturition.

OBJECTIVE: Interleukin-8 (IL-8) is known to play a crucial role in human parturition. We aimed to study the effect of mechanical stretching on the expression of IL-8 in fetal membranes (amniochorion) and decidua. STUDY DESIGN: We examined the expression of IL-8 and its receptor in fetal membranes (amniochorion) and decidua by immunohistochemical staining. Also, we studied the synthesis of IL-8 messenger RNA (mRNA) in the fetal membranes before and after stretching. RESULTS: We found that mechanical stretching within physiological limit increased IL-8 messenger RNA (mRNA) synthesis in fetal membranes and decidua in a time- and load-dependent manner. Application of mechanical force led to markedly increased staining of IL-8 receptor in decidual cells but not in amnion or chorion cells. CONCLUSION: These results suggested that mechanical stretching was a candidate for one of the signals important for production of IL-8 in fetal membranes and decidua and probably for initiation of a cytokine network at amniochorio-decidual interface through increased expression of IL-8 receptors.

Amnion↗