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To evaluate regional myocardial function, we developed a curvature sensor for direct and instantaneous measurement of the regional curvature radius of the LV wall. The sensor is a bimorph of two sheets of thin piezoelectric polymer film. The relation between output voltage of the sensor and the reciprocal of the known curvature radius has been shown to be linear. In anesthetized dogs, we inserted the curvature sensor into the subepimyocardium with a specially designed introducer. Special care was taken to insert it parallel to the epicardial surface. Circumferential regional curvature radius, which is defined as the reciprocal of regional curvature, showed the same phasic changes as the short-axis diameter under control conditions. Under regional ischemia caused by transient occlusion of the coronary artery, amplitude of the phasic change in regional curvature radius decreased, whereas that of the short-axis diameter did not change or slightly increased. Phasic changes in regional curvature radius cannot be estimated from short-axis diameter during regional ischemia. We calculated regional wall tension from the directly measured regional curvature radius and LV pressure and found that tension-length loop clearly differentiates between regional myocardial function under control and ischemic conditions. We have concluded that our newly developed curvature sensor is accurate, that its practical use is feasible, and that measurement of the regional curvature radius of the LV wall provides detailed and accurate information on regional shape and function of the left ventricle.

Akita Prefecture has an especially high mortality rate from stroke, and its age-adjusted death rate from stroke is the highest in Japan. We have carried out an epidemiological survey of cardio- and cerebrovascular diseases (CVD) in farming villages in this prefecture since 1963, with a response rate of 84%. During our 8-year follow-up, 94 new stroke cases were observed among 1,814 subjects. Multiple logistic function analysis was carried out on nonstroke and stroke cases from subjects aged 40 to 69 years at time of initial examination, in order to clarify the risk factors for stroke. The analysis used eight variables: age, sex, systolic blood pressure, obesity index, urinary sugar, urinary protein, serum total cholesterol, and total protein. The results showed that hypertension was the most important risk factor for stroke. However, regarding cholesterol, multivariate analysis showed that among men and women aged 40 to 69 years at entry, subjects with low serum total cholesterol levels were more prone to cerebral hemorrhage, but that serum cholesterol level had no weight as a risk factor for cerebral infarction. These results correspond well with the observed fact that stroke incidence or death rate in Japan is higher in populations with high prevalence of hypertension and low concentration of cholesterol, and also with the fact that death rate from hemorrhage declines with the increment of serum total cholesterol and the westernization of diet.

In the present study, we attempted to test the hypothesis that ejection timing rather than peak left ventricular pressure is a primary determinant of ventricular relaxation rate. In cross-circulated isolated canine hearts instantaneous left ventricular volume was controlled by a servo-pump system. To eliminate the effects of end-systolic and end-diastolic volumes and ejection velocity on left ventricular relaxation rate, these parameters were clamped, and only the ejection timing (onset and end of ejection) was altered, keeping the duration of ejection unchanged. Left ventricular relaxation rate was assessed by time constants of left ventricular pressure decline during the isovolumic relaxation phase calculated by both a semilogarithmic method, assuming that the asymptote is zero, and a best exponential fitting method. In 25 runs, a pair of contractions with ejection timings which differed by 53.1 +/- 2.1 (SE) msec were imposed, while end-systolic and end-diastolic left ventricular volumes and ejection duration were unchanged. All pairs of contractions demonstrated early ejection resulted in significantly (P less than 0.001) slowed relaxation as indicated by a prolongation of the time constants of isovolumic left ventricular pressure decay (delta 4.2 +/- 0.7, sec and delta 15.4 +/- 2.1 msec by semilogarithmic plot and the best exponential fit respectively), although peak left ventricular pressures (104.6 +/- 2.4 mm Hg) were even lower than those (116.6 +/- 2.8 mm Hg) in contractions with later ejection timing. Furthermore, in seven experiments, the heart was allowed to eject at five different timings; onset and end of ejection were progressively delayed in steps of 20 or 30 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

The sympathetic inhibitory mechanism in dog urinary bladder studied. The bladder contractions induced by electrical stimulation of the pelvic nerve both proximal and distal to the pelvic plexus and by intraarterial administration of tetramethylammonium (TMA) were inhibited by stimulation of the hypogastric nerve and intraarterial injection of catecholamines. The inhibition by hypogastric nerve stimulation was more potent at the low frequency of pelvic nerve stimulation than at the high frequency. The inhibition of contraction induced by stimulation of the pre-plexal pelvic nerve was antagonized by phentolamine and propranolol, whereas the inhibition of contraction induced by stimulation of the post-plexal pelvic nerve and by TMA treatment were antagonized only by propranolol. It is concluded that inhibition by hypogastric nerve stimulation of bladder contraction induced by pelvic nerve stimulation is composed of two different components. One occurs at the ganglia in the pelvic plexus and is mediated by alpha-adrenoceptors. The other occurs at the post-plexal pelvic pathway, probably at the ganglia in the bladder wall or on the muscle cells, and is mediated by beta-adrenoceptors. Moreover, the alpha-adrenergic action facilitated the pelvic nerve excitation in its pathway from the ganglionic cell bodies to the muscle cells.

A significant positive relationship was found between alcohol intake and blood pressure for men 40-69 years old living in urban Osaka (492 men) and in rural Akita (395 men), Japan, surveyed from 1975 to 1977. Both mean blood pressure and the prevalence of hypertension were related to alcohol intake in a graded fashion. Stepwise multiple regression also showed that both systolic and diastolic pressure were associated with alcohol intake independent of ponderosity index, serum cholesterol, triglycerides, hemoglobin, uric acid, smoking, and age. This cross-sectional study indicates a continuous--and not a threshold--relationship between alcohol and blood pressure, with the effect of even moderate consumption, e.g. 28-55 g per day (equivalent to about 2-4 U.S. drinks per day).

The afterload dependency of relaxation rate was reappraised in isolated canine hearts both in isovolumic and isobaric contractions by using the reliable exponential method in which the asymptote LV pressure (P chi) is variable. This method provided a closer correlation (r = 0.999 +/- 0.001) between the measured LV pressure decay and the model estimate than the semilogarithmic method assuming P chi = 0 (r = 0.992 +/- 0.001). Time constants of isovolumic LV pressure decay obtained by the exponential method demonstrated a significant (p less than 0.01) decrease during volume loading both in isovolumic and isobaric contractions, indicating that the relaxation rate is augmented as afterload increases. In contrast, if we assume P chi = 0, the time constant of LV pressure decay was independent of peak LV pressure as previously reported. Thus, we conclude that the load insensitive relaxation rate implied by the semilogarithmic method (P chi = 0) may be erroneous due to an invalid assumption, ie, P chi = 0, but the relaxation rate is augmented as afterload increases both in isovolumically contracting and isobarically ejecting isolated canine hearts.

Isometric relaxation in cardiac sarcomeres is characterised by an early, very slow phase of tension fall which is terminated by a 'give' in tension. A 'give' which occurs during relaxation in cardiac muscle can not be attributed to decrease in myofilament overlap. After the 'give' asynchronous motion occurs between sarcomeres, but the duration and extent of their displacement is limited. Intriguingly, the effect of isotonic displacements on the early fall in the velocity of sarcomere shortening indicates that an internal resistance increases near the peak of contraction. The complex shape of the sarcomere's complete force-velocity relation, with lengthening motions in particular, was consistent with an idealized model of cross-bridge cycling. The sarcomere's resistance to stretch is high at low velocity, but it diminishes to reveal yielding at larger velocities. Relative to tension, the resistance to yielding does not decrease during relaxation, and it may actually increase. The decay of isometric tension after a controlled stretch also slows during relaxation. Consequently, cycling slows in those cross-bridges which form (or persist but produce less force) later in contraction. Changes in cross-bridge properties may restrict sarcomere shortening, prolong activation, but promote a disequilibrium which favors rapid relaxation in cardiac muscle.

A high resolution laser Doppler velocimeter using an optical fiber was developed to evaluate detailed characteristics of phasic blood flow in the coronary artery. Local blood flow velocities were measured in the proximal (0.27 +/- 0.05 cm i.d.) and the distal portion (0.09 +/- 0.02 cm i.d.) of the left circumflex coronary artery of anesthetized, open-chest dogs. The velocity waveform in the central axial region of the vessel and the velocity profile across the vascular lumen were compared in the proximal and the distal portions.

The hypotensive effect of FR35447 was comparable to that of prazosin and was more potent than that of hydralazine, but its duration of action was shorter. Repeated administration of FR35447 or prazosin to hypertensive rats for 5 consecutive days induced no significant difference in the intensity or duration of the hypotensive effect. In contrast, marked tachyphylaxis to hydralazine or phentolamine was observed. FR35447 as well as prazosin induced only a transient increase in cardiac output in anesthetized dogs, whereas hydralazine induced a longlasting increase. This difference may contribute to no development of tolerance to FR35447 or prazosin. FR35447 decreased the pressor response to noradrenaline, but not that to angiotensin II or vasopressin in pithed rats, which indicates that FR35447 is an alpha-adrenoceptor antagonist. FR35447 has some selectivity for alpha 2-adrenoceptors, but the selectivity was far less than that of yohimbine. Since FR35447 induced only slight hypotension following intracerebroventricular injection in anesthetized cats, the hypotensive effect of the drug does not appear to be mediated through the central nervous system. Whereas prazosin induced a dose-dependent increase in blood glucose in rats, FR35447 showed no significant effect.

To elucidate the role of loading sequence in afterload-dependent slowed relaxation in hearts in situ, the time constants (Texp from best exponential fitting method and TL from semilogarithmic method) of isovolumetric left ventricular (LV) pressure decay were studied in nine anesthetized open-chest dogs under the pharmacological blockade of autonomic nerve activity. An afterload change was imposed by clamping the ascending or descending aorta to make the peak LV pressure early or late in systole. During afterload interventions, in contractions with the peak LV pressure in late systole Texp and TL were significantly (P less than 0.05) larger than in those with the peak LV pressure in early systole in any comparable peak LV pressure range. Moreover, both time constants were directly correlated (P less than 0.01) with the time of peak LV pressure irrespective of peak LV pressure and clamp mode of aorta. In another protocol, marked differences both in Texp and TL were also observed between each of 25 pairs of contractions with different loading sequence but with comparable peak LV pressure and LV dimension (segment length). Thus afterload-dependent slowed relaxation in hearts in situ could not be attributed to an increased total load but to the altered loading sequence associated with an increase in afterload.

Poststenotic blood flow velocities were evaluated in nine patients with 75% to 99% stenosis of the left anterior descending coronary artery (LAD) during coronary artery bypass graft surgery. We used the 20 MHz 80-channel pulsed Doppler velocimeter developed in our laboratory. An operator placed a specially designed probe on the native LAD with his fingers. Before induction of extracorporeal circulation, LAD blood velocities were measured at several locations distal to the stenosis. The poststenotic flow velocities were rich in systolic flow component with reduced diastolic component. The velocity configuration in the poststenotic portions was characterized by the presence of reverse flow velocities and/or irregularity of the velocity pattern near the vessel wall, indicating the existence of flow separation and recirculation in the regions. The broadening of the velocity spectrum observed at central axial regions suggested the occurrence of flow disturbances. After grafting, the velocity waveform in the LAD beyond a vein bypass graft changed to a diastolic-predominant pattern with a relatively small systolic component. A transient bypass graft occlusion caused a marked reduction in diastolic flow velocity. The systolic-to-diastolic velocity ratio increased from 0.27 +/- 0.07 to 1.50 +/- 0.50 (p less than .01) by the graft occlusion.

A synthesized mouse vasoactive intestinal contractor peptide, which belongs to a novel member of the endothelin family, induced a prolonged contraction in mouse ileum as well as porcine coronary artery in vitro. Studies comparing the effects of vasoactive intestinal contractor and endothelin on different tissues revealed that the maximum ileum contraction of vasoactive intestinal contractor was much higher than that of endothelin in both guinea pig and mouse systems, but that the vasoconstriction activity of vasoactive intestinal contractor was weaker than that of endothelin in porcine artery. These results show that vasoactive intestinal contractor might be a novel gastrointestinal hormone.

The relation between the site and severity of coronary artery lesion and infarct size was investigated in 59 patients with acute myocardial infarction. All patients had no prior myocardial infarction and had at least one significant coronary narrowing (greater than or equal to 75%) in one of the major coronary arteries or in the first diagonal branch. Left ventriculography and selective coronary arteriography were performed on average 2.2 months after the onset of infarction to identify the site and severity of coronary narrowing and to assess the extent of the non-contracting segment (akinetic, dyskinetic, or aneurysmal). Thirty-four of 59 patients were studied enzymatically and total CK released was taken as an indication of infarct size. Non-contracting segment and total CK released in group L-I (narrowing proximal to the first diagonal branch) were significantly larger than those in group L-II (a coronary lesion distal to the branch). The data also indicate that the perfusion area of the first diagonal branch is as large as that of the left anterior descending artery below the first diagonal branch. In contrast to left anterior descending artery disease, the involvement of the right ventricular branch did not significantly influence the infarct size. However, infarct size was significantly larger in eight patients with the left ventricular branch of the right coronary artery supplying the predominantly large area of posterior wall of the left ventricle than in nine patients with small left ventricular branches. It was also shown that the severity of coronary narrowing does not correlate with the infarct size in either left anterior descending or right coronary artery disease.

The effects of increasing heart rate (HR) on the hemodynamics of acute mitral regurgitation (MR) were studied in 8 open-chest dogs. Filling volume, regurgitant volume and stroke volume were calculated from electromagnetic probe measurements of mitral and aortic flows. The left atrial-left ventricular systolic pressure gradient was measured with micromanometers. The calculated effective mitral regurgitant orifice area varied from 10 to 128 mm2, with a consequent regurgitant fraction (regurgitant volume/filling volume) of 24 to 62%. After crushing the sinus node, HR was increased stepwise from 90 to 180 beats/min by atrial pacing while maintaining aortic pressure constant. With increasing HR, filling volume, stroke volume, regurgitant volume and regurgitant time decreased; total cardiac output, forward cardiac output, regurgitant output, systolic pressure gradient, regurgitant fraction and the regurgitant orifice did not change; left ventricular end-diastolic pressure decreased; and left atrial v-wave amplitude increased. These results indicate that in acute experimental MR with a wide spectrum of incompetence, the relative distribution of forward and regurgitant flows did not change with large increases in HR. At rates greater than 150 beats/min the atrial contraction occurs early and increases the amplitude of the left atrial v wave. This may contribute to the severity of pulmonary congestion in patients with MR.

A case of cutaneous leiomyoma of the male nipple is reported. This is the second case reported by dermatologists to the best of our knowledge.