Biomedical subjects

M Akaishi

Publications and source records attributed to M Akaishi.

At least 55 records · Page 3Linked to original sources

PubMed1988

A non-linear elastic model of contraction of ischaemic segments.

Previous studies have characterised the motion of the myocardium using a linear time varying elastance model, ie, they have sought to characterise the relationship between left ventricular volume and internal pressure as linear, but with time varying slopes over the cardiac cycle. However, the motion of myocardium during regional ischaemia has not been characterized by such models. Studies of totally ischaemic tissue and of myocardium in diastole have characterised the relationship between tension or stress and segment length as exponential. It is the purpose of this study to present a new model in which myocardial contraction is expressed as an exponential, but time varying elastic relationship. In this model tension, T, is related to segment length according to the formula T = e alpha(t)L + beta, where alpha(t) rises with systole and falls in diastole. This model was applied to the motion of hypokinetic segments noted in a series of conscious dogs studied for other purposes. Hypokinetic segments display early systolic bulging, decreased systolic shortening, and early diastolic recoil. These particular types of segment motion are naturally predicted by this model. Furthermore, the motion of myocardial segments as they become increasingly ischaemic may be predicted, including a gradual shift to the right and narrowing of the tension-length loop. alpha was noted to be independent of loading change, and thus may be viewed as an index of contractility. This model thus predicts the pattern of motion of hypokinetic segments and provides new insight into myocardial contractility.

Animals↗

PubMed1987

Absence of coronary vascular reserve in myocardium distal to a fixed coronary stenosis.

In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 mumol.min-1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml.min-1) decreased from 41(3) to 29(6) (p less than 0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p less than 0.05) with adenosine and to 50(10) (p less than 0.05) with stenosis adjustment. Subendocardial flow (ml.g-1.min-1) decreased from 0.89(0.26) to 0.78(0.23) (p less than 0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

PubMed1987

Myocardial segment motion during regional ischemia--regional contraction and relaxation.

Several aspects of regional ischemic myocardial function determined by segment motion are discussed, based on our studies. Although global left ventricular function decreased progressively as the global severity of myocardial ischemia increased, there are several possible factors which may modify this relationship. As for the site of the ischemic area, occlusion of the left anterior descending artery resulted in a greater decrease in the left ventricular ejection fraction than occlusion of the left circumflex artery. Interaction between the ischemic myocardium and the non-ischemic myocardium may be a multifactorial phenomenon rather than simple tandem stretching. The segment length motion during acute ischemia appears to be complicated. The segment motion of the severe ischemic myocardium during systole and diastole was explained for the most part by a uniform tension-length curve which was independent of changes in the loading condition. This non-linear elastic property was fundamental to the production of segment motion asynchrony. The wall motion of the hypokinetic segment might be explained by a combination of the active change in myocardial stiffness and the non-linear elastic property of the myocardium.

Animals↗

PubMed1987

[Contraction of the interventricular septum in right ventricular overload studied by two-dimensional echocardiography].

This study clarified the relationship between right ventricular (RV) overload and contraction of the interventricular septum using two-dimensional echocardiography. Seventeen patients with atrial septal defect (RV systolic pressure: 36 +/- 14 mmHg), 13 with mitral stenosis (49 +/- 19 mmHg), nine with primary pulmonary hypertension (87 +/- 21 mmHg) and 17 normal subjects (23 +/- 3 mmHg) were evaluated using two-dimensional echocardiography and cardiac catheterization. The circumferential lengths of the septum (Civs) and the left ventricular (LV) free wall (Cfw) were measured in the LV short-axis view at the level of the papillary muscles. In normal subjects, Civs was 3.4 +/- 0.5 cm and Civs/Cfw was 0.40 +/- 0.07. All patients with RV overload had longer Civs and greater Civs/Cfw as compared with the normal subjects. There was no significant difference in the Cfw among the cases with mitral stenosis and primary pulmonary hypertension and the normal subjects. Cfw in atrial septal defect was shorter than in the normal subjects. The percent contraction of Civs was decreased in mitral stenosis and primary pulmonary hypertension as compared with the normal subjects. No significant difference was found in the percent contraction of Civs between the normal subjects and the 11 patients with atrial septal defect with normal RV systolic pressure. However, in six patients with atrial septal defect with high RV systolic pressure, the percent contraction of Civs was decreased. There was an inverse correlation between RV systolic pressure and the percent contraction of Civs (r = -0.39, p less than 0.01), and RV ejection fraction (r = -0.52, p less than 0.01) defined by multiplegated equilibrium scintigraphy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1986

The significance of underlying coronary stenosis for recovery of myocardial function after transient ischemia in the dog.

The rate of recovery of myocardial function after transient coronary occlusion (CO) has been considered to depend on the duration and frequency of CO. However, underlying coronary stenosis has not been previously demonstrated to be a determinant of the rate of myocardial functional recovery. Thus, 12 open-chest dogs were studied to examine the influence of critical coronary stenosis (CCS) on functional recovery after transient CO. Regional functional recovery following 2-minute CO was examined under two different conditions in eight dogs: patent coronary artery stenosis and fixed CSS that exhausted coronary reserve but did not cause a deficit in resting coronary flow or regional function. Following reperfusion with the coronary artery patent, regional function in the ischemic zone was fully recovered (100 +/- 18.0% of pre-CO value) at 30 seconds and was significantly increased (postischemic hypercontraction) compared to pre-CO value at 1 and at 2 minutes after reperfusion. Following CO and reperfusion in the setting of CCS, regional functional recovery was delayed and regional function remained depressed until 2 minutes after reperfusion. No cumulative effect on functional recovery following repeated 2-minute CO was demonstrated in a control group of four dogs. We conclude that coronary artery patency is a determinant of the rate of myocardial function recovery after a transient ischemic episode, and postischemic hypercontractility was suppressed by the underlying CCS.

Animals↗

PubMed1986

Analysis of phases of contraction during graded acute myocardial ischemia.

The quantitative effects of graded ischemia on the phases of contraction in ischemic and nonischemic myocardium were studied in 10 open-chest dogs. During progressive coronary stenosis, an index of the overall severity of ischemia, total myocardial blood flow deficit (TMFD), was measured using microspheres. Segment shortening (% delta L) during the isovolumic and ejection phases of systole in the ischemic and nonischemic zones was obtained with ultrasonic crystals. In the ischemic zone, total systolic and ejection phase % delta L decreased progressively as stenosis increased; isovolumic phase % delta L showed segment elongation (bulging) during mild ischemia, which was unchanged as ischemia became severe. Total % delta L in the nonischemic zone increased progressively with increasing stenosis, reaching 132 +/- 20% of the control value when TMFD was 24.8 +/- 6.5% of total expected left ventricular (LV) myocardial blood flow. The increase in total % delta L was entirely attributable to increased ejection % delta L and correlated with indices of preload (multivariate r = 0.65) and afterload (multivariate r = 0.62). Multiple linear regression analysis revealed that augmented contraction in the nonischemic zone was best described (multivariate r = 0.94) by a combination of four hemodynamic variables estimating LV preload and afterload, which correlated in turn with the overall severity of ischemia. Thus systolic bulging in the ischemic zone is primarily an isovolumic phase phenomenon that develops initially with mild ischemia. Little additional change occurs in the isovolumic phase as ischemic severity increases, although further reductions in shortening occur in the ejection phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1986

Analysis of systolic bulging. Mechanical characteristics of acutely ischemic myocardium in the conscious dog.

To determine the mechanical factors affecting regional segmental motion after acute coronary occlusion, we studied seven conscious dogs, instrumented with sonomicrometers. Loading conditions were changed by the withdrawal of 500 ml of blood and the transfusion of 800 ml of blood. To express segmental motion, percent systolic shortening, percent systolic elongation, and early diastolic shortening were calculated. Blood withdrawal decreased left ventricular preload, increased percent systolic elongation (from 6.9 +/- 3.1% to 9.9 +/- 3.5%) and early diastolic shortening (12.9 +/- 5.3% to 16.6 +/- 5.3%), and decreased percent systolic shortening. Blood transfusion increased left ventricular preload, decreased percent systolic elongation (to 5.2 +/- 1.8%) and early diastolic shortening (8.8 +/- 2.9%), and increased percent systolic shortening. Manipulation of loading did not change regional myocardial blood flow. In acutely ischemic myocardium, the tension-length loop showed an exponential upstroke during isovolumic systole and a nearly superimposed exponential downstroke during the isovolumic relaxation phase after systole, compatible with essentially passive movement as seen with an elastic material. The changes in loading conditions affected the tension-length curve to a very minor extent. The uniformity of the curve and its exponential shape explain the load-dependency of systolic bulging and segmental motion. It is concluded that systolic bulging depends on the change in the preload tension due to the compliant portion of tension-length curve, and that shortening of ischemic myocardium during the isovolumic relaxation phase is a completely passive phenomenon.

Animals↗

PubMed1985

Relation between left ventricular global and regional function and extent of myocardial ischemia in the canine heart.

To develop a quantitative relation between the overall severity of acute ischemia and left ventricular global and regional function, two minor axis internal diameters and myocardial wall thickness were determined using ultrasonic crystals in 10 open chest dogs with carotid-left anterior descending artery cannulation. The overall extent of ischemia produced by graded stenosis of the cannulation system was estimated by total myocardial blood flow deficit, calculated using radioactive microspheres and a balloon-reservoir perfusion technique permitting precise separation of ischemic from nonischemic tissue. Although cardiac output and left ventricular stroke work were maintained through chamber enlargement until total myocardial blood flow deficit was about 10%, ejection indexes of left ventricular function decreased progressively with increasing ischemia and correlated inversely with total myocardial blood flow deficit (r = -0.55 to -0.73). Ejection indexes of left ventricular global function correlated directly with regional function in the ischemic zone (r = 0.67 to 0.83), although global function decreased at a far slower rate than regional contraction during progressive coronary stenosis with an ischemic region comprising about 25% of total left ventricular weight. During myocardial ischemia, regional dysfunction resulted in progressive global contractile dysfunction; left ventricular hemodynamic status was maintained until ischemia was severe.

Animals↗

PubMed1985

Left ventricular ejection fraction after acute coronary occlusion in conscious dogs: relation to the extent and site of myocardial infarction.

The change in left ventricular radionuclide ejection fraction after acute occlusion of the left anterior descending (LAD) or circumflex (LC) coronary artery was compared with the ultimate histologic extent of myocardial infarction in conscious dogs. The acute change in ejection fraction correlated with size of infarction in 14 dogs with occlusions of the LAD coronary artery (r = .89, y = 1.12x + 14.2) and in 27 dogs with occlusions of the LC coronary artery (r = .71, y = 0.73x + 7.9); the slope of the regression equation was greater (p less than .05) for those with LAD than for those with LC occlusions. Multivariate analysis revealed no independent contribution of left ventricular weight, the subendocardial extent of infarction, or change in heart rate to the acute change in ejection fraction. These data indicate that the decrease in ejection fraction after coronary occlusion is determined primarily by the size of the ischemic area, which also determines size of infarction. In dogs instrumented over a long term, infarcts in the LAD myocardial distribution result in greater decreases in ejection fraction than infarcts of comparable size in the LC distribution.

Animals↗

PubMed1985