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Biomedical subjects

D Franklin

Publications and source records attributed to D Franklin.

At least 91 records · Page 5Linked to original sources
PubMed1977

In situ measurement of papillary muscle dynamics in the dog left ventricle.

In five open-chest dogs, pairs of ultrasonic dimension gauges were implanted in the anterior papillary muscle and in a circumferential subendocardial segment of the anterior left ventricular free wall, and simultaneous recordings were made with intracardiac pressure. The average shortening of the anterior segment in isovolumetric systole was 6% of end-diastolic length (EDL), with a total shortening of 19%. In the papillary muscles, isovolumetric shortening averaged 2%, total shortening was 10%, and shortening velocity was only 0.60 length/s. With acute pressure and volume overload, or inotropic interventions, changes in EDL were relatively less in papillary muscles than in the free wall. During acute occlusion of the anterior descending coronary artery, shortening of anterior segments and papillary muscles was replaced by holosystolic lengthening, and occlussion of the circumflex artery produced augmentation of shortening in both these regions, with lengthening of the posterior papillary muscle. The present study documents shortening of the anterior left ventricular papillary muscle throughout systole that is substantially less than that of the circumferential free wall, and demonstrates severe papillary muscle dysfunction with systolic elongation during regional ischemia.

Animals↗
PubMed1977

Loss of regional ventricular postextrasystolic potentiation after coronary occlusion in dogs.

Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.

Animals↗
PubMed1977

Regional myocardial function and dimensions early and late after myocardial infarction in the unanesthetized dog.

Pairs of ultrasonic dimension gauges and a micromanometer implanted in the subendocardium of the left ventricles of unanesthetized dogs were used to analyze serial changes in hemodynamic status and segmental function for up to 4 weeks after permanent circumflex coronary artery occlusion. Regional function was studied in control segments and in segments identified as marginal (hypokinetic) and ischemic. In three dogs, after transient regional dysfunction, no myocardial infarction developed, whereas in five dogs regional dysfunction at 3 hours after occlusion was followed by the development of persistent dysfunction and infarction. Left ventricular end-diastolic segment length (EDL) changes over time; EDL of the control segments increased progressively, but in marginal segments EDL was 12% below control and in the ischemic segments 30% below control by 4 weeks. Progressive increases in percent active shortening occurred in control segments; but holosystolic bulging was replaced by akinesia in ischemic segments, and persistent reduction in shortening was present in marginal segments at 4 weeks. Correlations were found between percent scar and reductions in percent shortening, EDL, and the ratio of change in diastolic length to change in diastolic pressure. These methods have detected hyperfunction in normal regions and variable segmental loss of contractile function, together with reduction of subendocardial dimensions and changes that may reflect decreased diastolic compliance in ischemic regions. We conclude that this model for the conscious animals may be useful for studying the influence of therapy on the extent of myocardial damage after experimental coronary occlusion.

Animals↗
PubMed1976

Coronary arterial reperfusion. III. Early and late effects on regional myocardial function and dimensions in conscious dogs.

Regional myocardial function was studied in five conscious chronically instrumented dogs for 4 weeks after coronary reperfusion following a 2 hour period of occlusion of the left circumflex coronary artery. A cuff and flowmeter were placed around the left circumflex coronary artery, and a micromanometer and three pairs of ultrasonic crystals were implanted 1 cm apart subendocardially in control, marginal and ischemic segments of the left ventricle. Control normal segments showed progressive increases in end-diastolic length and extent of active shortening. Ischemic segments tended to show slight improvement early after reperfusion, but in succeeding weeks, despite some improvement in shortening, they showed progressive decreases in end-diastolic length compatible with subendocardial tissue loss. In marginally ischemic segments, shortening initially remained depressed after reperfusion, but showed late recovery so that shortening and end-diastolic length were not different from control values by 4 weeks. These results contrasted with findings in five similarly studied dogs subjected to permanent coronary occlusion; in that group the data suggested greater tissue loss and less recovery of function in marginal and ischemic segments. The late return of segmental function and reduced loss of subendocardial tissue several weeks after coronary reperfusion suggest that substantial time periods may be required to assess the ultimate effect of therapeutic interventions. The findings further indicate that in this experimental model the usual time constraints for occurrence of irreversible tissue damage do not apply to all of the myocardium within the ischemic zone.

Action Potentials↗
PubMed1976

Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog.

The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic valueof9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.

Animals↗
PubMed1976

Regional Myocardial function in the conscious dog during acute coronary occlusion and responses to morphine, propranolol, nitroglycerin, and lidocaine.

Regional myocardial function following occlusions of the circumflex coronary artery was studied in unanesthetized dogs using minature ultrasonic crystal pairs implanted subendocardially within the left ventricle for measurement of control, marginal, and ischemic lengths. As early as five beats after coronary occlusion, reduced function was apparent in ischemic zones, and an increase in heart rate occurred (78 to 115 beats/min) at an average of 25 sec. In the control zones, shortening initially increased from a constant end-diastolic length, but later end-diastolic length also increased by 7.5%. Shortening in the marginal zones was reduced by 50% at 90 sec as holosystolic expansion developed in the ischemic zones. On reperfusion, systolic function returned to normal within a few minutes while protodiastolic abnormalities persisted for up to 45 min. With coronary occlusions longer than two minutes most dogs exhibited arousal and further tachycardia; this reaction was prevented by morphine. During two minute occlusions morphine also decreased the heart rate increase by 37%, and marginal segment shortening was improved by 40%. Prior administration of propranolol also decreased heart rate during coronary occlusion and produced similar improvement in marginal segment function; however, in contrast to morphine, there was depression of contraction in the control segments. Nitroglycerin given during coronary occlusion caused decreases in end-diastolic length of all segments and increased shortening in the marginal segment by 28%. Lidocaine administered during coronary occlusion produced a mild depression of myocardial function in all regions of the heart.

Animals↗
PubMed1976

Adaptations of the left ventricle to chronic pressure overload.

Left ventricular (LV) function during the adaptation to chronic pressure overload produced by an ascending aortic constriction was analyzed in conscious dogs, instrumented with intraventricular micromanometers and pairs of ultrasonic crystals for measurement of LV wall thickness (WTh) and internal LV chamber diameter. During inflation of the cuff to produce LV pressures averaging 220 mg Hg, calculated peak wall stress (WSt) increased by 55% above control while percent shortening decreased by 24% and mean circumferential shortening velocity (VCF) decreased by 39% from control. By 9 days (mean) after aortic constriction, the cross-sectional area (CSA) of the LV wall increased by 10% and peak WSt fell to 37% above control. End-diastolic diameter (EDD) increased to 4% above control, while percent shortening and mean VCF remained reduced at -12% and -20% of control, respectively. During the phase of concentric hypertrophy (mean 2 1/2 weeks), CSA increased further to 15% above control and WSt fell to 22% above control, while EDD and percent shortening returned to control and mean VCF increased to -7% of control (not significant). At 24 hours after release of the cuff WSt, percent shortening, mean VCF, and peak velocity of LV pressure rise (peak dP/dt) were not significantly different from control. Rapid, partial regression of hypertrophy was observed in some dogs. Thus, the left ventricle responds to chronically elevated pressure by initial dilation with increased WSt followed by gradual wall thickening and consequent reduction of WSt to near normal. After successful adaptation to the pressure overload, hypertrophy per se did not produce intrinsic depression of the myocardial inotropic state.

Animals↗