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Biomedical subjects

J C Rembert

Publications and source records attributed to J C Rembert.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of atrial fibrillation on atrial blood flow in conscious dogs.

This study was undertaken to examine the independent effects of atrial tachycardia, ventricular tachycardia, and atrial fibrillation (AF) on atrial and ventricular blood flow in conscious, heart-blocked dogs using radioactive microspheres. Atrial blood flow averaged 0.54 +/- 0.08 ml/min/g during the control period at an atrial rate of 124 beats/min and a ventricular rate of 90 beats/min. Atrial flow increased to 0.72 +/- 0.12 ml/min/g during atrial pacing at 236 beats/min, but was not significantly altered by ventricular pacing at 200 beats/min. AF at a ventricular rate of 90 beats/min resulted in atrial flow values of 0.91 +/- 0.08 ml/min/g. The ratio of atrial flow to left ventricular flow during AF averaged 1.18 +/- 0.08. Administration of a maximal vasodilating dose of adenosine during AF further increased atrial flow to 2.18 +/- 0.16 ml/min/g. Atrial tachycardia or AF did not significantly affect ventricular blood flow. These data indicate (1) that atrial blood flow increases significantly during AF, reaching flow values per gram of tissue comparable to those of the left ventricle, and (2) that this flow is regulated by the metabolic needs of the atrial tissue and does not represent maximal vasodilation.

Adenosine↗
PubMed1983

Relation of left ventricular mass to geometry of the proximal coronary arteries in the dog.

Proximal epicardial coronary artery luminal diameters were measured from silicone casts formed in situ in freshly excised hearts under a constant pressure of 100 mm Hg. Twenty-five coronary arteries from 15 normal dogs and 22 coronary arteries in 13 dogs with either chronic pressure or volume overload hypertrophy were studied. Mean left ventricular (LV) body weight ratios were 4.75 +/- 1.01 g/kg in the normal dogs, 8.4 +/- 1.7 g/kg in the pressure-overload dogs, and 6.2 +/- 0.6 g/kg in the volume-overload dogs. The cross-sectional area of the left circumflex (LC) coronary artery was determined at 11 branch sites. The ratio of the area of the branches to the area of the parent vessel was 1.095 +/- 0.105, indicating that the cross-sectional area after a branch point increased. A poor correlation existed between LV mass and coronary artery diameter in both normal and hypertrophy groups for the LC (r = 0.44), the left anterior descending (LAD) (r = 0.63), and the combined LC and LAD (r = 0.52). The mean cross-sectional area of the combined LC and LAD was 0.12 cm2 in the normal group and 0.15 cm2 in the hypertrophy group; this increase was not statistically significant (p = 0.13). When the mean cross-sectional area of the combined vessels was adjusted for heart weight, there was a decrease in the cross-sectional area/100 g of myocardium in the hypertrophy group compared with the control group. These data demonstrate that coronary artery luminal diameter in the dog does not increase commensurately with the increase in mass associated with myocardial hypertrophy.

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PubMed1983

Mitochondrial function in canine experimental cardiac hypertrophy.

Concentric left ventricular hypertrophy was produced in puppies by coarctation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 +/- 16 mmHg in experimental dogs compared with 115 +/- 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 +/- 4 and 64 +/- 7, respectively. The left ventricular end-diastolic pressure was 6.0 +/- 0.4 in control and 8.4 +/- 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.

Animals↗
PubMed1983

Myocardial blood flow and function during gradual coronary occlusion in awake dog.

The purpose of this study was to correlate dimensions and transmural blood flow in a segment of myocardium supplied by a coronary artery undergoing gradual closure. Nine adult dogs were instrumented with an electromagnetic flow probe, pneumatic occluder, and an ameroid constrictor on the circumflex coronary artery. Ultrasonic crystals were implanted 10 mm from the external surface of the left ventricle in a segment perfused by the circumflex artery. Regional blood flow was determined with 7- to 10-microns radiolabeled microspheres. Data were collected in the awake state at rest before closure began (control), during partial closure, and immediately after total closure. Seven of the nine animals were studied after occlusion during treadmill exercise. During both partial and total closure at rest the rate and extent of systolic shortening as well as the transmural blood flow were unchanged from control. During treadmill exercise mean flow increased. However, flow was redistributed away from the inner two layers causing deterioration in both the rate and extent of shortening of this segment. These data suggest that, although regional myocardial function and flow can be maintained at rest by the immature canine collateral circulation, these parameters are impaired markedly during augmented flow with exercise.

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PubMed1980

Effect of hyperoxia on regional blood flow after coronary occlusion in awake dogs.

The effect of 100% oxygen inhalation on regional transmural myocardial blood flow following 45 s of actue total left circumflex coronary artery occlusion was studied in six awake dogs chronically instrumented with a coronary occluder and catheters in the aorta and left atrium. After inhalation of either room air or 100% oxygen for at least 30 min and following the 45-s occlusion, transmural myocardial blood flow was determined with radioactive microspheres (7--10 micrometers). Each dog underwent two occlusions of the left circumflex coronary artery; one during inhalation of rrom air and the other during 100% oxygen. During room air inhalation, mean regional myocardial blood flow to nonischemic, intermediate, and ischemic regions was 0.92 +/- 0.05, 0.51 +/- 0.08, and 0.10 +/- 0.02 ml . min-1 . g-1, respectively. During 100% oxygen administration, flow was significantly diminished in each region to 0.75 +/- 0.04, 0.41 +/- 0.07, and 0.06 +/- 0.01 ml . min-1 . g-1, respectively. Transmural blood flow to each layer was uniformly reduced in all regions. These data indicate that 100% oxygen further reduces myocardial blood flow to ischemic regions.

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PubMed1980

Effect of adenosine on transmural myocardial blood flow distribution in the awake dog.

Studies were conducted to determine the effects of adenosine on transmural myocardial blood flow distribution. Both maximal and submaximal vasodilatory doses of adenosine were infused into awake resting dogs chronically instrumented with coronary flow probes and aortic and left atrial pressure catheters. Radioactive microspheres (8-10 micron) were used to determine regional coronary blood flow. Four experimental protocols were evaluated: 1) the effects of maximal (1.00 mg . kg-1 . min-1) as well as submaximal (0.45 mg . kg-1 . min-1) vasodilatory levels of adenosine, 2) the dose-response characteristics of adenosine, 3) the dose-response characteristics of dipyridamole, and 4) the effects of adenosine in the presence of an increased arterial PO2. The data indicate that maximal vasodilatory doses of adenosine have little effect on the endocardial-to-epicardial blood flow ratio, whereas submaximal doses result in a marked preferential endocardial perfusion. This relative increase in endocardial perfusion was not altered by hyperoxia. Dipyridamole, in submaximal doses, produced a similar preferential flow to the endocardial layer. These data demonstrate that the vasodilator reactivity to adenosine infusion is greater in the endocardial layer,

Adenosine↗
PubMed1978

A reproducible model of moderate to severe concentric left ventricular hypertrophy.

A reproducible model for the production of moderate to severe concentric left ventricular hypertrophy has been developed in this laboratory. Coarctation-banding of the ascending aorta was performed successfully in 10 puppies. There were no late deaths related to aortic rupture, and in the dogs surviving for 1 yr no evidence of congestive heart failure was present. A second operative procedure was performed in seven dogs for chronic instrumentation, and all survived. Severe supravalvular aortic stenosis with a marked peak systolic pressure gradient was noted in each dog. Postmortem examination revealed a substantial increase in left ventricular mass and in the ratio of left ventricular to body weight.

Animals↗
PubMed1978

Regional myocardial blood flow after sudden aortic constriction in awake dogs.

Hemodynamic and regional myocardial blood flow responses were studied 5 seconds (early) and 30 seconds (late) after abrupt proximal aortic constriction in chronically instrumented awake dogs. During the early phase, left ventricular end-diastolic pressure (LVEDP) increased and stroke volume (SV) decreased significantly. During the late phase, there was a positive inotropic response manifested by a decrease in LVEDP and increase in SV (Anrep effect). The late inotropic response was closely associated with a recovery from subendocardial underperfusion. Hemodynamic and regional flow responses after beta-adrenergic blockade with propranolol (0.4 mg/kg) were similar to those observed during control. Studies during coronary vasodilation induced by adenosine (0.75--1.0 mg/kg per minute) showed that, if subendocardial flow was elevated during the early phase, the early increase of LVEDP and decrease of SV were less than control; however, if subendocardial flow did not change from control in the early phase and did not subsequently increase, there was no late inotropic response. These data suggest that the Anrep effect in the awake dog is closely related to a recovery from subendocardial ischemia.

Animals↗
PubMed1978

Myocardial blood flow distribution in concentric left ventricular hypertrophy.

Regional myocardial blood flow during both control conditions and ischemia-induced vasodilatation was studied in eight chronically instrumented awake dogs. Seven of these animals had coarctation-banding of the ascending aorta performed at 6 wk of age, and the other dog had congenital subvalvular aortic stenosis. The mean left ventricular weight for the group was 157+/-7.6 g, and the left ventricular body weight ratio was 8.76+/-0.47 g/kg. None of the animals exhibited signs of congestive heart failure. During the control state, the mean left ventricular systolic pressure was 249+/-12 mm Hg and the left ventricular end-diastolic pressure was 11.5+/-0.5 mm Hg. The aortic diastolic pressure was 74+/-6 mm Hg. Mean left circumflex coronary artery blood flow was 71+/-6 cm(3)/min. In the animals with coarctation-banding, 52+/-6% of the flow occurred during systole. In the dog with congenital subvalvular aortic stenosis, 5% of the coronary flow was systolic. Mean transmural blood flow during resting conditions was 0.97+/-0.08 cm(3)/min per g, and the ratio of endocardial to epicardial flow (endo/epi) was 0.88+/-0.07. During reactive hyperemia, the mean transmural blood flow increased to 3.5+/-0.30 cm(3)/min per g; however, the endo/epi decreased to 0.52+/-0.06.THESE STUDIES DOCUMENT A DIFFERENCE IN TRANSMURAL BLOOD FLOW DISTRIBUTION BETWEEN THE NORMAL AND THE HYPERTROPHIED LEFT VENTRICLE: during resting conditions, in the normal ventricle, the highest flow occurs in the endocardial layer, whereas in the hypertrophied ventricle, the highest flow is in the middle layers with the endocardial flow less than the epicardial flow. During ischemia-induced vasodilatation, the abnormal endo/epi becomes accentuated markedly. These data demonstrate that, in situations requiring high flow, the endocardial layer of a heart with marked concentric left ventricular hypertrophy may not be perfused adequately.

Animals↗
PubMed1975

Shunt dynamics in experimental atrial septal defects.

Inorder to study the hemodynamic variables involving the magnitude, direction, and timing of phasic shunt flow, both the interatrial pressure gradient and blood flow along with other pertinent hemodynamic variables were measured instantaneously across a surgically created atrial septal defect (ASD) in seven awake dogs. Atrial and ventricular pacing and infusion of phenylephrine and isoproterenol were used to alter hemodynamic conditions. The wave form of phasic ASD flow was similar both in configuration and timing to the interatrial pressure gradient. During the cardiac cycle, both left-to-right (L-R) and right-to-left (R-L) shunting occurred: atrial contraction augmented L-R flow; the onset of ventricular contraction was associated with R-L flow; during the latter part of ventricular contraction, flow returned to L-R with the maximum L-R shunting occurring in early diastole. Tachycardia, infusion of phenylephrine and isoproterenol did not alter the phasic flow pattern. Both spontaneous and positive pressure respiration decreased net L-R shunting.

Animals↗
PubMed1975

Effects of nitroglycerin on transmural myocardial blood flow in the unanesthetized dog.

This study was designed to determin the effect of nitroglycerin upon transmural distribution of myocardial blood flow in the awake dog during normal conditions and in the presence of ischemia-induced coronary vasodilation. Studies were performed in chronically prepared dogs with electromagnetic flowmeters and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow was estimated by using radionuclide-labeled microspheres, 7-10 mum in diameter, injected into the left atrium. During control conditions endocardial flow (0.86 plus or minus SEM 0.05 ml/min per g) slightly exceeded epicardial flow (0.72 plus or minus 0.03 ml/min per g, P smaller than 0.05), and this distribution of flow was not significantly altered by nitroglycerin. After a 5-s coronary artery occlusion, reactive hyperemia occurred with excess inflow of arterial blood effecting 360 plus or minus 15% repayment of the blood flow debt incurred during occlusion. When arterial inflow was limited to the preocclusion rate during coronary vasodilation after a 5-s total coronary artery occlusion, flow to the subepicardial myocardium was increased at the expense of underperfusion of the subendocardial myocardium, and the delayed reactive hyperemia was markedly augmented (mean blood flow debt repayment =775plus or minus 105%, P smaller than 0.01). Tese data suggested that subendocardial underperfusion during the interval of coronary vasodilation in the presence of a flow-limiting proximal coronary artery stenosis caused continuing subendocardial ischemia which resulted in augmentation of the reactive hyperemic response. In this experimental model both the redistribution of myocardial blood flow which occurred during an interval of restricted arterial inflow after a 5-s coronary artery occlusion and augmentation of the subsequent reactive hyperemic response were returned toward normal by nitroglycerin. This effect of nitroglycerin may have resulted, at least in part, from its ability to vasodilate the penetrating arteries which deliver blood from the epicardial surface to the subendocardium.

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