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Biomedical subjects

R J Bache

Publications and source records attributed to R J Bache.

At least 163 records · Page 9Linked to original sources
PubMed1982

Influence of systolic intracavity pressure on right ventricular perfusion in the awake dog.

This study tested the hypothesis that an acute increase in right ventricular pressure would result in selective impedance of blood flow into the right ventricular subendocardium (ENDO) similar to that seen normally in the left ventricle. Since tachycardia (reduces diastolic time) and vasomotor paralysis will reveal impedence to blood flow by a decrease in ENDO to subepicardial (EPI) myocardial blood flow (MBF) ratio, MBF was measured with microspheres in eight awake dogs during rapid pacing at 176 +/- 2 beats . min-1 (mean +/- SE) after acute pulmonary artery constriction (PAC) before and during adenosine (A) infusion (1.00 mg . kg-1 . min-1). AP was held constant by aortic constriction. During control pacing the ENDO/EPI ratios were 1.38 +/- 0.08 and 1.46 +/- 0.12 in the RV and LV, respectively. During adenosine infusion the ENDO/EPI decreased to 0.85 +/- 0.08 (P less than 0.05) in the LV but did not change in the RV (1.17 +/- 0.10). During PAC and pacing alone the RV ENDO/EPI was 1.24 +/- 0.05 (NS vs control), but during adenosine fell to 0.88 +/- 0.07 (P less than 0.05). Transmural blood flow to the interventricular septum (IVS) was also affected by increased RV pressure. During control the ratio of blood flow to the left and right side (LV/RV) of the IVS was 1.32 +/- 0.12. PAC alone caused a redistribution of MBF toward the right side and the LV/RV fell to 0.66 +/- 0.06 (P less than 0.05). During PAC and adenosine, however the LV/RV rose to 1.38 +/- 0.08. These data demonstrate that increased RV systolic pressure produces systolic impedance to blood flow to the right ventricular ENDO and the right side of the interventricular septum.

Adenosine↗
PubMed1982

Effect of perfusion pressure distal to a coronary stenosis on transmural myocardial blood flow.

We tested the hypothesis that reductions of perfusion pressure distal to a flow-limiting coronary artery stenosis can directly impair perfusion of the subendocardial myocardium. Dogs were instrumented with an electromagnetic flowmeter probe and a variable occluder on the proximal left circumflex coronary artery. Coronary perfusion pressure was measured with a catheter distal to the occluder. Coronary autoregulation was abolished by intraarterial infusion of adenosine to produce maximal coronary vasodilation. The transmural distribution of myocardial blood flow was measured with radioactive microspheres during unimpeded arterial inflow, when the occluder was progressively narrowed to reduce distal coronary pressure to approximately 70%, 50% and 35% of the control coronary perfusion pressure, and during total coronary occlusion. Heart rate, left ventricular diastolic pressure and the fraction of coronary artery flow during systole remained constant throughout the study. Progressive reductions of coronary perfusion pressure were accompanied by direct reductions of the subendocardial/subepicardial blood flow ratio (r = 0.83). Examination of the relationship between myocardial blood flow and coronary perfusion pressure showed that blood flow decreased linearly with perfusion pressure, with flow ceasing at a positive pressure (zero-flow pressure). Blood flow data from four transmural myocardial layers from epicardium to endocardium showed that this zero-flow pressure increased progressively from 10 +/- 2.1 mm Hg in the subepicardium to 18 +/- 2.3 mm Hg in the subendocardium (p less than -.01). Consequently, as coronary pressure was reduced, the zero-flow pressure represented a progressively greater fraction of coronary pressure in the subendocardium than in the subepicardium. This effect appeared to account for the progressive redistribution of blood flow away from the subendocardium that occurred as coronary pressure was decreased. Myocardial vascular resistance did not change as a result of changes in coronary perfusion pressure.

Animals↗
PubMed1982

Myocardial lactate and adenosine metabolite production as indicators of exercise-induced myocardial ischemia in the dog.

To determine the value of lactate and the adenosine metabolites inosine and hypoxanthine as indicators of myocardial ischemia, we measured the levels of these metabolites in arterial and coronary sinus blood of nine chronically instrumented dogs subjected to exercise stress before and during reversible circumflex coronary artery occlusion. The degree of circumflex bed hypoperfusion was measured by 15-mu microspheres and the reduction in circumflex coronary flow was measured with a proximal flow probe. Adenosine metabolites, although below the level of accurate detection in our laboratory in arterial blood (i.e., 0.5 microM/l), were detected in coronary sinus blood (range 2.7--18.7 microM/l) in 26 of 33 studies with partial circumflex occlusion when circumflex flow was reduced to less than 80% of that seen during exercise without occlusion and when only subendocardial perfusion was reduced. Global left ventricular flow and transmural flow in nonischemic beds did not correlate with positive studies. Myocardial lactate extraction was a less accurate test for determining circumflex bed hypoperfusion. Thus, myocardial production of adenosine metabolites is a sensitive qualitative test of exercise-induced ischemia responding to a modest fall in coronary flow when only subendocardial hypoperfusion is present.

Adenosine↗
PubMed1982

Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve.

Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 microM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 +/- 0.09 ml/min per g (mean +/- SEM) during control conditions to 1.69 +/- 0.27 ml/min per g during moderate pulmonary artery occlusion (P less than 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-to-subepicardial blood flow ratio fell from 1.36 +/- 0.14 to 0.77 +/- 0.06 (P less than 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 +/- 0.18 (P less than 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 +/- 0.10 to 2.25 +/- 0.30; P less than 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted.

Adenosine↗
PubMed1982

Effect of diltiazem on myocardial blood flow.

We examined the effects of diltiazem on transmural myocardial blood in the presence of a flow-limiting stenosis and during acute total coronary artery occlusion in awake, chronically instrumented dogs. Regional myocardial perfusion was estimated with left atrial injections of 15-mu-diameter radionuclide labeled microspheres. An electromagnetic flowmeter probe and hydraulic occluder were used to monitor blood flow and produce total and subtotal occlusions of the left circumflex coronary artery. A 10-second total arterial occlusion produced intense coronary vasodilation and a pronounced reactive hyperemic response. When a proximal coronary stenosis prevented reactive hyperemia, ischemic coronary vasodilation after a 10-second arterial occlusion caused transmural redistribution of blood flow toward the subepicardium. resulting in subendocardial underperfusion despite a normal net volume of arterial flow. Although diltiazem did not increase coronary collateral flow during acute arterial occlusion, it did blunt the vasodilation that occurred in response to a 10-second total coronary occlusion, and partially corrected the subendocardial underperfusion that occurred with a proximal flow-limiting coronary stenosis.

Animals↗
PubMed1980

Effect of selective beta-adrenergic blockade and stimulation on regional myocardial blood flow following acute coronary artery occlusion in the awake dog.

This study was designed to evaluate the effects of alterations of beta-receptor activity on intercoronary collateral blood flow after acute coronary artery occlusion in the awake dog. Blood flow following acute circumflex coronary occlusion was measured during: 1) control conditions; 2) selective beta1-blockade with practolol; 3) combined beta1 and beta2 blockade with propranolol; and 4) selective beta2 stimulation. Neither practolol nor propranolol significantly altered the volume or distribution of blood flow into the normally perfused or ischaemicmyocardial areas, while beta2 stimulation increased blood flow to the normally perfused myocardium from 1.13 +/- 0.12 to 1.28 +/- 1.10 cm3 .min-1 .g-1 (P <0.05). This increase in flow, which was directed preferentially to the subepicardium, was mediated by a significant decrease in coronary vascular resistance. In contrast to the effect on normally perfused myocardiu, beta2 stimulation resulted in a 47 +/- 12% decrease in collateral flow into the central ischaemic zone (P <0.05), which was mediated by a combination of decreased arterial pressure and increased collateral vascular resistance during beta2-agonist administration. Thus, although beta2 stimulation produced a modest increase in blood flow to normally perfused myocardium, in the setting of acute myocardial ischaemia, beta2 stimulation resulted in a significant decrease in intercoronary collateral flow.

Adrenergic beta-Agonists↗
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.

Animals↗
PubMed1980

Effect of heart rate on myocardial blood flow in dogs with left ventricular hypertrophy.

Because of the previous suggestion that subendocardial perfusion may be inadequate in the hypertrophied heart, this study was carried out to examine the response of transmural myocardial blood flow to pacing induced tachycardia in dogs with chronic left ventricular hypertrophy. Myocardial hypertrophy, produced by banding the ascending aorta of puppies at 5-6 wk of age, resulted in an 87% average increase in relative left ventricular mass compared with the control dogs. Myocardial blood flow was examined during ventricular pacing at heart rates of 100, 200, and 250 beats/min using radionuclide-labeled microspheres. Mean blood flow per unit myocardial mass was similar in the two groups of dogs at a heart rate of 100 beats/min and increased regularly during pacing in both groups of animals. Increasing heart rates did not change the transmural pattern of myocardial blood flow in the normal dogs, but in the animals with left ventricular hypertrophy pacing at 250 beats/min resulted in a significant redistribution of perfusion away from the subendocardium, with the ratio of subendocardial/subepicardial blood flow falling from 1.03 +/- 0.08 at 100 beats/min to 0.83 +/0 0.06 at 250 beats/min (P < 0.01). This redistribution of blood flow away from the subendocardium was especially marked in the regions encompassing the papillary muscles and the intervening left ventricular lateral wall.

Animals↗
PubMed1979

Effect of increases in afterload before and after coronary occlusion in awake dogs.

Ventricular function curves relating stroke work and left ventricular end-diastolic pressure were generated in awake dogs during increases in preload produced by infusion of fluid and during increases in afterload produced by administration of phenylephrine. The ventricular function curves produced by preloading were steeply upsloping whereas those produced by afterloading were essentially horizontal. Coronary occlusion produced downward displacement of these horizontal curves, but no change in slope. This increases in afterload did not help to demonstrate the functional impairment produced by coronary occlusion.

Animals↗