PubMed Health⌕ Search

Biomedical subjects

G A Pantely

Publications and source records attributed to G A Pantely.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effect of coronary sinus occlusion on coronary flow, resistance, and zero flow pressure during maximum vasodilatation in swine.

The effects of coronary sinus occlusion on the relation between coronary artery pressure and flow during maximum vasodilatation were studied in seven swine. The left anterior descending (LAD) coronary artery was instrumented with two catheters, a hydraulic occluder, and a flowprobe. Mean flow was measured at a series of pressures produced by partial LAD occlusion during maximum vasodilatation induced by an intracoronary infusion of adenosine. Observations were made under control conditions and during occlusion of the coronary sinus produced by inflating the balloon on the catheter positioned in the coronary sinus. Systemic haemodynamic variables did not change significantly after the coronary sinus was occluded. The mean right atrial pressure was 4 mmHg. At any given LAD perfusion pressure mean flow during coronary sinus occlusion was always less than during the control state: at LAD pressure 30 mmHg, control flow was 53 ml.min-1 vs occluded flow 24 ml.min-1; at LAD pressure 40 mmHg, control flow 79 ml.min-1 vs occluded flow 49 ml.min-1; and at LAD pressure 50 mmHg, control flow 105 ml.min-1 vs occluded flow 74 ml.min-1; p less than 0.001 for all comparisons. The mean (SD) LAD pressure at which flow stopped (Pzf) when the coronary sinus was unobstructed was 10(2) mmHg. The Pzf during occlusion of the coronary sinus was significantly higher at 20(4) mmHg (p less than 0.001). The slopes of the mean pressure-flow relations were not significantly different during the control state (2.62(0.65) ml.min-1 per mmHg) vs the occluded state (2.47(0.63) ml.min-1 per mmHg), indicating no change in vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

No reflow and extent of infarction during maximal vasodilation in the porcine heart.

To explore the relation between myocardial and vascular injury in the generation of the no-reflow phenomenon, the pressure-flow relation during maximal vasodilation after coronary artery reperfusion was studied in the open-chest porcine model. During both endogenous and maximal vasodilation with intracoronary adenosine, pressure-flow (P/Q) plots were constructed before and after 20-minute (n = 9) or 40-minute (n = 17) circumflex artery occlusions. Decreases in circumflex vascular bed conductance were represented by downward shifts in P/Q plot regression lines. No significant change occurred in P/Q line slope or pressure at zero flow 30 minutes after release of the 20-minute occlusion, and no infarction was found. After release of the 40-minute occlusion, a small but insignificant decrease in P/Q line slope occurred during endogenous vasodilation. However, during maximal vasodilation, a significant (p less than 0.01) decrease in P/Q line slope was present during reperfusion compared with preocclusion corresponding to a decrease in vasodilatory reserve (P/Q line slope = 1.52 +/- 0.14 ml/min/mm Hg preocclusion vs. 1.03 +/- 0.13 at 15 minutes reperfusion). Pretreatment with aspirin did not prevent this decrease in vascular conductance during maximal vasodilation. Total circumflex, as well as subendocardial, midmyocardial, and subepicardial blood flows, was measured with radioactive microspheres. There was a good correlation between the extent of infarction measured by triphenyltetrazolium chloride staining and the decrease in vascular conductance during maximal vasodilation for all three myocardial layers as well as for the total circumflex vascular bed. Hence, the degree of no-reflow correlates closely with the extent of infarction during maximal vasodilation (but not during endogenous vasodilation) and is not altered by aspirin therapy.

Animals↗
PubMed1987

Relation of lactate production to postischaemic reduction in function and myocardial oxygen consumption after partial coronary occlusion in swine.

Postischaemic myocardial dysfunction (stunning) induced by partial occlusion of the left anterior descending coronary artery and its relation to lactate production during reperfusion were studied in nine swine. A 40% reduction in regional left ventricular wall thickening, as measured by ultrasonic crystals, was prospectively defined as stunning. A perfusion pressure of 20 mmHg was maintained with a hydraulic occluder for each ischaemic period and was monitored by a distal arterial catheter. To achieve a 40% reduction in function, four animals required three ischaemic periods (mean ischaemic flow reduction 73%), four two (86% flow reduction), and one one (93% flow reduction). At 25 min of reperfusion transmural flow was slightly reduced from 0.67 ml.g-1.min-1 at control to 0.58 ml.g-1.min-1 (p less than 0.05), whereas regional flow endocardial to epicardial flow ratio was unchanged. At 60 min reperfusion, percentage systolic wall thickening was reduced to 25% from a control of 39% (p less than 0.01) and parallel reductions in regional myocardial oxygen consumption from 4.3 ml.min-1 to 2.7 ml.min-1 occurred (p less than 0.01). Lactate extraction was depressed at 15 min reperfusion (-4.0% compared with control +18.0% (p less than 0.05)) but returned to control values by 30 min. It is concluded that postischaemic myocardial dysfunction (stunning) can be induced by partial coronary occlusions and that the extent of dysfunction depends on the degree of flow reduction. The reductions in myocardial oxygen consumption parallel those of wall thickening during reperfusion after stunning. Finally, lactate production occurs during early reperfusion but does not persist with the postischaemic reductions in function and myocardial oxygen consumption.

Animals↗
PubMed1987

Increased vascular resistance during complement-activated plasma infusion in swine.

To investigate the acute effects of complement activation on blood flow, we infused complement-activated plasma into the femoral artery of the isolated hindlimb of 19 anesthetized swine. Femoral artery blood flow decreased abruptly, was lowest at 1 min of the infusion, and thereafter slowly increased despite continued infusion. There was no significant change in femoral artery pressure or femoral vein pressure, confirming an acute increase in vascular resistance. Control infusion of heat-decomplemented-activated plasma caused no change in pressure or flow. Slope of the femoral artery pressure-flow relationship during maximal vasodilation with adenosine was significantly lower after infusion of complement-activated plasma, confirming a persistent increase in vascular resistance. Neither the acute nor the persistent increase in vascular resistance was prevented by alpha-adrenergic blockade with phentolamine or granulocytopenia produced by cyclophosphamide. We conclude that complement-activated plasma infusion in the femoral circulation causes an abrupt increase in vascular resistance that persists during pharmacologically maximal vasodilation, is not due to alpha-mediated vasoconstriction, and is not altered by severe granulocytopenia.

Adrenergic alpha-Antagonists↗
PubMed1987

Coronary vasodilator reserve persists despite tachycardia and myocardial ischemia.

During myocardial ischemia, we tested whether coronary blood flow would increase in response to tachycardia, thereby employing known coronary flow reserve. We instrumented the left anterior descending (LAD) coronary circulation in anesthetized pigs and performed three sets of experiments while coronary pressure was controlled and several heart rate increases were produced. Pacing-induced tachycardia at normal LAD pressure was characterized by increased LAD flow and myocardial oxygen consumption, without production of lactate. Tachycardia at a mean LAD pressure of 38 mmHg was associated with a lower, fixed coronary flow and oxygen consumption. At average heart rates of 90 and 150 beats/min, LAD flow was 19.6 and 19.4 ml/min and corresponding myocardial blood flows were 0.59 and 0.54 ml X g-1 X min-1. Lactate was produced at all rates and local myocardial function declined progressively. Coronary flow at low LAD pressure doubled during tachycardia when intracoronary adenosine was added. The increase to the subepicardium was greater than 100%, whereas subendocardial flow changed little. There is persistent coronary flow reserve during moderately severe myocardial ischemia, even when metabolic demand is increased by tachycardia. This reserve, however, is predominantly subepicardial.

Adenosine↗
PubMed1986

A quantitative study of the anatomy and distribution of coronary arteries in swine in comparison with other animals and man.

The coronary circulation of swine was studied to establish adequate baseline information for using swine in cardiovascular research. Of 65 hearts from domestic and miniature pigs, 45 were injected with a methacrylate plastic and prepared as coronary artery casts whose branches were described and measured, and 20 were injected with different coloured dyes in the right, left anterior descending, and circumflex coronary arteries so that horizontal sections of the heart showed the distribution of each artery and the source of blood supply to particular areas or structures of the heart. Like man, the swine had a left coronary artery that was larger in diameter and longer than the right coronary artery. The right coronary artery was almost always dominant (78%), supplying the posterior septum and atrioventricular node via the posterior descending coronary artery. Eight (17%) of the hearts possessed a balanced blood supply. Two (5%) hearts had a left dominant supply. The intracoronary artery dye injections showed that 72.4% of the right ventricular mass was supplied by the right coronary artery and 27.6% by the left anterior descending coronary artery. In the left ventricle 49% of the mass was supplied by the left anterior descending coronary artery, 25.5% by the right coronary artery, and 25.5% by the circumflex coronary artery. The left anterior descending coronary artery supplied 58% of the interventricular septal mass, while the posterior descending coronary artery supplied 42%. The distribution of the left anterior descending coronary artery branches to the ventricular wall varied inversely in number and size of its diagonal branches (2-9) with the obtuse marginal branches of the circumflex coronary artery which were occasionally more numerous or extended to the apex. The blood supply to the sinoatrial node was always by a branch of the right coronary artery. This analysis shows that not only the coronary anatomy but also the distribution of blood supply to particular areas or structures of the swine heart are very similar to that of humans.

Animals↗
PubMed1985

Vasopressin-induced coronary constriction at low perfusion pressures.

We studied the effects of intracoronary vasopressin on the relationship between pressure and flow in the coronary circulation of anaesthetised swine. In addition to measurements at control levels, diastolic pressure-flow relationships were constructed from steady-state points below a coronary pressure of 50 mmHg, where endogenous vasodilatation is strongly stimulated. At baseline pressures, flow fell 28% with maximal vasopressin effect. At all levels of diastolic pressure below 50 mmHg vasopressin also decreased flow, eg, at 30 mmHg flow was depressed by 40%. The slope of the steady-state pressure-flow relationship fell from 1.21 to 0.75 ml.min-1.mmHg-1. The diastolic pressure at which coronary flow ceased rose slightly from 13 to 15 mmHg. Intracoronary adenosine completely prevented vasopressin's effect, and the vasodilator response to adenosine was not attenuated by simultaneous administration of vasopressin. The porcine coronary circulation will constrict in response to vasopressin, not only at normal perfusion pressure, but also at low levels when metabolic vasodilatation is intense. Our study has implications about the therapeutic use of vasopressin, and demonstrates interaction of vasoactive stimuli in the coronary circulation.

Adenosine↗
PubMed1985

Incomplete coronary vasodilation during myocardial ischemia in swine.

To determine if endogenous (ENDG) vasodilation was maximum during myocardial ischemia, left anterior descending (LAD) mean pressure (P) was reduced for 20 min in 13 swine. At LAD P of 45 mmHg (LAD P45) flow fell during ENDG = 25 but rose to 44 ml/min during adenosine (AD) infusion (P less than 0.01). Flow increased to subendocardium (ENDG 0.65 vs. AD 1.04 ml X min-1 X g-1) and to subepicardium (ENDG 0.99 vs. AD 1.83 ml X min-1 X g-1; P less than 0.05). No significant change occurred in myocardial O2 consumption (MVO2; ENDG 2.91 vs. AD 3.18 ml X min-1 X g-1), lactate extraction (ENDG = -5 vs. AD-1%), and wall thickening (WTh; ENDG + 16 vs. AD + 17%). At LAD P35, flow during ENDG was 12 but rose to 19 ml/min during AD (P less than 0.01). Flow increased to subendocardium (ENDG 0.24 vs. AD 0.46 ml X min-1 X g-1; P less than 0.02) and subepicardium (ENDG 0.51 vs. AD 0.87 ml X min-1 X g-1; P less than 0.01). No significant change occurred in MVo2 (ENDG 1.38 vs. AD 1.59 ml/min), lactate extraction (ENDG -38 vs. AD -22%), WTh (ENDG -1 vs. AD + 1%). Thus endogenous vasodilation reserve was not used fully during ischemia. AD increased flow but did not improve abnormalities in myocardial function or metabolism.

Adenosine↗
PubMed1984

Low zero-flow pressure and minimal capacitance effect on diastolic coronary arterial pressure-flow relationships during maximum vasodilation in swine.

During maximum dilation with adenosine in dogs, the diastolic coronary pressure at which flow ceases (Pzf) has been observed to be up to 27 mm Hg above coronary sinus and right atrial pressures. We studied swine to measure the Pzf and to determine the effects of interventions that change collateral flow and coronary capacitance. In 44 swine, the left anterior descending coronary artery (LAD) was instrumented with two catheters, a hydraulic occluder, and a flowmeter. Late diastolic and mean pressure-flow relationships were constructed at a series of pressures produced by partial LAD occlusions during maximum vasodilation. The late diastolic Pzf was 7.0 +/- 2.2 mm Hg (mean +/- SD), less than 4 mm Hg above right atrial pressure; the mean Pzf was 12.1 +/- 3.1 mm Hg, less than 9 mm Hg above right atrial pressure. The Pzf in the LAD did not change significantly (1) during transient simultaneous occlusion of the right coronary artery (RCA) in seven swine (late diastolic Pzf with the RCA open was 6.6 +/- 1.5 mm Hg and with the RCA closed it was 6.0 +/- 1.5 mm Hg), (2) during increased left ventricular systolic pressure (LVSP) in seven swine (late diastolic Pzf with LVSP of 123 mm Hg was 5.5 +/- 2.2 mm Hg and with LVSP of 184 mm Hg it was 7.3 +/- 2.8 mm Hg), or (3) during increased heart rate in eight swine (late diastolic Pzf at heart rate of 107 per minute was 10.8 +/- 2.9 mm Hg and at 180 per minute it was 12.7 +/- 2.1 mm Hg). Similar results were obtained from analysis of the mean pressure and flow data. The Pzf in the LAD of swine is very close to right atrial pressure, and it did not change significantly during interventions that would modify collateral flow (reduced by RCA occlusion and enhanced by increased LVSP) and coronary capacitance (increased LVSP and increased heart rate). This low Pzf is beneficial in maintaining flow at lower coronary arterial perfusion pressures.

Adenosine↗
PubMed1983

Late exercise test results from a prospective randomized study of bypass surgery for stable angina.

A prospective randomized study comparing coronary bypass surgery (group 1, 51 patients) to drug therapy (group 2, 49 patients) was initiated in 1981. Supine graded exercise testing (SGXT) was performed initially, at 6 months, and annually with a bicycle ergometer. The presence or absence of ischemic ST segment changes (positive or negative SGXT) and chest pain were recorded. Initially, 63% of all patients had positive SGXT. For group 2, the frequency of positive SGXT results did not change significantly at 6 months (58%) or at 5 years (52%). At 6 months the number of patients without chest pain increased in group 1 compared with group 2 (28/41 vs 13/41, respectively; p less than .002), but there was no difference in the frequency of positive SGXT results (20/41 vs 24/41, respectively; p = NS). This occurred because a majority of the group 1 patients with positive SGXT no longer had associated chest pain (group 1, 11/20, group 2, 3/24; p less than .007). This response was associated with incomplete revascularization in eight of these 11 group 1 patients and may result from "silent ischemia." At 5 years, no significant difference existed in the incidence of positive SGXT (group 1, 10/32 vs group 2, 12/23; p = NS), but group 1 patients continued to have a reduction (although not statistically significant) in the number of patients without chest pain (group 1, 19/32 vs group 2, 7/23). The incidences of death and myocardial infarction were not significantly different between groups. Fewer episodes of unstable angia occurred in group 1 (10/51 vs 19/49; p less than .05). The prognosis of group 1 patients with positive SGXT and no chest pain and incomplete revascularization was not different from that of the entire group.

Adult↗
PubMed1981

Improvement in the relationship between flow to ischemic myocardium and the extent of necrosis with glycolytic intermediates that decrease blood oxygen affinity in dogs.

Reducing blood oxygen affinity may enhance myocardial oxygen delivery during ischemia. We evaluated this hypothesis in awake, previously instrumented dogs that received a 20 ml/kg infusion of a solution of dihydroxyacetone, phosphate, and pyruvate after acute occlusion of either the left anterior descending or circumflex coronary artery. This infusion reduced blood oxygen affinity (BOA) after 2 hours; the P50 increased from 29.9 +/- 0.7 torr (mean +/- SD) to 32.1 +/- 0.6 torr; P less than 0.01 (BOA group). Four dogs received 20 ml/kg of phosphate and pyruvate solution to assess volume effects (V group), and five dogs were controls (C group). The 2-hour P50 values in V and C were unchanged. Regional flow (15-mum spheres) reduction 2 hours postocclusion was compared to the percent tissue infarcted determined by histology 7-9 days after occlusion for multiple samples from the endocardial layer of the left ventricle. When flow was less than 40% of normal, V and C had 55% infarction while BOA had 37% (P less than 0.05); at flow less than 20% of normal, V and C had 79% infarction while BOA had 38% (P less than 0.001); and at less than 10% of normal, V and C 87% and 94% infarction, respectively, while BOA had 56% (P less than 0.001). Reducing blood oxygen affinity after coronary artery occlusion significantly decreased the extent of myocardial necrosis for the same degree of ischemia. Reducing BOA may increase oxygen delivery to ischemic myocardium when flow is restricted.

Animals↗
PubMed1979

Failure of antiplatelet and anticoagulant therapy to improve patency of grafts after coronary-artery bypass: a controlled, randomized study.

Fifty patients who underwent aortocoronary saphenous-vein bypass-graft surgery were randomly assigned to one of three groups to determine the effects of antiplatelet or anticoagulant therapy on graft patency. Twenty-four patients served as controls; 13 patients received aspirin (325 mg three times a day) and dipyridamole (75 mg three times a day); and 13 patients received closely regulated warfarin therapy. Medications were begun on the third post-operative day. Six months after surgery, all patients underwent coronary angiography to assess graft patency. There were no statistically significant differences between groups in various clinical, hemodynamic and angios, 27 of 33 grafts (82 per cent) with aspirin and dipyridamole and 29 of 37 grafts (78 per cent) with warfarin (P less than 0.5), all patients had at least one patent graft. Postoperative treatment either with aspirin and dipyridamole or with warfarin failed to improve the patency of the grafts.

Aged↗
PubMed1979

Reduction of human blood O2 affinity using dihydroxyacetone, phosphate, and pyruvate.

Human blood oxygen affinity (BOA) was measured after blood from six normal donors was incubated with 4 concentrations of dihydroxyacetone (0.022, 0.044, 0.088, and 0.175 M) plus equimolar disodium phosphate and pyruvate (sodium salt) (0.013, 0.025, 0.05 and 0.1 M) in solutions labeled DDP X 1, DDP X 2, DDP X 4, and DDP X 8, respectively. Blood P50 rose (BOA was reduced) from a control value of 26.0 +/- 0.4 Torr (mean +/- SD) to 29.4 +/- 0.6, 30.6 +/- 0.4, 31.9 +/- 0.15 and 33.3 +/- 1.4 Torr after 2 h of incubation at 37 degrees C with solutions DDP X 1, DDP X 2, DDP X 4, and DDP X 8, respectively. P50 changes at 2 h were 75% complete within 30 min. During these incubations, erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentration rose from 0.76 +/- 0.09 mol/mol Hb (control) to 1.09 +/- 0.17, 1.14 +/- 0.10, 1.33 +/- 0.15, and 1.45 +/- 0.25 mol/mol Hb with increasing solution concentration. BOA is decreased by an increase in erythrocyte 2,3-DPG. Reduced BOA may improve oxygen delivery to ischemic tissues.

Animals↗
PubMedDate not supplied

Microvascular and collateral adaptation in swine hearts following progressive coronary artery stenosis.

We chronically implanted hygroscopic occluders around the left circumflex coronary artery in 49 anesthetized young male domestic pigs and we studied the development of a collateral circulation at 4, 8, 12, and 26 weeks after implantation. At these time intervals groups of animals were again anesthetized, the hearts were explanted and perfused in Langendorff-fashion with leucocyte-filtered pig blood. Maximal coronary vasodilation was induced with adenosine and global (electromagnetic), and regional (tracer microspheres) blood flow was measured at 40, 60, 80, and 100 mm Hg of perfusion pressure. At 4 weeks after occluder implantation maximal left circumflex collateral blood flow was about 20% of normal maximal flow. Collateral flow rose to 60% of maximal normal flow between 4 and 8 weeks and did not improve further with longer time intervals. In contrast to the canine heart numerous small vessels develop in response to ischemia in the pig heart. These vessels develop throughout the entire risk region with a slight preference for the subendocardium. They appear on tomographic angiograms as a dense "blush". The study of the relationship between peripheral coronary pressure vs collateral flow showed a relationship much steeper than that of normal maximal flow vs aortic perfusion pressure which indicates that the minimal resistance of the risk region was decreased as part of the mechanism to ensure adequate blood supply in a situation of progressive coronary narrowing.

Adaptation, Physiological↗
PubMedDate not supplied

Ischemic cardiomyopathy.

The term "ischemic cardiomyopathy" was used initially to describe a clinical syndrome that was indistinguishable from primary congestive cardiomyopathy but due to severe, diffuse coronary artery disease. The term has been expanded to include the larger category of myocardial disease secondary to coronary artery disease. Using this expanded definition, we have discussed the varied clinical presentations of congestive ischemic cardiomyopathy and restrictive ischemic cardiomyopathy (stiff heart syndrome and right ventricular infarction), and how the effects of ischemia on left ventricular systolic and diastolic performance may cause these varied presentations. The prognosis of any ischemic cardiomyopathy is related primarily to the degree of ventricular dysfunction and the extent of coronary artery disease. Therapy is aimed at preventing or ameliorating myocardial ischemia and halting the progression of, or even reversing, the deterioration in myocardial function.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Cleft in the anterior and posterior leaflet of the mitral valve: a rare anomaly.

A rare entity that causes congenital mitral regurgitation is an isolated cleft mitral valve. The cleft in the mitral valve can be seen in either the anterior or posterior leaflet of the valve. We present a unique case of an individual with a history of congenital mitral regurgitation caused by a cleft in both the anterior and posterior leaflets of the mitral valve.

Adult↗