Biomedical subjects

J R Stratton

Publications and source records attributed to J R Stratton.

At least 73 records · Page 4Linked to original sources

PubMed1988

Postinfarction left ventricular pseudoaneurysm: echocardiographic diagnosis and prolonged survival in three patients.

Both echocardiography and radionuclide angiography have been proposed as noninvasive modalities for the diagnosis of left ventricular pseudoaneurysm. In the only three cases seen at our institution over the past five years, this diagnosis was missed with radionuclide blood pool imaging, while two-dimensional echocardiography demonstrated the typical features of a pseudoaneurysm. Our patients were asymptomatic and diagnosis was made incidentally 4 to 6 years after myocardial infarction. Although the patients survived an extended period without surgery, the reported incidence of rupture is high, and prophylactic surgical repair probably is indicated. It is likely that the increased use of noninvasive cardiac imaging techniques will lead to the detection of other cases of unsuspected left ventricular pseudoaneurysm. Two-dimensional echocardiography appears superior to planar radionuclide ventriculography in establishing the diagnosis.

Aged↗

PubMed1988

Relation of global and regional left ventricular function to tomographic thallium-201 myocardial perfusion in patients with prior myocardial infarction.

To determine the relation between regional myocardial perfusion and regional wall motion in humans, tomographic thallium-201 imaging and two-dimensional echocardiography at rest were performed on the same day in 83 patients 4 to 12 weeks after myocardial infarction. Myocardial perfusion and wall motion were assessed independently in five left ventricular regions (total 415 regions). Regional myocardial perfusion was quantitated as a percent of the region infarcted (range 0 to 100%) using a previously validated method. Wall motion was graded on a four point scale as 1 = normal (n = 266 regions), 2 = hypokinesia (n = 64), 3 = akinesia (n = 70), 4 = dyskinesia (n = 13) or not evaluable (n = 2). Regional wall motion correlated directly with the severity of the perfusion deficit (r = 0.68, p less than 0.0001). Among normally contracting regions, the mean perfusion defect score was only 2 +/- 4. Increasingly severe wall motion abnormalities were associated with larger perfusion defect scores (hypokinesia = 6 +/- 5, akinesia = 11 +/- 7 and dyskinesia = 18 +/- 5, all p less than 0.01 versus normal. Among regions with normal wall motion, only 3% had a perfusion defect score greater than or equal to 10. Conversely, among 68 regions with a large (greater than or equal to 10) perfusion defect, only 13% had normal motion whereas 87% had abnormal wall motion. The relation between perfusion and wall motion noted for the entire cohort was also present in subgroups of patients with anterior or inferior infarction. In patients with prior myocardial infarction, the severity of the tomographic thallium perfusion defect correlates directly with echocardiographically defined wall motion abnormalities, both globally and regionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

PubMed1988

Fate of left ventricular thrombi in patients with remote myocardial infarction or idiopathic cardiomyopathy.

Although left ventricular thrombi that form acutely after myocardial infarction frequently resolve spontaneously or with anticoagulant therapy, the fate of left ventricular thrombi in patients with remote myocardial infarction or with idiopathic cardiomyopathy remains unknown. To determine the natural history of such chronic left ventricular thrombi, we performed serial echocardiograms on 51 patients with remote myocardial infarction (greater than or equal to 3 months; mean, 31 +/- 41 months) and on nine patients with idiopathic dilated cardiomyopathy. Mean follow-up was 24 +/- 22 months during which 3.5 +/- 1.4 echocardiograms were obtained. Studies were interpreted by blinded observers, and an increase or decrease of more than 5 mm in maximal thrombus thickness was defined as significant. Among all 60 patients left ventricular thrombi were unchanged in 24 (40%), completely resolved in 24 (40%), decreased in size in four (7%), increased in size in five (8%), and decreased and then increased in size in three (5%). Results in patients with remote infarction and idiopathic cardiomyopathy were similar. Warfarin therapy, which was at the discretion of the primary physician, was associated with a higher prevalence of thrombus resolution compared with no therapy (59% vs. 29%, p = 0.02). Definite systemic emboli occurred in seven patients (12%), all at times while they were not anticoagulated. Among the 48 thrombi that were present on two or more echocardiograms, changes in thrombus shape (classified as protruding or flat) occurred in only 16%, and changes in thrombus movement (classified as mobile or immobile) occurred in only 10%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Increased embolic risk in patients with left ventricular thrombi.

Although left ventricular thrombi are associated with an increased embolic risk in the first few weeks after acute myocardial infarction, the long-term risk remains undefined. To ascertain the incidence of strictly defined systemic emboli, we followed 85 patients with echocardiographically documented left ventricular thrombi. At the time of the entry echocardiogram, most patients (n = 57) had remote myocardial infarction, while 19 had recent (less than 1 month) infarction, and nine had idiopathic cardiomyopathy. Because of the difficulty in classifying events as embolic in patients with advanced atherosclerosis, a matched control group of 91 patients without thrombi was also studied. The thrombus and control groups were similar with regard to recent myocardial infarction, remote infarction, anterior infarction, ejection fraction, atrial fibrillation, echocardiographic referral for source of emboli, and warfarin therapy. During a mean follow-up of 22 months after echocardiography, embolic events occurred in 13% (11 of 85) of patients with thrombi compared with 2% (two of 91) control patients (p less than .01). The actuarial probability of being embolus free at 2 years after echocardiography was 86% in patients with thrombi compared with 97% in control patients (p less than .01). All embolic events occurred greater than 1 month after myocardial infarction (range 1 to 96 months). The only clinical or echocardiographic features predictive of embolization were protrusion and mobility of thrombus (both p less than .02). We conclude that the incidence of embolic events is definitely increased in patients with left ventricular thrombi compared with control subjects during long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiography↗

PubMed1987

The hemodynamic effects of sympathetic stimulation combined with parasympathetic blockade in man.

To define the effects of circulating norepinephrine and epinephrine on cardiac function and to determine whether left ventricular function is influenced by parasympathetic mechanisms during catecholamine stimulation, hemodynamic changes were investigated in healthy young human subjects who were supine and awake during infusion of intravenous norepinephrine alone (125 ng/kg/min) (n = 6), norepinephrine (125 ng/kg/min) plus epinephrine (50 ng/kg/min) (n = 6), and norepinephrine plus epinephrine plus parasympathetic blockade induced by atropine (2 mg intravenously) (n = 5). Ejection fraction and changes in cardiac volumes were measured by radionuclide ventriculography. During the infusion of norepinephrine plus epinephrine, plasma norepinephrine increased from 358 +/- 35 to 1782 +/- 123 pg/ml (mean +/- SE) and plasma epinephrine increased from 31 +/- 5 to 355 +/- 90 pg/ml (both p less than .01 vs baseline). These increases in plasma catecholamines were associated with increases in the heart rate (58 +/- 3 to 67 +/- 2 beats/min, p = NS), systolic blood pressure (113 +/- 3 to 140 +/- 6 mm Hg, p less than .01), ejection fraction (0.64 +/- 0.02 to 0.72 +/- 0.02 ejection fraction units, p less than .01), stroke volume (+41 +/- 5%, p less than .01), and cardiac output (+54 +/- 8%, p less than .01), and a decrease in systemic vascular resistance (-31 +/- 3%, p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Mechanisms of thrombocytopenia in chronic autoimmune thrombocytopenic purpura. Evidence of both impaired platelet production and increased platelet clearance.

Mechanisms of thrombocytopenia were studied in 38 patients with mild to moderately severe chronic autoimmune thrombocytopenia (AITP). 51Cr and 111In-labeled autologous platelet turnover studies and in vitro analysis of committed megakaryocyte progenitors (CFU-Meg) were used as independent measures of platelet production. Autologous 111In-labeled platelet localization studies were performed to assess platelet clearance. Although there was no increase in the frequency of marrow CFU-Meg, a specific increase in the CFU-Meg [3H]TdR suicide rate was seen which was inversely correlated with the platelet count (P less than 0.001). Platelet turnover studies showed significant numbers of patients had inappropriate thrombopoietic responses to their reduced platelet counts. Platelet-associated antibody levels correlated inversely with platelet turnover suggesting that antiplatelet antibody impairs platelet production. The circulating platelet count was best predicted by an index relating platelet production (i.e., turnover) to the spleen-liver platelet clearance that correlated directly with platelet survival (P less than 0.001). In summary, both depressed platelet production and increased platelet clearance by the liver and spleen contribute to the thrombocytopenia of AITP.

Autoantibodies↗

PubMed1986

Effect of suloctidil on tomographically quantitated platelet accumulation in Dacron aortic grafts.

Platelet deposition contributes to the thrombotic and embolic complications of prosthetic materials in man. To determine if the investigational platelet inhibitory drug suloctidil (200 mg 3 times daily) reduces platelet deposition on Dacron aortic grafts, a randomized, double-blind, crossover trial was conducted in 12 men with grafts that had been in place more than 9 months. Platelet deposition in the graft was assessed by quantitative analysis of planar images obtained at 24, 48 and 72 hours after injection of indium-111-labeled platelets. Also, a tomographic method of imaging and quantitating labeled platelet deposition in the graft was developed. Tomographic imaging was performed at 24 and 72 hours after platelet injection and was quantitated by a graft/blood ratio that compared indium-111 platelet activity in summed 1.8-cm-thick transaxial tomographic slices of the aortic graft to indium-111 platelet activity in well-counted whole blood. Compared with placebo, suloctidil failed to decrease the tomographic graft/blood ratio at 24 hours (6.2 +/- 1.3 vs 5.7 +/- 0.8) and 72 hours (11.4 +/- 2.9 vs 10.7 +/- 2.2). Similarly, the graft/blood ratio determined by planar imaging was not different between placebo and suloctidil therapy at 24 hours (1.7 +/- 0.3 vs 1.6 +/- 0.2), 48 hours (2.2 +/- 0.4 vs 2.4 +/- 0.4) or 72 hours (2.6 +/- 0.5 vs 2.8 +/- 0.5) after labeled platelet injection. Thus, suloctidil does not significantly reduce platelet deposition on chronically implanted Dacron grafts in humans.

Adult↗

PubMed1986

Reduction of indium-111 platelet deposition on Dacron vascular grafts in humans by aspirin plus dipyridamole.

Aspirin plus dipyridamole reduces platelet accumulation on short-term Dacron vascular grafts in man. To determine whether drug inhibition of platelet deposition is sustained on older grafts, we studied 18 men aged 41 to 87 years who had Dacron aortic bifurcation grafts in place a mean of 43.4 months (range 9.8 to 121.0) before and during short-term therapy with aspirin (325 mg tid) plus dipyridamole (75 mg tid). During both the baseline and drug studies, indium-111 (111In) platelet deposition was quantitated by two techniques, standard planar imaging performed at 24, 48, and 72 hr after injection of platelets and single photon emission computed tomographic imaging performed at 24 and 72 hr after injection. All analyses were performed in a blinded fashion. On both the planar and tomographic images, platelet accumulation on the graft was quantitated by a graft/blood ratio that compared activity in the graft to simultaneously collected whole blood 111In platelet activity. Aspirin plus dipyridamole reduced the tomographic graft/blood ratio at 24 hr (20.6 +/- 3.5 vs 17.3 +/- 2.5) (+/-SEM) and at 72 hr (29.0 +/- 4.8 vs 25.0 +/- 4.1) after injection of platelets (p = .02). Dacron vascular grafts. Similarly, the planar graft/blood ratio was reduced at 24 hr (2.7 +/- 0.5 vs 2.4 +/- 0.5), 48 hr (3.7 +/- 0.9 vs 3.1 +/- 0.7), and 72 hr (4.0 +/- 0.9 vs 3.6 +/- 0.8) (p = .04). We conclude that aspirin (325 mg tid) plus dipyridamole (75 mg tid) reduces platelet accumulation on long-term Dacron vascular grafts.

Adult↗

PubMed1985

Effect of a benzodiazepine (alprazolam) on plasma epinephrine and norepinephrine levels during exercise stress.

To determine whether a benzodiazepine central nervous system depressant, alprazolam, inhibits sympathetic discharge during exercise stress, 11 healthy men, aged 21 to 35 years, performed symptom-limited treadmill tests before and on the third day of drug therapy (0.5 mg 3 times daily). Plasma epinephrine and norepinephrine levels were measured at rest and at 8 minutes, 11 minutes and maximal exercise. Owing to catheter malfunction during vigorous exercise, paired samples could be obtained from only 8 subjects at 8 minutes and from only 4 subjects at 11 minutes of exercise. During drug treatment, the plasma epinephrine level was lower at rest (30 +/- 4 vs 53 +/- 7 pg/ml, p less than 0.01), and at 8 minutes (60 +/- 13 vs 117 +/- 19 pg/ml, p less than 0.01), 11 minutes (120 +/- 39 vs 193 +/- 52 pg/ml, p less than 0.05), and maximal exercise (520 +/- 125 vs 970 +/- 324 pg/ml, p = 0.13). Plasma norepinephrine was unchanged at rest (452 +/- 57 vs 413 +/- 45 pg/ml) but lower at 8 minutes (730 +/- 75 vs 886 +/- 82 pg/ml, p less than 0.01), 11 minutes (1,077 +/- 197 vs 1,447 +/- 301 pg/ml, p less than 0.05) and at maximal exercise (3,453 +/- 487 vs 5,590 +/- 1,100 pg/ml, p = 0.09). Exercise duration (17 +/- 1 and 17 +/- 1 minutes) was unchanged on drug. Thus, alprazolam reduces the plasma catecholamine response to exercise stress, possibly by inhibiting centrally mediated sympathetic discharge. Blunting of sympathetic activation may be beneficial in cardiac disorders in which increased sympathetic tone is potentially deleterious.

Adult↗

PubMed1985

Left ventricular volume determination using single-photon emission computed tomography.

A new method for measuring left ventricular (LV) volume based on gated single-photon emission computed tomography (SPECT) is described. Preliminary phantom studies showed an excellent correlation between SPECT and observed volumes (r = 0.99, standard error of the estimate [SEE] = 4.9 ml). SPECT was performed 24 hours after biplane contrast LV angiography in 36 patients. Transaxial blood pool tomograms were reconstructed by filtered back projection and reoriented to views orthogonal to the cardiac axes. Volume was calculated from serial short-axis tomograms by determining the base, apex and lateral borders of the LV blood pool, ascertaining the number of pixels in this volume and multiplying by the known volume of a pixel. Gated SPECT volumes were compared with contrast angiographic volumes. At end-systole, r = 0.96 and SEE = 12 ml; at end-diastole, r = 0.81 and SEE = 27 ml. For ejection fraction, r = 0.85 and SEE = 0.06. To test interobserver variation in processing, count data from 5 patients were processed twice (r = 0.98, SEE = 8.3 ml). There is an excellent correlation between SPECT and contrast angiographic volumes at end-systole; at end-diastole the relation is good. SPECT requires no arbitrary background correction, allows systematic isolation of the left ventricle from other overlapping cardiac chambers and requires no geometric assumptions for volume determination. It has promise as a direct method for measuring LV volume in a minimally invasive manner.

Adult↗

PubMed1985

The effect of sulfinpyrazone on platelet deposition on Dacron vascular grafts in man.

To determine if sulfinpyrazone inhibits platelet deposition on chronically implanted (greater than 9 months) Dacron aortic bifurcation grafts in man, we performed indium-111 platelet imaging over 24 to 96 hours after labeled platelet injection in 10 males with grafts before and during sulfinpyrazone therapy (200 mg four times daily). Platelet accumulation was quantitated by a graft/blood ratio that compared indium-111 platelet image activity in the graft to platelet activity in well-counted whole blood. In addition, independent visual analysis compared platelet accumulation in the graft area to adjacent native arteries. By quantitative evaluation, sulfinpyrazone did not decrease the graft/blood ratio compared to baseline at 24 hours (3.2 +/- 0.4 vs 3.3 +/- 0.5, mean +/- SEM), 48 hours (4.6 +/- 0.6 vs 4.6 +/- 0.9) , 72 hours (6.8 +/- 0.8 vs 6.7 +/- 1.3), or 96 hours (9.7 +/- 1.6 vs 9.7 +/- 1.6) after labeled platelet injection. Visual interpretation also revealed no decrease in deposition in any patient during sulfinpyrazone therapy. We conclude that sulfinpyrazone does not inhibit platelet deposition on chronically implanted Dacron arterial graft surfaces in man. The techniques described provide a useful method of evaluating antithrombotic drug effects in patients with intravascular prosthetic materials.

Aged↗

PubMed1985

Late effects of intracoronary streptokinase on regional wall motion, ventricular aneurysm and left ventricular thrombus in myocardial infarction: results from the Western Washington Randomized Trial.

To determine whether intracoronary streptokinase improves late regional wall motion or reduces left ventricular aneurysm or thrombus formation in patients with acute myocardial infarction, two-dimensional echocardiography was performed at 8 +/- 3 weeks after infarction in 83 patients randomized to streptokinase (n = 45) or standard therapy (n = 38) in the Western Washington Intracoronary Streptokinase Trial. Among the patients treated with streptokinase, the average time to treatment was 4.7 +/- 2.5 hours after the onset of chest pain, and 67% had successful reperfusion. Regional wall motion was assessed in nine left ventricular segments on a scale of 1 to 4 (normal, hypokinetic, akinetic and dyskinetic). Left ventricular thrombus formation was interpreted as positive, equivocal or negative. All patients received anticoagulant therapy in the hospital and 52 received such therapy after hospital discharge. The mean (+/- SD) global (1.5 +/- 0.4 in both groups) and regional wall motion scores in the streptokinase-treated and control groups were not significantly different. The prevalence of aneurysm was 16% in both groups. Left ventricular thrombus was identified in only five patients (positive identification in four, and equivocal in one), all in the streptokinase-treated group (p = NS). There were also no differences between streptokinase and control treatment in any of the echocardiographic variables in subgroups of patients with anterior infarction, inferior infarction, no prior infarction or reperfusion with streptokinase. It is concluded that intracoronary streptokinase given relatively late in the course of acute myocardial infarction does not result in improved global or regional wall motion or a reduction in left ventricular thrombus or aneurysm formation in survivors studied 2 months after myocardial infarction.

Aged↗

PubMed1985

Hemodynamic effects of epinephrine: concentration-effect study in humans.

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

Adult↗

PubMed1984

The effects of antithrombotic drugs in patients with left ventricular thrombi: assessment with indium-111 platelet imaging and two-dimensional echocardiography.

Patients with left ventricular thrombi not caused by recent myocardial infarction were prospectively studied by indium-111 platelet imaging and two-dimensional echocardiography to determine the reproducibility of these techniques and the short-term effects of sulfinpyrazone (200 mg four times daily), aspirin (325 mg three times daily) plus dipyridamole (75 mg three times daily), and full-dose warfarin. At baseline, all patients underwent indium-111 platelet imaging and echocardiography, and the results were positive for thrombus. In six patients on no antithrombotic drug therapy, repeat platelet scans and echocardiographic studies at 6.0 +/- 3.3 weeks remained positive and were unchanged. In seven patients studied on sulfinpyrazone, three platelet scans became negative, two became equivocal, and two were unchanged; the presence and size of thrombus was constant by echocardiography in all seven patients. Of the six patients studied on aspirin plus dipyridamole, one platelet scan became negative, those of three became equivocal, and two were unchanged; all echocardiographic findings remained positive, but one patient had decreased thrombus size. Among four warfarin-treated patients, three had resolution of platelet deposition and one was unchanged; by echocardiography, thrombus resolved in one patient, was decreased in size in one, and was unchanged in two. We conclude that, in the absence of antithrombotic drug therapy, platelet imaging and echocardiographic findings are stable in patients with left ventricular thrombi not caused by recent myocardial infarction. Sulfinpyrazone, aspirin plus dipyridamole, and warfarin all interrupt platelet deposition in some patients with chronic left ventricular thrombi.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Failure of ticlopidine to inhibit deposition of indium-111-labeled platelets on Dacron prosthetic surfaces in humans.

In a randomized double-blind trial we sought to determine whether short-term therapy with ticlopidine (250 mg bid for 14 days) inhibited platelet deposition on Dacron aortic bifurcation grafts that had been in place a year or longer. A total of 10 men, 42 to 69 years old, underwent indium-111 platelet imaging during both placebo and drug phases of the trial at 24, 48, and 72 hr after the injection of labeled platelets. Platelet accumulation was quantitated by a graft/blood ratio that compared background-corrected activity of indium-111-labeled platelets in the graft with whole-blood activity of indium-111-labeled platelets. Additionally, blinded qualitative visual analysis of the unprocessed images was used to compare graft area activity with activity in adjacent native arteries. Ticlopidine significantly prolonged the template bleeding time from 5.3 +/- 0.5 to 17.1 +/- 3.1 min (+/- SEM) (p = .003). However, by quantitative analysis there was no significant reduction in platelet deposition in the graft during ticlopidine therapy compared with placebo at 24 hr (graft/blood ratio 2.3 +/- 0.4 vs 2.6 +/- 0.3), 48 hr (3.1 +/- 0.5 vs 3.2 +/- 0.4), or 72 hr (3.9 +/- 0.7 vs 4.0 +/- 0.6) after injection of labeled platelets. By visual analysis, nine patients had positive results for abnormal platelet deposition when on placebo that were unchanged when on ticlopidine. The tenth patient had an equivocal result for abnormal platelet deposition when on placebo and a negative result for abnormal platelet deposition when on ticlopidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Quantitation of size of relative myocardial perfusion defect by single-photon emission computed tomography.

The purpose of this study was to validate a semiautomatic method for quantitating the size of relative myocardial perfusion defects from single-photon emission computed tomographic (SPECT) images. We compared the size of the image defect in vivo, expressed as percent of involved left ventricle, as determined by this method with the anatomic size of the defect in vitro in 19 dogs. To test the method under optimal conditions, we first labeled the left ventricular myocardium in nine dogs by left atrial injection of 99mTc-labeled macroaggregated albumin particles after acute occlusion of one coronary artery. The "defect volume" was defined as the volume of the left ventricular myocardium for which counts fell 2 or more SDs below the distribution of counts in the myocardium supplied by a normal coronary artery in a series of animals. The relative in vivo defect volume by SPECT occupied 26.46 +/- 12.7% of the left ventricular volume (mean +/- SD), compared with a relative defect size in vitro of 33.3 +/- 13.7% (p = NS) of left ventricular volume as determined by well counting of myocardial samples. There was a close correlation between the two measurements (r = .92). However, myocardial relative defect volumes involving less than 5% of myocardium were not identified by SPECT. The defect volume weighted for the relative reduction in flow within the defect zone or the relative "reduced perfusion volume" was also determined. The correlation between the estimates by SPECT and those made in vitro for relative reduced perfusion volume was also high (r = .94).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1984

Plasma catecholamines and hemodynamic responses to stress states in man.

The relationship between the plasma catecholamine and hemodynamic responses to stress in man was studied using radionuclide left ventricular angiography to assess changes in cardiac volumes. In 10 healthy men, the maximum plasma norepinephrine (NE) and epinephrine (EPI) responses to symptom-limited supine bicycle exercise were considerably greater than the responses to isometric handgrip exercise or to a cold pressor test. Similarly, increases in heart rate, systolic blood pressure, stroke volume, ejection fraction, and cardiac output were greatest with bicycle exercise. Both the plasma catecholamine and hemodynamic responses to handgrip exercise tended to be intermediate, and the smallest responses were observed during cold pressure testing. The plasma NE and EPI responses to symptom-limited upright treadmill exercise in another group of 10 men were greater than the responses to supine bicycle exercise. During bicycle exercise and during handgrip exercise there were significant correlations between plasma NE and EPI levels and changes of heart rate, blood pressure, and cardiac output. In addition, when data from all three stresses were combined and effects of heart rate and subject differences were controlled for, plasma NE and EPI levels were significantly correlated with ejection fraction. These findings suggest that release of EPI and NE during stress states may contribute to some of the hemodynamic responses that occur during stress.

Adult↗

PubMed1983

Platelet adenine nucleotide levels in patients with Dacron vascular prostheses.

Platelets adenine nucleotide levels were determined in 11 patients with Dacron bifemoral aortic prostheses using high performance liquid chromatography. Total platelet and dense granule adenine nucleotide levels were measured in neutralized perchloric acid extracts prepared from gel-filtered platelet suspensions and from platelet supernatants following thrombin-induced release of granule constituents respectively. Dense granule adenine nucleotide levels were significantly decreased in the patient group compared with age and sex-matched controls (p less than 0.01), whereas no differences in cytoplasmic adenine nucleotide levels were observed (p greater than 0.2). Platelet survival measurements were made on 3 patients; when grouped with control subjects, a positive correlation was observed between platelet survival and platelet dense granule ADP (r = 0.96; p less than 0.01). These results suggest that platelet dense granule adenine nucleotide content may be a clinically significant indicator of vascular graft thrombogenesis.

Adenine Nucleotides↗