Biomedical subjects

C M Dyke

Publications and source records attributed to C M Dyke.

24 records · Page 2Linked to original sources

PubMed1991

Arterial-ureteral fistula: case study with review of published reports.

Arterial-ureteral fistula, a rare cause of gross hematuria, may be associated with life-threatening hemorrhage if not rapidly diagnosed and treated. Recently, a patient at the Hunter H. McGuire Veterans Administration Medical Center developed an arterial-ureteral fistula at the site of the confluence of the external iliac artery and a superior mesenteric artery bypass graft. Review of the world's literature revealed 31 additional reported cases of arterial-ureteral fistulas. This current case is only the second one reported in which the diagnosis was made with arteriography. Several common features of arterial-ureteral fistulas were present in this case: a history of ureteral obstruction and urinary tract infections, upper urinary tract disease, and previous vascular surgery. The condition is usually associated with either prior upper urinary tract instrumentation or vascular surgery, and an antecedent period of intermittent hematuria, followed by life-threatening hematuria, is common. A high index of suspicion and early surgical intervention are required for successful management. The major surgical challenges are to establish unobstructed urinary drainage and restore vascular continuity. Exclusion of prosthetic material from potentially infected areas is mandatory.

Fistula↗

PubMed1991

Inotropic stimulation and oxygen consumption in a canine model of dilated cardiomyopathy.

Inotropic support for the dilated, failing ventricle results in complex hemodynamic changes affecting preload, afterload, contractility, and heart rate, each of which affects myocardial oxygen consumption. Appreciation of a hierarchy of hemodynamic determinants of myocardial oxygen consumption may be helpful to the clinician trying to balance oxygen demands and hemodynamic performance. We tested the hypothesis that epinephrine alters the hierarchy of hemodynamic determinants of myocardial oxygen consumption in a canine model of dilated cardiomyopathy created by rapid ventricular pacing. Dogs (n = 10) were instrumented to record left ventricular pressure and dimension, and a modified right heart bypass preparation was used to control left ventricular workload. Coronary sinus effluent was quantitatively collected and analyzed for oxygen content and used to calculate myocardial oxygen consumption. Epinephrine administration significantly increased myocardial oxygen consumption in the empty, beating heart; however, when the relationships of multiple determinants of left ventricular work and load were compared before and after epinephrine administration, no oxygen wasting effect was observed. Using multivariate linear regression analysis, a hierarchy of hemodynamic determinants of myocardial oxygen consumption was created. In the untreated heart, stroke work and cardiac output were the primary hemodynamic determinants of oxygen consumption; epinephrine significantly altered the determinants such that wall stress became the dominant hemodynamic determinant of myocardial oxygen consumption. Focused manipulation of wall stress in the treated, failing heart may limit the potentially deleterious effects of inotropic stimulation in this setting.

Adenine Nucleotides↗

PubMed1991

Triiodothyronine-enhanced left ventricular function after ischemic injury.

Hypothyroidism is associated with profound left ventricular dysfunction. Brain-dead organ donors and patients undergoing cardiopulmonary bypass are chemically hypothyroid with significantly reduced circulating free triiodothyronine (T3). To test the hypothesis that T3 enhances left ventricular function in a hormonally deficient environment, a total of 36 healthy New Zealand White rabbit hearts were studied using a modified Langendorff preparation with Krebs-Henseleit perfusate and intra-ventricular balloon. In 9 normal rabbit hearts a cumulative dose-response curve with logarithmically increasing doses of T3 was obtained. The vehicle solution for T3 dissolution served as control (n = 9). Left ventricular function was assessed from peak developed pressure at baseline and after T3 administration. Triiodothyronine had no effect in normal hearts on peak developed pressure or end-diastolic pressure. In 18 rabbits, the acute effect of T3 administration after ischemia was investigated. Preischemic left ventricular function was measured to serve as baseline, and hearts were subjected to 37 degrees C global ischemia. Triiodothyronine (n = 9) or vehicle (n = 9) was infused during reperfusion, and left ventricular peak developed pressure was measured at 30 and 60 minutes of reperfusion. Recovery of function (expressed as percent return of left ventricular peak developed pressure) was significantly improved within 15 minutes of reperfusion (65.0% +/- 2.1% versus 80.2% +/- 4.1%) and remained significantly improved throughout the reperfusion period (p less than 0.05 by analysis of variance). These data suggest that although T3 possesses no inotropic properties, it significantly improves postischemic left ventricular function. The rapidity of the functional improvement suggests that these effects may be due to plasma membrane-mediated mechanisms.

Animals↗

PubMed1991

Theoretical considerations in the use of dynamic cardiomyoplasty to treat dilated cardiomyopathy.

Clinical data describing the hemodynamic benefits of cardiomyoplasty are inconclusive, and there has not been any study detailing the mechanisms by which dynamic cardiomyoplasty may improve the functional and mechanical impairments of the failing heart. The left ventricle in dilated cardiomyopathy is characterized by increased end-diastolic volume, inadequate systolic myocardial wall thickening, increased wall stress, and decreased stroke volume. Based on experimental and preliminary clinical data, we propose that cardiac assistance by dynamic cardiomyoplasty is the consequence of enhanced volume translocation rather than increased potential for pressure generation. A small augmentation of dimensional shortening results in a large increment of stroke volume because of the enlarged resting chamber volume. Key geometric effects are enhanced systolic chamber shortening and increased wall thickening, resulting in a net decrease of myocardial wall stress. The contractile skeletal muscle may improve myocardial mechanics, and normalization of the afterload mismatch may be an important mechanism by which dynamic cardiomyoplasty augments cardiac output.

Assisted Circulation↗

PubMed1991

Effects of dynamic cardiomyoplasty on left ventricular performance and myocardial mechanics in dilated cardiomyopathy.

We tested the hypothesis that dynamic cardiomyoplasty produces beneficial changes in the functional mechanics of the dilated, failing left ventricle. Chronic dilated cardiomyopathy was induced in seven mongrel dogs by rapid ventricular pacing (260 beats/min) for 3 to 4 weeks. After completion of the induction period, dynamic cardiomyoplasty was performed with the left latissimus dorsi muscle, paced synchronously with the R waves of the electrocardiogram (Medtronic SP1005). Instruments included an aortic flow probe, a left ventricular Millar pressure catheter, and piezoelectric sonomicrometric crystals on the left ventricle for measurements of wall thickness and minor and major axis dimensions. Data were obtained with the stimulator off and on. Statistical comparisons were made with Student's t test for paired data. Dynamic cardiomyoplasty increased the cardiac output of the failing heart (966 +/- 124 versus 1166 +/- 112 ml/min; p less than 0.01). Systolic shortening of both minor and major axis dimensions increased (3.1 +/- 0.3 versus 4.7 +/- 0.3 mm, p less than 0.01, and 4.6 +/- 0.3 versus 7.3 +/- 0.9 mm, p less than 0.05, respectively). Left ventricular end-diastolic pressure decreased by 16% (18 +/- 1 versus 15 +/- 1 mm Hg, p less than 0.01). Although skeletal muscle contraction increased the pressure development in the left ventricular chamber, mean systolic wall stress was diminished by concomitant changes in left ventricular dimensions (116,144 +/- 11,530 versus 101,268 +/- 7464 dynes/cm2, p less than 0.05). At end-systole, wall thickness increased (11.8 +/- 1.1 versus 12.7 +/- 1.1 mm, p less than 0.01), minor axis dimension decreased (51.3 +/- 1.4 versus 49.2 +/- 1.8 mm, p less than 0.01), and major axis dimension also decreased (85.6 +/- 3.3 versus 79.0 +/- 2.3 mm, p less than 0.05). Our detailed evaluation of left ventricular chamber mechanics suggests that dynamic cardiomyoplasty may have a role in ameliorating the functional and mechanical derangements associated with progression of dilated cardiomyopathy both by augmenting cardiac performance and by diminishing determinants of myocardial oxygen consumption. (All values are expressed as mean +/- standard error of the mean.)

Animals↗

PubMed1987

Preload dependence of right ventricular blood flow: I. The normal right ventricle.

Right ventricular (RV) failure is commonly treated with intravascular volume expansion to increase the RV-left atrial pressure gradient and improve left-sided filling. As RV pressure rises, chamber distention occurs and wall tension increases. These studies were designed to determine if increased wall tension might impede RV myocardial blood flow in the normal canine right ventricle and thus contribute to RV failure. Hemodynamic data, the septal-RV free wall dimension, and RV myocardial blood flow were obtained at low and high levels of preload and in both the autoregulated and vasodilated (adenosine, 2 mg per kilogram of body weight per minute) states. Elevated filling pressure decreased RV myocardial blood flow in both the autoregulated (0.85 +/- 0.18 to 0.67 +/- 0.15 ml/min/gm; p less than .05) and vasodilated (2.25 +/- 0.50 to 0.85 +/- 0.25 ml/min/gm; p less than .05) states but did not change the transmural distribution of blood flow to the right ventricle. Vasodilator reserve was markedly impaired in the high-preload state. These observations suggest that preload is an important determinant of RV myocardial blood flow. Volume loading to treat RV dysfunction may be limited by impairment of RV myocardial blood flow.

Animals↗