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M L Hess

Publications and source records attributed to M L Hess.

At least 127 records · Page 7Linked to original sources
PubMed1981

Left ventricular mass by M-mode echocardiography in cardiac transplant patients with acute rejection.

Serial determination of left ventricular mass, right ventricular and left atrial size, fractional shortening and left ventricular systolic time intervals were made from M-mode echocardiograms in 13 long-term survivors with cardiac allografts These measurements were correlated with presence or absence of acute rejection as determined by myocardial biopsy. Left ventricular mass increased significantly, from a baseline of 129.8 +/- 11.8 (mean +/- SEM) to 310.5 +/- 13.0 g during 12 episodes of rejection. In contrast during eight episodes without rejection, the left ventricular mass did not increase significantly (baseline 175.2 +/- 11.8 to 211.9 +/- 25.6 g). There was no relationship between changes in right ventricular and left atrial size, fractional shortening or systolic time intervals and presence or absence of rejection of myocardial biopsy. An increase in left ventricular mass by M-mode echocardiography offers a reliable noninvasive method for detection of acute rejection of a cardiac allograft.

Echocardiography↗
PubMed1981

Augmented venous return: a model of left ventricular afterload reduction during the course of endotoxin shock.

Utilizing a canine model of endotoxin shock (E coli, 4 mg/kg, B6:026) the major determinants of cardiac output (preload, afterload, contractility, and heart rate) were simultaneously followed for 5 hr in four study groups: Group I: time-matched controls, Group II: endotoxin shock, Group III: endotoxin shock and femoral-femoral A-V shunt, and Group IV: A-V shunt control. Groups II and III demonstrated an initial, abrupt increase in total peripheral resistance (TPR), coronary vascular resistance (CVR), and pulmonary vascular resistance (PVR), and a decrease in cardiac output (CO), coronary flow (CF) and heart rate (HR) and stroke work (P less than 0.05). Group II then demonstrated a decrease in TPR, CVR, PVR with an increase in CO and CF but systemic arterial pressure did not return to control values. At approximately 3 hr, Group II developed a progressive increase in TPR, CVR, and PVR, and a decrease in CO, CF, and SW. Heart rate did not change. In contrast, at 3 hr Group III demonstrated no significant increase in TPR, CVR, or PVR, a progressive increase of CO and CF, and preservation of SW. It is hypothesized that endotoxin shock is characterized by an initial phase characterized by an increase in resistance and decrease in flow that is not affected by an augmented venous return. However, in the intermediate and latter stages of shock, there is a progressive increase in resistance and decrease in flow, increasing impedance to left ventricular ejection that results in an imbalance between myocardial oxygen supply and demand, contributing to the observed myocardial failure. An augmented venous return, by decreasing resistance (afterload) and increasing venous return (preload) preserves cardiac output and myocardial function and thus serves as a model of left ventricular afterload reduction during the course of endotoxin shock.

Animals↗
PubMed1981

Hemodynamics, hypoglycemia, and hepato-pancreatic pathology during the course of endotoxin shock.

The interrelationships between hemodynamics and hypoglycemia during the course of endotoxin shock (ES) has not been fully defined. In the following study, ES (E. coli, 1 mg/kg; n = 7) was induced in a canine model and systemic hemodynamics, glucose metabolism, and hepatic and pancreatic function monitored for 5 hr and compared to time-matched controls (TMC, n = 7). Total peripheral resistance (TPR, dynes-sec-cm-5) increased from 3227 +/- 430 to 4050 +/- 750 at 30 min and then declined to 3050 +/- 1100 at 90 minutes. TPR progressively increased to 6225 +/- 749 by 5 hours. Plasma glucose did not significantly differ from control values (105 +/- 4 mg%) for the first 90 min but then declined to 68 +/- 6 mg% at 4.5 hours. (TMC = 103 +/- 17, P less than 0.05). Serum amylase during the 5 hr protocol was not elevated (TMC = 110.9 +/- 2.4; ES = 100 +/- 1.97%; P greater than 0.1), and light microscopy of the exocrine pancreas demonstrated normal acinar structure. Islet cell structure from the ES group is not significantly different from the TMC. Hepatic histology in the ES group demonstrated periportal and perilobular degranulation and hepatocyte disruption not seen in the TMC. It is hypothesized that ES results in a circle of positive feedback initiated by an increase in TPR and subsequent decrease in flow resulting in hepato-pancreatic ischemia. Ischemic damage is most apparent at the liver and leads to changes in hepatic metabolic activities which contribute to the developing hypoglycemia of the late phase of ES.

Animals↗
PubMed1980

Myocardial failure and excitation--contraction uncoupling in canine endotoxin shock: role of histamine and the sarcoplasmic reticulum.

Subendocardial and subepicardial sarcoplasmic reticulum (SR) were isolated from five groups of dogs following five hours of hemodynamic monitoring: Group 1, 6-8 mg/kg diphenhydramine (n = 5); Group 2, 0.5 mg/kg histamine phosphate, IV bolus; Group 3, 4.0 mg/kg Escherichia coli endotoxin (n = 5); Group 4, 6-8 mg/kg diphenhydramine, followed by 4.0 mg/kg E coli endotoxin (n = 5); and Group 5, time-matched, sham-operated controls (n = 5). The velocity of calcium uptake and ATP hydrolysis and the integrity of the transport system were determined (coupling ratio = mumoles Ca++/mumoles Pi). Control SR calcium-uptake velocities averaged 1.13 +/- 0.3 mumoles Ca++/mg-min, with no significant difference between the endocardium and epicardium. SR calcium uptake from the endotoxin shock group averaged 0.64 +/- 0.06 (endocardium) and 0.56 +/- 0.05 (epicardium) mumoles Ca++/mg-min (P < 0.01 from control).ATPase activity from the control group = 1.23 +/- 0.04 mumoles Pi/mg-min; and the endotoxin-shocked group exhibited an activity of 0.99 +/- 0.06, with no significant difference between the endocardial and epicardial populations (P > 0.1). Diphenhydramine-control SR calcium-uptake rates averaged 1.12 +/- 0.6 mumoles Ca++/mg-min, with no difference between endocardium and epicardium. Diphenhydramine pretreatment plus endotoxin-shock epicardial SR calcium uptake = 0.94 +/- 0.08 mumoles Ca++/mg-min, while the endocardial SR was significantly depressed at 0.72 +/- 0.04 mumoles Pi/mg-min, with no difference between endocardium and epicardium. Bolus histamine infusion resulted in a small but significant depression of both SR calcium-uptake rates (0.93 +/- 0.04 mumoles Ca++/mg-min) and ATPase activity (0.93 +/- 0.04 mumoles Pi/mg-min), with no significant difference between epicardium and endocardium. This study confirms that the calcium transport system of cardiac sarcoplasmic reticulum isolated from endotoxin-shocked animals is depressed. However, this depression is not due entirely to a depression of the Mg++-dependent, Ca++-stimulated ATPase enzyme, but is also associated with a significant uncoupling of ATP hydrolysis from calcium transport. The histamine blocker, diphenhydramine, was only able to protect the epicardial SR; the endocardial SR still exhibited an uncoupling of ATP hydrolysis from calcium transport. Bolus histamine infusion produced a small but significant depression of both calcium transport and ATP hydrolysis. These results are formulate d into a "proton-lysosome" hypothesis that appears to be able to explain excitation-contraction uncoupling in the endotoxin-shocked myocardium.

Animals↗
PubMed1980

Cardiogenic endotoxin shock: coronary flow and contractile protein dysfunction as determinants of depressed cardiac contractility.

Cardiogenic endotoxin shock (ES) refers to the intermediate and latter stages of ES characterized by a progressive myocardial dysfunction. This laboratory has been developing the hypothesis that a major etiology of this observed myocardial failure is a progressive state of global ischemia. In order to further test this hypothesis, ES (E coli, Difco Labs, 026:B6, 4 mg/kg) was induced in the canine model (n = 6) and coronary flow, myocardial contractility (dP/dtmax), and systemic hemodynamics were continuously monitored for five hours, following which the cardiac contractile proteins were isolated and characterized. In the ES group, control coronary flow (CF) = 90.5 +/- 3.6 ml/min/100 gm LV, coronary vascular resistance (CVR) = 61.82 X 10(3) +/- 2.28 X 10(3) dyne . sec. cm--5 and dP/dtmax 2,200 +/- 160 mm Hg/sec. Between four and five hours, CF decreased to 58.6 +/- 16 ml/min/100 gm LV, CVR increased to 128.6 X 10(3) +/- 18 X 10(3) dyne . sec. cm--5, and dP/dtmax decreased to 968 +/- 62 mm Hg/sec. Sham animals (n = 7) demonstrated no significant difference in CF, CVR, or dP/dtmax. Control myofibrillar ATPase activity demonstrated 50% activation (specific activity = 0.072 +/- 0.002 mumoles Pi/mg protein . min) at p Ca++ = 6.4, with no significant difference between endocardium and epicardium. ES myofibrils demonstrated 50% activation (specific activity = 0.060 +/- 0.002 mumoles Pi/mg protein . min endocardial, and 0.068 +/- 0.005 mumoles Pi/mg protein . min epicardial at pCa++ = 6.48 and 6.45, respectively, incriminating a change in affinity for Ca++ binding to the regulatory proteins. Thus, it would appear that the documented decrease in myocardial contractility is due in part to a depression of myofibrillar ATPase activity, which is related to a decrease in coronary flow, an increase in coronary vascular resistance, and a state of global myocardial ischemia.

Adenosine Triphosphatases↗
PubMed1980

Cardiac transplantation at the Medical College of Virginia.

The world's second largest experience in orthotopic cardiac transplantation has been achieved at the Medical College of Virginia, where significant progress has been made in the refinement of surgical technique, use of immunosuppression, and treatment of post-transplant complications. The procedure may now be regarded with cautious optimism, according to the authors, who document the MCV experience and describe the criteria for heart transplant candidates.

Graft Survival↗
PubMed1980

Cardiac transplantation--1980: The Medical College of Virginia program.

Within the last three years, advances in the fields of cardiac surgery and immunology have established the value of cardiac transplantation for patients with irreversible myopathic disease. Long-distance donor procurement has increased the availability of the donor pool and made possible a more critical selection of donor hearts. The development of antithymocyte globulin and the concept of individual immune monitoring has decreased the incidence of acute rejection and the dosage of prednisone and azathioprine necessary to achieve optimal graft protection. These advances are reflected in the survival statistics. Since 1977, the three-month mortality rate has decreased to 40%, as compared to 77% from 1968 to 1976. Ptatients who are discharged from the hospital are currently demonstrating an 88% one-year survival rate and are functional class I-II status. We conclude that in properly selected patients, cardiac transplantation is a viable option for end-stage cardiomyopathic disease.

Antilymphocyte Serum↗