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Biomedical subjects

D F Larson

Publications and source records attributed to D F Larson.

50 records · Page 3Linked to original sources
PubMed1982

Concurrent left and right ventricular hypertrophy in dog models of right ventricular overload.

In two pressure and volume overload models of canine right ventricular hypertrophy, we have demonstrated significant hypertrophy of both the left and the right ventricles. The extent of hypertrophy was correlated positively to the extent of the increase in plasma epinephrine in both volume and pressure overload models. Attenuation or ablation of plasma epinephrine through the administration of propranolol, a beta-adrenergic blocker, or by denervation of the adrenal medulla prevented the hypertrophy process. No hemodynamic parameter was altered consistently in a parallel manner to hypertrophy. This is the first report of concurrent right and left ventricular hypertrophy in response to pressure or volume overload of the right ventricle. These studies further implicate epinephrine as a major trophic hormone of the heart.

Animals↗
PubMed1981

Comparison of two closed systems for thermodilution cardiac outputs.

The authors used an in vitro flow system to evaluate the sources of error in a previously described closed system thermodilution method for cardiac output determinations. Cardiac outputs were overestimated by as much as 49% because the injectate warmed as it was drawn through the connecting tubing. Submerging the tubing in the ice bath prevented this problem. The authors also evaluated a new closed system thermodilution cardiac output method. The method employed a bypass line and a spring loaded autosyringe which enables the user to flush the system with cold fluid, thereby ensuring accurate injectate temperatures. Cardiac output determinations with this method were as accurate as those obtained with a CO2 powered injector. Additionally, this method is easy to use, accommodates injection volumes of 1-10 ml, and is inexpensive.

Cardiac Output↗
PubMed1980

Platelet loss during experimental cardiopulmonary bypass and its prevention with prostacyclin.

Prostacyclin (PGI2), a newly discovered short-acting prostaglandin that inhibits platelet aggregation, was evaluated as an agent for prevention of cardiopulmonary bypass-induced thrombocytopenia. Ten adult, splenectomized greyhounds were divided into three treatment groups prior to beginning 120 minutes of partial cardiopulmonary bypass. Group 1 animals received 300 units of heparin per kilogram of body weight, Group 2 animals received 300 units of heparin per kilogram plus PGI2, 1.5 micrograms per minute, and Group 3 animals received 300 units of heparin per kilogram plus PGI2 3.0 micrograms per minute. Bypass and PGI2 infusion were started simultaneously. Mean platelet counts of each group at 5 minutes were approximately 40% of prebypass levels. Additional platelet loss was seen in Groups 1 and 2 at 30, 60, and 120 minutes. However in Group 3, platelet counts at 30 and 60 minutes were essentially unchanged from prebypass levels. At 30, 60, and 120 minutes of cardiopulmonary bypass, the differences between Groups 1 and 3, and 2 and 3 are highly significant (p less than 0.01). We conclude that PGI2 is an effective agent for preserving platelet levels during experimental cardiopulmonary bypass. Furthermore, it is possible that platelet loss during cardiopulmonary bypass may be caused, in part, by an imbalance between PGI2 and thromboxane A2, which results in excessive platelet adhesion and aggregation.

Animals↗
PubMed1979

Unusual complication of the Hancock porcine heterograft: strut compression in the aortic root.

A 65-year-old man underwent aortic valve replacement and triple coronary artery bypass grafting which were followed by gradual late postoperative thrombosis of his 25 mm. Hancock porcine aortic heterograft. At reoperation, the valve struts were noted to be angled centrally into the aortic lumen and dense thrombus completely filled all three sinuses. After valve removal and extensive debridement of the aortic anulus, including relaxing incisions, a diameter of only 23 mm. was obtained. A 23 mm. Björk-Shiley aortic prosthesis was inserted and the patient's recovery was uneventful. This previously unreported complication resulted from the insertion of a too-large Hancock porcine heterograft into a relatively small aortic root, resulting in circumferential strut compression, impedance of central flow, and subsequent valve thrombosis.

Aged↗
PubMed1977

Hemolysis due to chemical contamination of clinical perfusion apparatus.

A chemical contaminant found on the interior surface of the extracorporeal apparatus manufactured by the William Harvey Corporation was believed to have caused severe hematuria in 2 children. The biological activity of the contaminant was tested by mixing 50 ml of whole blood in contaminated cardiotomies; after 5 minutes of exposure lysis of one-sixth of the red blood cells was found. This hemolytic agent was concluded to be bisphenol A dissolved in an organic solvent, but the mechanism of contamination was never found.

Benzhydryl Compounds↗
PubMedDate not supplied

Validation of conductance catheter system for quantification of murine pressure-volume loops.

The purpose of this study was to define the validation methods and outcomes of a conductance catheter system specifically for in vivo murine cardiac hemodynamic analysis. To express the relationship between conductance and blood volumes, we used an in vitro model to derive a volume-conductance line. The volume-conductance line was used to compute raw volume from the modified conductance signals. The parallel volume was calibrated with hypertonic (15%) saline injected from extrajugular vein. The ventricular volume was computed by raw volume minus parallel volume. The accuracy of conductance volumetric measurements was validated with a static in situ infusion of calibrated volumes of whole blood injected into arrested left ventricles. In vivo dynamic measurements were performed with 24 C57B1/6 mice, 6 months old; for comparison of established values. The in situ model showed that after calibration, the experimental coefficient, alpha, was equal to 1 and the measured volume by conductance catheter was equal to the true volume of the left ventricle (y = 0.982x + 0.513, p < .0001). For the in vivo models, the end-diastolic volumes and the stroke volumes and cardiac output determined with the conductance catheter system were 17.3 +/- 1.0 microL, 10.6 +/- 0.9 microL, and 6.0 +/- 0.5 mL/min, respectively. We validated the relationship between measured volume by conductance catheter and the true volume and demonstrated the accuracy of the volume-conductance line for conversion of conductance to volume.

Animals↗
PubMedDate not supplied

Low-pressure perfusion results in effective microvascular perfusion of isolated rabbit hearts during hypothermic preservation for twenty-four hours.

Hypothermic, low-pressure coronary artery perfusion with oxygenated electrolyte solutions containing oncotic agents has resulted in successful orthotopic transplantation of hearts after extended preservation periods. Coronary flow may not, however, be consistently maintained during preservation. Previous research has demonstrated that coronary flow during preservation is related to contractile function after preservation. Specific mechanisms leading to reduced coronary flow during preservation remain undefined. This study was designed to determine whether low-pressure perfusion is a mechanism for decreased coronary flow and decreased microvascular perfusion during preservation. With India ink used as a marker of flow, microvascular perfusion was measured in rabbit hearts immediately after isolation (controls) or after 24 hours of hypothermic perfusion at 13 mm Hg (preserved hearts). There were no differences in the percentage of perfused microvessels in the control hearts perfused at either 13 or 80 mm Hg (94% +/- 2% and 99% +/- 1%, respectively). Nor was there a difference in the percentage of perfused microvessels in hearts perfused at either 13 or 80 mm Hg after 24 hours of hypothermic, low-pressure perfused preservation (67% +/- 9% and 74% +/- 6%, respectively). There was a significant difference, however, between the percentage of perfused microvessels in control hearts and in hearts preserved for 24 hours. These differences were independent of the pressure at which the India ink solution was administered. A perfusion pressure of 13 mm Hg is as effective as is 80 mm Hg in providing perfusion of the coronary microvascular beds during long-term hypothermic perfused preservation.

Analysis of Variance↗
PubMedDate not supplied

Recovery of heart function following 24 hours preservation and ectopic transplantation.

We examined the capacity of hearts injured during 24 hours of preservation to recover function over 96 hours when placed in an ectopic transplant configuration. Standard Langendorff techniques employing an intraventricular balloon and fixed perfusion pressure of 80 mm Hg were used to measure parameters of myocardial function, including maximal systolic pressure, left ventricular end diastolic pressure, and left ventricular balloon volume. Hearts preserved for 24 hours and held ischemic for 1 hour at room temperature exhibited significantly depressed contractility (maximal systolic pressure decreased by 26%) and diastolic compliance (left ventricular balloon volume decreased by 61%). During 96 hours in the ectopic transplant configuration, 24-hour preserved hearts recovered 52% of the lost diastolic compliance. These data demonstrate that 24-hour preserved and transplanted hearts recovered function over 96 hours.

Animals↗
PubMedDate not supplied

Derivation of sieving coefficients to determine the efficacy of the hemoconcentrator in removal of four inflammatory mediators produced during cardiopulmonary bypass.

Cardiopulmonary bypass has been implicated in triggering a multisystem inflammatory response caused by blood contact with the artificial surfaces of the circuit. This leads to increased morbidity levels because of cytotoxic enzymes released from activated neutrophils. Recently, it was discovered that certain inflammatory mediators are permeable to the membrane of the hemoconcentrator. As a result, this study was undertaken to quantitatively characterize the nature of this movement by deriving a sieving coefficient (S) for four inflammatory mediators: myeloperoxidase, elastase, interleukin-6, and lactoferrin. The results show no permeability through the hemoconcentrator for the two neutrophil derived enzymes myeloperoxidase and elastase (S = 0, p > 0.05). Conversely, although larger than the pore size of the hemoconcentrator, lactoferrin sieves through unrestricted (S = 1.030 +/- 0.037, p < 0.0001). Interleukin-6 is removed in concentrations greater than those found in the blood, which yields a sieving coefficient significantly greater than 1.0 (S = 1.246 +/- 0.042, p < 0.0001). In addition to sieving coefficients, this study offers theories as to why these mediators acted as such. One conclusion is that certain mediators are efficaciously removed by the hemoconcentrator and, with additional study, may result in an attenuated inflammatory response.

Aged↗