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Biomedical subjects

R S Stuart

Publications and source records attributed to R S Stuart.

At least 37 records · Page 2Linked to original sources
PubMed1993

Centrifugal ventricular assist device for support of the failing heart after cardiac surgery.

OBJECTIVE: To determine the morbidity and mortality associated with use of centrifugal ventricular assist devices for postcardiotomy cardiogenic shock and to determine factors that might influence outcome and thus, aid in patient selection. DESIGN: A retrospective study. SETTING: Surgical intensive care unit in a university hospital. PATIENTS: During a 6-yr period, a total of 7,385 adult patients underwent cardiac operations requiring cardiopulmonary bypass. Myocardial protection consisted of single-dose cold crystalloid cardioplegia and continuous topical hypothermia by saline lavage. A total of 72 (1%) patients developed postcardiotomy cardiogenic shock. Of 72 patients, 28 met the institutional criteria and were placed on centrifugal ventricular assist devices. INTERVENTIONS: Twenty-eight adult patients with postcardiotomy cardiogenic shock were supported with centrifugal ventricular assist devices. MEASUREMENTS AND MAIN RESULTS: A total of 15 patients received left ventricular assist devices, five received right ventricular assist devices, and eight received both right and left ventricular assist devices. Mean age of ventricular assistance patients was 50.8 +/- 12.9 yrs (range 22 to 72), and mean duration of ventricular assistance was 2.8 +/- 2.5 days (range 4 hrs to 10 days; median 2 days). Twenty-five complications occurred in 16 patients and included bleeding (13), tamponade (2), systemic embolism (6), seizures (2), and sepsis (2). Nine patients required reexploration for bleeding or tamponade. Nine (32%) of 28 patients were discharged from the hospital. Ventricular assistance for cardiac failure after transplantation was associated with improved survival (p < .10), while age > 50 yrs and postoperative tamponade each showed trends toward association with mortality (p = .10). Survival was not predicted by gender, weight, time on cardiopulmonary bypass, aortic cross-clamp time, urgency of operation, or preoperative congestive heart failure. At 27 +/- 20 months follow-up, all survivors were alive and New York Heart Association functional class I or II. CONCLUSIONS: These results document a low incidence of ventricular assist device use in a surgical practice that employs a relatively simple method of myocardial protection. When postcardiotomy ventricular assistance was necessary, a centrifugal pump was used and successful outcome and satisfactory long-term results were possible in nearly one third of patients. Ventricular assistance for cardiac failure after transplantation was associated with improved survival. Older age is a relative contraindication to mechanical ventricular assistance.

Adult↗
PubMed1993

Abnormal responses to pulmonary vasodilators in conscious dogs after left lung autotransplantation.

We investigated the extent to which left lung autotransplantation (LLA) alters endothelium-dependent (bradykinin and acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilation in the pulmonary circulation of conscious dogs. Continuous left pulmonary vascular pressure-flow (LPQ) plots were generated in conscious dogs 3-4 wk post-LLA and in sham-operated controls. LLA resulted in a marked upward shift in the baseline LPQ relationship compared with the control group (P < 0.01), i.e., LLA caused a chronic increase in pulmonary vascular resistance. The thromboxane analogue, U-46619, was used to acutely preconstrict the pulmonary circulation in control dogs, which shifted the control LPQ relationship to the same position measured post-LLA. Under these circumstances, bradykinin, acetylcholine, and nitroprusside caused pulmonary vasodilation in the control group, whereas these responses were either attenuated or reversed to vasoconstriction post-LLA. After acute preconstriction with U-46619 post-LLA, the pulmonary vasodilator responses to bradykinin and acetylcholine were again attenuated, but the response to nitroprusside was unaltered compared with control. These results indicate that a significant component of the chronic increase in pulmonary vascular resistance post-LLA is passively mediated and does not reflect an active increase in baseline vasomotor tone. Moreover, LLA results in an impairment in endothelium-dependent, but not endothelium-independent, pulmonary vasodilation in conscious dogs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Pulmonary vascular alpha 1-adrenoreceptor activity in conscious dogs after left lung autotransplantation.

We investigated the extent to which sympathetic alpha 1-adrenoreceptor activation is involved in chronic pulmonary vascular regulation in conscious dogs after left lung autotransplantation (LLA). Continuous left pulmonary vascular pressure-flow plots were generated in conscious dogs 3-4 wk post-LLA and in identically instrumented conscious dogs not subjected to LLA (sham-operated controls). LLA resulted in a marked upward shift in the baseline left pulmonary vascular pressure-flow relationship compared with the control group (P < 0.01), i.e., LLA caused a chronic increase in pulmonary vascular resistance. The sympathetic alpha 1-adrenoreceptor antagonist prazosin partially reversed (P < 0.01) the LLA-induced increase in pulmonary vascular resistance. Circulating concentrations of norepinephrine and epinephrine at 2 and 4 wk post-LLA were not significantly different from values measured in control dogs. However, the dose-response relationship to the exogenous administration of the sympathetic alpha 1-adrenoreceptor agonist phenylephrine was shifted (P < 0.05) to the left post-LLA compared with control, which indicates an increase in pulmonary vascular reactivity to alpha 1-adrenoreceptor activation. This effect was not due to a generalized increase in pulmonary vascular reactivity to vasoconstrictor stimuli because the dose-response relationship to the thromboxane analogue U-46619 was not significantly altered post-LLA compared with control. Thus LLA results in a chronic increase in pulmonary vascular resistance in conscious dogs. A component of the increase in pulmonary vascular resistance resulting from LLA is mediated by an enhanced reactivity to sympathetic alpha 1-adrenoreceptor activation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Pulmonary vascular beta-adrenoreceptor activity in conscious dogs after left lung autotransplantation.

Our objective was to determine whether chronic denervation associated with left lung autotransplantation (LLA) results in an alteration in sympathetic beta-adrenoreceptor regulation of the pulmonary circulation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LPQ) plots were generated in conscious dogs 2-4 wk post-LLA and in sham-operated control conscious dogs. We tested the hypothesis that endogenous sympathetic beta-adrenoreceptor activation via circulating catecholamines acted to attenuate the chronic increase in pulmonary vascular resistance post-LLA. Administration of the sympathetic beta-adrenoreceptor antagonist propranolol had no significant effect on the LPQ relationship post-LLA. We also tested the hypothesis that pulmonary vascular reactivity to sympathetic beta-adrenoreceptor activation would be increased post-LLA. The thromboxane analogue U-46619 was used to acutely preconstrict (P < 0.01) the pulmonary circulation in control dogs; this preconstriction shifted the LPQ relationship to the same position measured post-LLA. Under these conditions, cumulative doses of the beta-adrenoreceptor agonist isoproterenol caused pulmonary vasodilation (P < 0.01) in the control group but had no effect post-LLA. However, after acute preconstriction with U-46619, the pulmonary vasodilator response (P < 0.01) to isoproterenol post-LLA was not significantly different from that in the control group. These differential responses to isoproterenol with and without acute preconstriction indicate that a significant component of the chronic increase in pulmonary vascular resistance post-LLA is mediated by passive nonvasoactive mechanisms. Moreover, sympathetic beta-adrenoreceptor reactivity of the pulmonary circulation is not enhanced by chronic denervation resulting from the LLA procedure.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Acute and chronic pulmonary vasoconstriction after left lung autotransplantation in conscious dogs.

We investigated the acute and chronic effects of left lung autotransplantation (LLA) on the left pulmonary vascular pressure-flow (LP/Q) relationship in conscious dogs. Continuous LP/Q plots were generated in chronically instrumented conscious dogs 2 days, 2 wk, 1 mo, and 2 mo after LLA. Identically instrumented normal conscious dogs were studied at equal time points post-surgery. LLA had little or no effect on baseline systemic hemodynamics or blood gases. In contrast, compared with normal conscious dogs, striking active flow-independent pulmonary vasoconstriction was observed 2 days post-LLA. The slope of the LP/Q relationship was increased from a normal value of 0.275 +/- 0.021 to 0.699 +/- 0.137 mmHg.ml-1.min-1.kg-1 2 days post-LLA. Pulmonary vasoconstriction of similar magnitude was also observed on a chronic basis at 2 wk, 1 mo, and even 2 mo post-LLA. Pulmonary vasoconstriction post-LLA was not due to fixed resistance at the left pulmonary arterial or venous anastomotic sites. Finally, systemic arterial blood gases were unchanged when total pulmonary blood flow was directed to exclusively perfuse the transplanted left lung. Thus, LLA results in both acute and chronic pulmonary vasoconstriction in conscious dogs. LLA should serve as a useful stable experimental model to assess the specific effects of surgical transplantation on pulmonary vascular regulation.

Animals↗
PubMed1991

Similarity of pulmonary rejection patterns among heart-lung and double-lung transplant recipients.

The transbronchial biopsy and clinical courses of 9 double-lung and 1 single-lung recipients surviving greater than 10 days were analyzed and compared to those of 15 heart-lung transplants performed during the same time period. Of these, 8 isolated lung (LT) and 11 heart-lung transplant (HLT) recipients survived greater than 50 days and were at risk of developing obliterative bronchiolitis believed to be a form of chronic rejection. Cyclosporine-based immunosuppression, in combination with azathioprine and steroids, was used for 22 of 25 patients. Two double-lung recipients and 1 heart-lung patient received FK506 as the sole immunosuppressive agent; 90% and 62% of LT, and 67% and 54% of HLT recipients developed acute and chronic rejection, respectively (P = NS). The average time to first episode of acute (30.2 days [LT] versus 21.5 days [HLT]) and chronic rejection (146 days [LT] versus 193.7 days [HLT]) was not different between groups (P = NS). Age (34.2 [LT] versus 29.1 [HLT]) and sex (M:F, 5:5 [LT] versus 5:10 [HLT]) were also not found to be discriminators. The histologic diagnosis of chronic rejection was associated with significant declines in FEV1.0 and FEF25-75 (P less than 0.02). There was only one instance of cardiac rejection among the heart-lung transplant recipients. Heart-lung and isolated lung transplant patients appear to be at similar risk for developing acute or chronic pulmonary rejection.

Adult↗
PubMed1991

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation.

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.

Animals↗
PubMed1989

Negative intrathoracic pressure decreases independently left ventricular filling and emptying.

The mechanism for the fall in left ventricular (LV) stroke volume with normal and obstructed inspiration is controversial with changes proposed in LV preload and afterload. During respiration extending over several cardiac cycles, changes in both LV filling and emptying could occur, rendering demonstration of any responsible mechanism difficult. To evaluate the independent effects of negative intrathoracic pressure (NITP) on LV filling and emptying, we have analyzed the effects of NITP confined to either diastole or systole using electrocardiogram (ECG)-triggered phrenic nerve stimulation in six anesthetized closed-chest dogs. Lung volume was either maintained by completely obstructing the airway or allowed to increase during NITP. With diastolic NITP and the airway obstructed during phrenic nerve stimulation, LV filling volume (integrated mitral flow) significantly decreased (-37 +/- 6.1% SE) associated with increases in LV and right atrial filling pressures at end diastole relative to both atmospheric and esophageal pressures. Right atrial pressure relative to either atmospheric or esophageal pressure increased significantly more than left atrial pressure. The ensuing LV stroke volume (integrated ascending aortic flow) decreased significantly (-30.8 +/- 5.9%). With NITP confined to systole and at constant LV preload, LV stroke volume also decreased (-12.9 +/- 2.5%) associated with an increase in LV systolic pressure relative to esophageal pressure. Similar significant changes were observed despite a smaller fall in esophageal pressure when lung volume was allowed to increase during either diastolic or systolic NITP. We conclude that 1) NITP confined to diastole decreases LV filling and the ensuing LV stroke volume, most likely by ventricular interdependence; 2) NITP confined to systole also decreases LV stroke volume, presumptively by imposing an increased afterload on the LV; 3) both diastolic and systolic mechanisms should contribute to a decreased LV stroke volume during normal and obstructed inspiration; and 4) if the effects of intrathoracic pressure changes were to extend over several cardiac cycles, mechanisms exist to account for either increases or decreases in LV volumes.

Airway Obstruction↗
PubMed1989

The risk of coronary bypass surgery for patients with postinfarction angina.

Three hundred consecutive patients who developed unstable postinfarction angina requiring isolated coronary artery bypass from 1982 through 1987 were analyzed. Hospital mortality was 5%; 15 (5.5%) additional late deaths occurred during the 69-month follow-up period (mean follow-up, 23.3 months). Significant independent predictors of perioperative mortality by univariate analysis were ejection fraction (p = 0.004); existence of an anterior, transmural infarction (p = 0.0001); and the requirement for preoperative intra-aortic balloon counterpulsation (p = 0.001). By multivariate analysis, only the occurrence of an anterior, transmural infarction (p = 0.001) and the preoperative use of an intra-aortic balloon pump (p = 0.004) were significant independent predictors of mortality. Actuarial survival in this group ranged from 96 +/- 1% at 1 year to 88 +/- 4% at 5 years.

Actuarial Analysis↗
PubMed1988

Mitral and aortic blood flows during spontaneous respiration in dogs.

Left sided hemodynamic events during respiration remain a controversial subject. Left ventricular (LV) hemodynamic events were evaluated during obstructed and partially obstructed inspiration in anesthetized dogs acutely instrumented with mitral (Qm) and ascending aortic (Qa) flow probes. This allows classification of the inspiratory decrease in LV stroke volume as either a diastolic event (e.g., ventricular interdependence) in which case the LV inflow volume (integral of Qm) should decrease before the LV outflow volume (integral of Qa), or a systolic event (e.g., afterload or contractility) in which case outflow (integral of QA) should decrease before inflow (integral of Qm). During either unobstructed (n =8) or partially obstructed (n = 5 spontaneous ventilation, Qm reached both its inspiratory minimum and expiratory maximum prior to the associated minimum and maximum values for integral of in 80% or more of the respiratory cycles. Thus, a diastolic event dominates both in reducing the subsequent LV outflow during the expiratory increase in intrathoracic pressure. However, because a diastolic event did not occur first at all times, a systolic event must occur first at all times, a systolic event must also be present. If a rapid change in intrathoracic pressure occurred during diastole, integral of Qm invariably immediately increased. If a rapid in intrathoracic pressure occurred during systole, integral of Qa could change independently of the preceding integral of Qm. Both systolic and diastolic mechanisms contribute to the inspiratory fall in LV output. These mechanisms will not be clearly delineated without evaluating the effects of intrathoracic pressure within a single cardiac cycle.

Airway Obstruction↗
PubMed1988

Effects of changes in left ventricular loading and pleural pressure on mitral flow.

The cause of the fall in left ventricular (LV) stroke volume (SV) during a fall in pleural pressure (Pp1) has been in dispute for over a century. We have defined the changes in the temporal relationship between LV inflow (Qm) and outflow (Qa) in a canine preparation to test the mutually exclusive hypotheses that the fall in LVSV is caused only by changes during diastole (e.g., ventricular interdependence) or only by changes during systole (e.g., afterload). The ability of the experimental preparation to measure the results of acute changes in right heart volume or output and acute changes in LV afterload was validated in open-chest studies with and without pericardial constraint. In closed-chest studies, with a fall in Pp1 during a Mueller maneuver Qm reached both its inspiratory minimum and expiratory maximum before Qa in 80% of the Mueller maneuvers, invalidating both hypotheses, which each required that one flow lead the other in 100% of the Mueller maneuvers. Review of individual records suggested that if the rapid changes in Pp1 occurred during systole, Qa could vary in a manner independent of the preceding Qm. These studies suggest that both diastolic and systolic events may contribute to the fall in SV, while causing opposite changes in LV volumes.

Animals↗
PubMed1988

Predictors of perioperative mortality in patients with unstable postinfarction angina.

Factors associated with increased operative mortality in patients with postinfarction angina have not been defined. Two hundred twenty-five patients underwent urgent coronary artery bypass grafting from 1982 through 1986. One hundred sixty-two men and 63 women averaged 62 years of age (range, 35-87 years). Operative mortality was 5.3%. To assess the predictors of perioperative mortality, 16 variables were evaluated by univariate and multivariate analyses. Significant independent predictors of perioperative mortality were the presence of a transmural anterior myocardial infarction (p less than 0.0005) and the need for preoperative intra-aortic balloon pumping for angina or congestive heart failure (p = 0.009). All perioperative mortalities (12 patients) occurred in this subset (anterior myocardial infarction, intra-aortic balloon pumping, or both) that included 101 patients. The mean follow-up period was 27.8 months (range, 1-69 months). There were 11 late deaths, resulting in an actuarial survival of 92 +/- 2%, 91 +/- 2%, 88 +/- 2.6%, and 88 +/- 4% at 1,2,3, and 4 years, respectively. Ninety-six percent of survivors were assigned to New York Heart Association Class I or II for congestive heart failure, and 96% were assigned to Class I or II for angina. Urgent coronary artery bypass grafting can be performed in patients with unstable postinfarction angina with acceptable mortality, although a significant increase in risk exists for patients with preoperative transmural anterior myocardial infarction, intra-aortic balloon pumping, or both.

Adult↗
PubMed1986

Anatomic and anesthetic considerations in experimental cardiopulmonary surgery in swine.

We have used immature commercial swine (13-25 kg) successfully in a variety of experimental cardiopulmonary surgical procedures in our laboratories since 1981. Multiple drug anesthetic protocols using barbiturates, narcotics, paralytic and antiarrhythmic agents have been employed in over 400 procedures per year. Complications, including fatal cardiac arrhythmias, have been greatly reduced by anesthetic protocols and surgical procedures developed through experience.

Acepromazine↗
PubMed1985

Twenty-four hour lung preservation by hypothermia and leukocyte depletion.

In lung preservation, as well as in other forms of pulmonary disease, injury is associated with sequestration of leukocytes. We hypothesized that leukocyte depletion could prevent reperfusion injury and prolong the period of safe lung preservation. The heart-lung block from 39 New Zealand white rabbits were harvested, flushed with 100 ml of a modified Collins solution, stored at 4 degrees C in a 30% inflation state, and reperfused with either whole blood or leukocyte depleted blood. Leukocyte depletion was accomplished using a blood filter and verified with selected leukocyte counts. Leukocyte readdition specimens were obtained from whole blood, the separation being done with hydroxyethyl starch and centrifugation at 4,000 rpm for five minutes. Six groups of rabbit lungs were studied. Group 1 consisted of control lungs that were not preserved and were reperfused with whole blood. Lungs in Group 2 underwent five-hour preservation and whole blood reperfusion. Lungs in Group 3 underwent five-hour preservation and leukocyte depleted blood reperfusion. Lungs in Group 4 underwent 24-hour preservation and leukocyte depleted blood reperfusion. Lungs in Group 5 also underwent 24-hour preservation, leukocyte depleted blood reperfusion, but with leukocyte readded at the onset of reperfusion. Lastly, lungs in Group 6 underwent 24-hour preservation, leukocyte depleted blood reperfusion, with leukocyte readdition after one hour of reperfusion. Group 5 showed pulmonary edema and complete reservoir emptying within the first hour of reperfusion. Group 2 had comparable poor results. Groups 3, 4, and 6 showed no significant differences from the control lungs in regard to pressure or reservoir loss.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗