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Biomedical subjects

M J Morton

Publications and source records attributed to M J Morton.

80 records · Page 5Linked to original sources
PubMed1981

Terbutaline and maternal cardiac function.

The effect of terbutaline sulfate on left ventricular size and performance was studied by M-mode echocardiography in pregnant women with premature labor. Patients with uterine activity initiated during either oxytocin challenge testing or induction of labor served as a comparison group. During terbutaline therapy, heart rate, ejection fraction, and cardiac output increased significantly. End-diastolic volume and systolic blood pressure (BP) were unchanged, and diastolic BP and end-systolic volume fell. No changes in echocardiographic or hemodynamic parameters were present during oxytocin-induced uterine activity. Terbutaline, as currently used to prevent premature labor, is a potent inotropic and chronotropic agent. Pulmonary edema accompanying terbutaline treatment is probably not due to cardiac failure.

Adolescent↗
PubMed1965

The family home.

Explore the source record for details and available documents.

Child↗
PubMedDate not supplied

Pulmonary function in nonsmokers following exposure to sidestream cigarette smoke.

Ten healthy male and 10 healthy female, "never-smoking" subjects (ages 21-50) participated in a 5-day environmental room study to determine if an acute exposure to a high level of fresh diluted sidestream smoke (FDSS) would alter pulmonary function. On Monday, Tuesday, Thursday and Friday, the twenty subjects sat in an environmental room for 7.33 hours and were exposed to filtered and humidified air. On Wednesday, the twenty subjects were exposed in an environmental room for 7.33 hours to an average respirable suspended particle (RSP) concentration of 179 micrograms per m3 of FDSS generated by machine smoking Kentucky 1R4F reference cigarettes. This level of FDSS is 3.3 times the 95th percentile concentration of workplace environmental tobacco smoke exposure levels previously measured in the US. FVC and FEV1 decreased approximately 1.6% (p < 0.05) in both males and females after exposure. Similarly, PEF decreased approximately 1.3% (p < 0.03) following exposure. The observed decrease in pulmonary function was consistent with a "stress" related norepinephrine-induced alteration in blood flow leading to transient bronchoconstriction. Alternatively, a cholinergic reflex due to activation of bronchopulmonary C fibers may have also played a role in the transient bronchoconstriction. These small exposure-related decrements in pulmonary function were reversible.

Adult↗
PubMedDate not supplied

Lack of progressive "restrictive" physiology after heart transplantation despite intervening episodes of allograft rejection: comparison of serial rest and exercise hemodynamics one and two years after transplantation.

It has been suggested that the cardiac allograft becomes less compliant either because of repeated episodes of rejection, chronic hypertension, or as a direct consequence of immunosuppression. A corollary to this hypothesis is that this reduction in compliance should be a progressive, rather than a static, change. To test this hypothesis, rest and exercise filling pressures, cardiac outputs, and radionuclide ventriculographic systolic and diastolic indices were measured in 20 patients at 1 and 2 years after heart transplant by means of identical protocols at both study times. Between studies 10 of 20 patients had no rejection, five of 20 had one rejection episode, and five of 20 had more than one rejection episode. There were no significant differences in resting or exercise heart rates, pulmonary wedge pressures, cardiac outputs, left or right ventricular ejection fractions, left ventricular peak filling rates, or time to peak filling between the studies at 1 and 2 years. Only resting right atrial pressure increased between year 1 and year 2 (6 +/- 2 mm Hg vs 8 +/- 4 mm Hg, p = 0.035). These data demonstrate that cardiac allograft function is unchanged between 1 and 2 years after transplantation, despite episodes of intervening rejection and continued immunosuppression. The data further suggest that the previously reported decrease in cardiac allograft compliance does not appear to be caused by a progressive intrinsic abnormality in the allograft, and that other mechanisms for "restrictive" allograft physiology should be sought.

Adolescent↗
PubMedDate not supplied

Relation between recipient: donor body size match and hemodynamics three months after heart transplantation.

Cardiac allograft hemodynamics were compared with respect to donor and recipient body weights to determine whether recipient: donor body size match played a significant role in subsequent recipient hemodynamics. Thirty-four stable outpatients underwent resting right-sided cardiac catheterizations 3 months after heart transplantation. As expected, resting cardiac output correlated positively with recipient body weight (r = 0.50, p = 0.002), and mean cardiac index (2.7 +/- 0.6 L/min/m2) was normal. There was, however, only a weak and statistically insignificant correlation between recipient body weight and stroke volume (r = 0.31, p = 0.072). There was a statistically significant negative correlation between donor: recipient body weight ratio and right arterial pressure (r = 0.41, p = 0.017), pulmonary wedge pressure (r = 0.38, p = 0.027), and heart rate (r = 0.39, p = 0.024). These data demonstrate that although cardiac output is maintained at levels appropriate for recipient size after heart transplantation, patients who receive small hearts rely on an increased heart rate and elevated filling pressures to achieve this end. These data suggest that the cardiac allograft may not adapt to recipient body size by 3 months after transplantation.

Body Constitution↗