The Widow and the Sperm: The Law of Post-Mortem Insemination

In this case we must decide whether a widow has the right to use her late husband\u27s frozen sperm to attempt to conceive a child where her late husband signed an agreement with the company storing the frozen sperm providing that the frozen sperm was to be discarded upon his death. We conclude that in determining the disposition of gametic material, to which no other party has contributed and thus another party\u27s right to procreational autonomy is not implicated, the intent of the donor must control. In this judgment roll appeal, the widow cannot challenge the probate court\u27s finding that the decedent\u27s intent was to have his frozen sperm discarded upon his death. Accordingly, we affirm the decision denying distribution of the frozen sperm to the widow

Widow and the Sperm: The Law of Post-Mortem Insemination

Just as there are moral and ethical implication in permitting the widow to use a sperm deposit for AIH, so are there moral and ethical implications in denying her this privilege. What is the rationale behind denying a widow access to that which would only be discarded? Suppose the sperm, rather than be discarded, were to be designated that of an unknown donor to be used in AID? If unmarred women have the right to procreate even using known donor sperm, what is the reason for prohibiting a woman to choose to be inseminated with the sperm of a man who was once her legal husband? Should not the widow, who knew her husband\u27s wishes and had presumably considered the disadvantages of posthumous parenting have a role in making the decision to create a child? Are there really any legal or public policy reasons that a vial of semen from a man who pays for it storage should not be considered part of his personal property to be made available to his heirs? These and other considerations must be fully explored by legislators before a case such as Parpalaix arises in the United States

Indications for immediate angiotensin-converting enzyme inhibition in patients with acute myocardial infarction

AbstractWhen initiated a few days after myocardial infarction, angiotensin-converting enzyme inhibition exerts beneficial effects on survival and morbidity in patients with asymptomatic left ventricular systolic dysfunction or symptomatic heart failure. During the acute phase of a myocardial infarction, angiotensin-converting enzyme inhibition appears to be well tolerated, to prevent the development of heart failure in patients with asymptomatic left ventricular systolic dysfunction and to improve the hemodynamic and clinical variables of heart failure when present. Accordingly, early angiotensin-converting enzyme inhibition is clearly indicated in patients with acute myocardial infarction associated with asymptomatic left ventricular dysfunction or clinical evidence of heart failure. Angiotensin-converting enzyme inhibition may also be beneficial when thrombolytic agents fail to restore coronary patency in patients with acute myocardial infarction

The Control of Myocardial Contraction with Skeletal Fast Muscle Troponin C.

The present study describes experiments on the myocardial trabeculae from the right ventricle of Syrian hamsters whose troponin C (TnC) moiety was exchanged with heterologous TnC from fast skeletal muscle of the rabbit. These experiments were designed to help define the role of the various classes of Ca2+-binding sites on TnC in setting the characteristic sensitivities for activations of cardiac and skeletal muscles. Thin trabeculae were skinned and about 75% of their troponin C extracted by chemical treatment. Tension development on activations by Ca2+ and Sr2+ was found to be nearly fully blocked in such TnC extracted preparations. Troponin C contents and the ability to develop tension on activations by Ca2+ and Sr2+ was permanently restored after incubation with 2-6 mg/ml purified TnC from either rabbit fast-twitch skeletal muscle (STnC) or the heart (CTnC, cardiac troponin C). The native (skinned) cardiac muscle is characteristically about 5 times more sensitive to activation by Sr2+ than fast muscle, but the STnC-loaded trabeculae gave response like fast muscle. Attempts were also made to exchange the TnC in psoas (fast-twitch muscle) fibers, but unlike cardiac muscle tension response of the maximally extracted psoas fibers could be restored only with homologous STnC. CTnC was effective in partially extracted fibers, even though the uptake of CTnC was complete in the maximally extracted fibers. The results in this study establish that troponin C subunit is the key in setting the characteristic sensitivity for tension control in the myocardium above that in the skeletal muscle. Since a major difference between skeletal and cardiac TnCs is that one of the trigger sites (site I, residues 28-40 from the N terminus) is modified in CTnC and has reduced affinity for Ca2+ binding, the possibility is raised that this site has a modulatory effect on activation in different tissues and limits the effectiveness of CTnC in skeletal fibers

Intravenous prenalterol in acute and chronic heart failure

The new inotropic agent prenalterol was administered intravenously in a canine model of acute ischemic heart failure and in patients with severe chronic heart failure. Experimental heart failure in anesthetized dogs was induced by two vessel coronary artery constriction and intravenous prenalterol (0.005–15 Μg/kg/min) was compared to dobutamine (0.001–30 Μg/kg/min) and saline. Significant dose–dependent increases in left ventricular dP/dt max ′ cardiac output and non–ischemic zone contractile force and significant reductions in systemic vascular resistance were present during infusions of both inotropic agents. High dose dobutamlne caused greater increases in mean arterial pressure and pressure rate product with a trend toward greater increases in heart rate. However, neither inotropic agent significantly improved ischemic zone contractile force. Prenalterol possessed a markedly longer hemodynamic half–life than dobutamlne (3.0 hours compared to 1.7 minutes). Nine patients with severe chronic heart failure (left ventricular ejection fraction mean ± SD 17 ± 5%, cardiac index 1.7±0.4 1/min/m 2 ) responded to intravenous prenalterol (1, 4, and 8 mg) with significant increases in cardiac index, left ventricular ejection fraction and left ventricular stroke work index. Left ventricular filling pressure, mean right atrial pressure and pulmonary arteriolar resistance were significantly reduced. No significant differences were present among peak responses to the three doses employed. An inverse correlation between basal heart rate and increase in left ventricular ejection fraction following prenalterol was noted. The mechanisms by which prenalterol causes hemodynamic improvement appear to include a direct inotropic effect, a reduction in left ventricular outflow resistance and a reduction in left and right ventricular filling pressure (venodilating effect). The net result is an upward and leftward shift of the depressed ventricular function curve. Both prenalterol and dobutamine were associated with sustained ventricular tachyarrhythmias in the experimental acute low output state and two digitalized patients with ischemic cardiomyopathy developed transient ventricular tachycardia after prenalterol administration. These findings indicated that adrenergic stimulants should be administered in severe ischemic states with careful monitoring.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73348/1/j.0954-6820.1982.tb00852.x.pd