Cerebral hemorrhagic risk of aspirin or heparin therapy with thrombolytic treatment in rabbits

We studied the incidence of cerebral hemorrhage in an animal model of embolic stroke to determine the safety of aspirin, heparin, and tissue plasminogen activator therapies. We occluded the middle cerebral arteries of rabbits with labeled blood clots and administered either tissue plasminogen activator, heparin, aspirin, tissue plasminogen activator plus aspirin, tissue plasminogen activator plus heparin, or saline at various times after stroke. Compared to saline controls, both the aspirin-only and the tissue plasminogen activator-plus-aspirin groups had a significantly higher incidence of cerebral hemorrhage, whereas the heparin and tissue plasminogen activator combination groups did not. We conclude that aspirin antiplatelet therapy alone may increase the risk of hemorrhagic infarction, whereas heparin or tissue plasminogen activator therapy appears to be relatively safe.     

Cognitive impairment in heart failure.

Heart failure is reaching epidemic proportions in the United States, causing a constellation of disabling symptoms. Cognitive impairment in people with heart failure may be more common than previously known with multiple etiologies from both the disease process and the treatment. Exemplars from a research study are used to illustrate the perspective of heart failure patients. Given the critical importance of memory deficits on patient education, potential nursing interventions to address the issue of cognitive impairment are described.     

Fetal beta-endorphin levels in response to reductions in uterine blood flow

Fetal beta-endorphin release has been associated with fetal hypoxia. The purpose of this study was to assess the degree of uterine blood flow reduction needed to elicit fetal beta-endorphin release in the sheep since there is a large reserve of oxygen supply to the fetus. Uterine blood flow was reduced by 26 +/- 2, 46 +/- 3 and 66 +/- 2%, producing fetal oxygen content concentrations of 5.7 +/- 0.6, 4.4 +/- 0.7 and 2.6 +/- 0.3 ml/dl, respectively. Although fetal oxygen concentrations were significantly decreased in the groups with a reduction in uterine blood flow of 46 and 66%, beta-endorphin was elevated only in the latter group. It is speculated that fetal beta-endorphin is released at a level of hypoxia which leads to a decrease in fetal oxygen consumption. A reduction in uterine blood flow of 66% appears to produce a stressful environment for the fetus as measured by fetal plasma beta-endorphin levels.