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Biomedical subjects

M L Armstrong

Publications and source records attributed to M L Armstrong.

At least 55 records · Page 3Linked to original sources
PubMed1990

Reading activities of registered nurses.

This national study was designed to gather baseline data about the reading activities of registered nurses. Questionnaires were administered by nurse continuing educators to subjects (N = 1406) at 44 sites in 25 states and the District of Columbia. In a week, the mean amount of time devoted to professional literature was four hours, 48 minutes (SD = 3.88) plus eight hours, 12 minutes (SD = 5.15) to general material. This translated to reading one hour and 51 minutes per day, slightly more than the average adult. Educational level, position, and memberships were the best predictors of how much time was spent reading job-related material that might lead to self-development and enhancement of nursing practice.

Adult↗
PubMed1990

Endothelium-dependent vascular relaxation is abnormal in the coronary microcirculation of atherosclerotic primates.

Atherosclerosis impairs endothelium-dependent relaxation of large conduit arteries. Because coronary resistance vessels are spared from the development of overt atherosclerosis, endothelium-dependent responses were examined in these vascular segments. Malaysian cynomolgus monkeys (n = 6) were made atherosclerotic by being fed a 0.7% cholesterol diet for 18 months. Control monkeys (n = 6) were fed a standard diet. Coronary microvessels (122-220 microns) were studied in a pressurized (20 mm Hg), no-flow state using a video-imaging apparatus. Relaxations of microvessels, preconstricted with the thromboxane analogue U46619, were determined in response to acetylcholine, bradykinin, the calcium ionophore A23187, adenosine, and sodium nitroprusside. Microvascular relaxations to bradykinin and A23187 were reduced in atherosclerotic monkeys compared with controls, whereas acetylcholine produced additional contraction in atherosclerotic monkeys. Responses of preconstricted microvessels to adenosine and sodium nitroprusside were identical in atherosclerotic and control animals. Indomethacin did not alter responses in control or atherosclerotic animals. Histologic examination revealed neither intimal thickening nor plaque formation in microvessels of this size class despite marked changes in conduit arteries. Electron microscopy showed minor alterations of endothelial cell morphology in microvessels of atherosclerotic animals. In conclusion, long-term hypercholesterolemia markedly impairs endothelium-dependent vascular relaxation in the coronary microcirculation where overt atherosclerosis does not develop. These changes in endothelial cell function may significantly alter regulation of myocardial perfusion by neurohumoral stimuli.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Texas nurses are reading, yet.

The time Texas nurses spend reading professional literature is similar with physicians, yet they also read almost twice as much general material. A significant relationship was demonstrated between nurses who are members of nursing organizations and reading. Supervisor encouragement also influences reading but was reported as often not occurring.

Humans↗
PubMed1990

What causes spasm of atherosclerotic arteries? Is regression of plaques beneficial?

We would like to emphasize three points. First, atherosclerosis produces a profound alteration of vascular responses, which may lead to spasm in several vascular beds. Second, we have proposed that leukocytes as well as platelets may play a critical role in the pathophysiology of vasospasm. Third, there is bad news and good news in relation to regression of atherosclerosis. Maximal vasodilator capacity does not improve consistently during regression of atherosclerosis, but endothelium-dependent relaxation improves, hypersensitivity of blood vessels subsides, and we speculate that susceptibility to vasospasm may be abolished.

Animals↗
PubMed1989

Vasa vasorum in the carotid sinus of atherosclerotic monkeys: implications for baroreceptor function.

The carotid sinus is unusually susceptible to development of severe atherosclerotic lesions. The purposes of this study were to examine effects of atherosclerosis on blood flow through vasa vasorum in the carotid sinus and to examine responses to humoral stimuli. Blood flow to vasa in the carotid sinus was measured with microspheres in 8 normal and 9 atherosclerotic cynomolgus monkeys. Blood flow to vasa in intima-media (in ml/min per 100 g) was 0.5 +/- 0.3 (mean +/- SE) in normal and 21 +/- 5 in atherosclerotic monkeys (P less than 0.05). Flow to adventitial vasa was 37 +/- 5 in normal monkeys and 50 +/- 7 in atherosclerotic monkeys (P greater than 0.05). Infusion of phenylephrine did not affect blood flow in normal or atherosclerotic monkeys. Infusion of serotonin did not affect blood flow to vasa in normal monkeys, but decreased flow to vasa in both intima-media and adventitia of atherosclerotic monkeys. In normal media, histological examination demonstrated the presence of a few vasa vasorum, which penetrated from adventitia. In atherosclerotic monkeys, medial vasa were much more frequent. Thus, (1) atherosclerosis produces marked increases in blood flow through vasa in intima-media of the carotid sinus, probably as a consequence of proliferation of vasa, and (2) in atherosclerotic monkeys, vasa constrict in response to serotonin. Based on these findings, we speculate that when serotonin is released as platelets aggregate at plaques in the carotid artery, serotonin may be delivered through vasa to nerves in the carotid sinus and thereby affect baroreceptor function.

Animals↗
PubMed1989

Hypothesis: vasoconstriction contributes to amaurosis fugax.

Platelets play a critical role in the pathophysiology of amaurosis fugax. Emboli to retinal vessels apparently produce amaurosis but, in addition, we propose that augmented vasoconstrictor responses and vasospasm may contribute to amaurosis. In this study we tested the hypothesis that constrictor responses of retinal vessels to serotonin, which is released when platelets aggregate, are potentiated in experimental atherosclerosis. Blood flow to the retina was measured in normal and atherosclerotic cynomolgus monkeys. In normal monkeys, infusion of serotonin did not alter flow to the retina. In atherosclerotic monkeys, infusion of serotonin reduced retinal blood flow (in milliliters per minute per 100 g) from 66 +/- 7 (mean +/- SE) to 5 +/- 2. Infusion of serotonin in atherosclerotic monkeys abolished the retinal response to light. Thus, atherosclerosis greatly potentiates constrictor responses to serotonin in the retinal circulation and produces a profound but reversible impairment of retinal function. We propose that altered responses to vasoactive substances that are released by platelets may contribute to the pathogenesis of amaurosis fugax.

Animals↗
PubMed1989

Response of the mesenteric circulation to serotonin in normal and atherosclerotic monkeys: implications for the pathogenesis of non-occlusive intestinal ischaemia.

We tested the hypothesis that atherosclerosis potentiates vasoconstrictor responses in the mesenteric circulation to stimulation of serotonergic and alpha-adrenergic receptors. In normal monkeys, infusion of serotonin had little effect on blood flow to the stomach, duodenum, and colon. In contrast, in atherosclerotic monkeys, serotonin produced a modest decrease in blood flow to the stomach and duodenum, and virtually abolished blood flow to the colon. Vasoconstrictor responses to phenylephrine in the stomach and duodenum were not altered by atherosclerosis, but responses were potentiated in the colon of atherosclerotic monkeys. In summary, atherosclerosis greatly potentiates vasoconstrictor responses to serotonin in the mesenteric circulation, particularly in vessels to the colon. We speculate that release of serotonin during adherence and aggregation of platelets at atherosclerotic lesions, coupled with augmented vasoconstrictor responses to serotonin, may play a role in the pathogenesis of non-occlusive mesenteric ischaemia.

Animals↗
PubMed1989

Mechanisms of abnormal endothelium-dependent vascular relaxation in atherosclerosis: implications for altered autocrine and paracrine functions of EDRF.

The present studies were performed to determine if abnormal endothelium-dependent vascular relaxation in atherosclerosis is due to decreased production or release of endothelium-derived relaxing factor (EDRF) by atherosclerotic rabbit vessels or if atherosclerotic vessels are less sensitive to the relaxing effects of EDRF. EDRF release was quantified using two approaches, by the response of bioassay detector vessels and also by the activation of guanylate cyclase within cultured endothelial cells. Using these assays, atherosclerotic vessels were found to release significantly less EDRF than normal vessels in response to both receptor- and nonreceptor-mediated stimuli. Relaxations of normal and atherosclerotic vessels to luminally applied EDRF (derived from normal rabbit aortas stimulated by the calcium ionophore, A23187) and nitric oxide, a putative EDRF, were also studied. Atherosclerotic vessels were more sensitive to EDRF than normal vessels, and equally sensitive to nitric oxide. Additional studies performed in organ chambers failed to demonstrate augmented constriction of atherosclerotic vessels in response to acetylcholine in the presence or absence of methylene blue or LY83583, compounds which inhibit the effect of EDRF. We conclude that decreased EDRF release is the principal underlying mechanism responsible for abnormal endothelium-dependent vascular relaxation in atherosclerosis.

Acetylcholine↗
PubMed1989

Effect of early and advanced atherosclerosis on vascular responses to serotonin, thromboxane A2, and ADP.

In monkeys with early and advanced atherosclerosis, we examined responses to the three major vasoactive agonists that are released when platelets aggregate. Measurements were obtained in normal cynomolgus monkeys and in monkeys fed an atherogenic diet for 4 +/- 1, 9 +/- 1, and 19 +/- 1 months (mean +/- SEM). Morphometry of femoral and iliac arteries indicated that 4 months of atherogenic diet produced only slight intimal thickening, 9 months produced early lesions, and 19 months produced approximately 5-10 fold greater intimal proliferation than did 9 months of atherogenic diet. Serotonin and adenosine 5'-diphosphate (ADP), which are endothelium-dependent agonists, and adenosine and phenylephrine, which are endothelium-independent agonists, were injected intra-arterially into the perfused hind limb. Thromboxane A2 analogue U46619 also was studied. Vasoconstrictor responses to serotonin were potentiated, and vasodilator responses to ADP were impaired by early and advanced atherosclerosis. In contrast, vasoconstrictor responses to phenylephrine and vasodilator responses to adenosine were similar in all groups. Vasoconstrictor responses to U46619 were potentiated by advanced atherosclerosis. Thus, vascular responses to serotonin, ADP, and thromboxane A2 are altered by atherosclerosis in a direction that would favor vasoconstriction when platelets aggregate. Furthermore, because responses to endothelium-dependent agonists are altered, these data suggest that endothelium is dysfunctional in early atherosclerosis. These findings may explain, in part, the propensity for exaggerated vasoconstriction even in arteries with minimal atherosclerotic lesions.

Adenosine Diphosphate↗
PubMed1989

Vascular responses to leukocyte products in atherosclerotic primates.

Little is known about the possible role of leukocytes in the pathogenesis of vasospasm. We hypothesized that vasoactive products released by leukocytes might produce constriction of atherosclerotic arteries. To test this hypothesis, we infused fmet-leu-phe (fMLP), a peptide that activates leukocytes to release their vasoactive products, into the perfused hind limb of normal and atherosclerotic cynomolgus monkeys. Infusion of fMLP did not change resistance of large arteries in normal monkeys. In contrast, fMLP produced pronounced constriction of large arteries in atherosclerotic monkeys. To determine whether leukotrienes, platelet-activating factor, or prostaglandin E2 (PGE2), which are released by leukocytes, may contribute to leukocyte-induced vasoconstriction in atherosclerotic monkeys, we injected leukotriene D4, platelet-activating factor, and PGE2 intra-arterially into the perfused hind limb. Leukotriene D4 and platelet-activating factor had minimal effects on large arteries in both normal and atherosclerotic monkeys. PGE2 produced marked constriction of large arteries in atherosclerotic, but not normal, monkeys. Thus, pronounced constriction in atherosclerotic, but not normal, arteries during infusion of fMLP suggests that products released by leukocytes may mediate vasoconstriction in atherosclerotic vessels. Vasoconstrictor responses to PGE2 are profoundly potentiated by atherosclerosis, which suggests that PGE2 may contribute to leukocyte-induced vasoconstriction.

Animals↗
PubMed1989

Atherosclerosis potentiates constrictor responses of cerebral and ocular blood vessels to thromboxane in monkeys.

The goal of our study was to examine the effects of infusion of serotonin and the thromboxane A2 analogue U46619 into one carotid artery to stimulate their release from platelets during aggregation. We measured blood flow to the brain and eye using microspheres and cerebral microvascular pressure in the pial arteries of normal and atherosclerotic cynomolgus monkeys. Unilateral intracarotid infusion of 10-30 micrograms/min serotonin did not affect cerebral blood flow in normal or atherosclerotic monkeys; serotonin did not alter blood flow to the eye in normal monkeys but decreased flow to the retina and choroid in atherosclerotic monkeys by 39 +/- 11% and 44 +/- 10% (mean +/- SEM), respectively. Infusion of 30 ng/min U46619 did not alter cerebral blood flow but increased the pressure gradient from the aorta to the pial artery, which is an index of large-artery resistance, in atherosclerotic monkeys. U46619 had no effect on blood flow to the eye in normal monkeys but decreased blood flow to the retina and choroid by 71 +/- 14% and 53 +/- 13%, respectively, in atherosclerotic monkeys. Thus, atherosclerosis potentiates the constrictor responses of large cerebral arteries to thromboxane and the responses of blood vessels of the eye to thromboxane and serotonin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Orchestrating the process of patient education. Methods and approaches.

Patient education is a must, yet many obstacles prevent the achievement of this important goal. Nurses need to examine methods and approaches that have application in today's practice. These include the nurse's assessment of the patient as well as a self-inventory so a multifaceted plan can be implemented to provide information during each patient care contact point. Suggested methods, such as contracting and use of computers in the education process, are additional ways to involve patients actively so they can maximize their fullest potential in self-care.

Aftercare↗
PubMed1988

Blood flow through new microvessels: factors that affect regrowth of vasa vasorum.

A segment of abdominal aorta in dogs was transplanted to its original position (high PO2) or to the femoral vein (low PO2), and a segment of thoracic aorta was transplanted to its original position. Two days after grafting to each location, there was no blood flow (measured with microspheres) through vasa vasorum. After 2 and 4 wk, blood flow through vasa was restored to normal, or above normal, levels in all grafts. Vasa in grafts did not have smooth muscle, and they were not responsive to adenosine. Medial necrosis occurred in grafts of thoracic aorta but not in grafts of abdominal aorta. There was cellular degeneration and medial atrophy in grafts of abdominal aorta to the femoral vein. We conclude that 1) revascularization of the aorta by vasa vasorum is rapid; 2) new vasa do not have smooth muscle, and they are not responsive to vasoactive stimuli; and 3) medial necrosis occurs in grafts in which delivery of oxygen to media is compromised, either by low luminal PO2 or by interruption of medial vasa (in thoracic aorta), but not when the abdominal aorta is excised and reanastomosed. Absence of medial necrosis in grafts of abdominal aorta indicates that diffusion from the lumen of the vessel is adequate to nourish the vessel. This finding provides evidence that adventitial vasa, in contrast to medial vasa, are not essential for nourishment of the vessel wall.

Adenosine↗
PubMed1988

Vasa vasorum in atherosclerotic coronary arteries: responses to vasoactive stimuli and regression of atherosclerosis.

The goals of this study were to determine whether vasa vasorum in atherosclerotic coronary arteries respond to vasoactive stimuli and to examine effects of regression of atherosclerosis on blood flow through vasa vasorum in coronary arteries. We studied three groups of monkeys: normal, atherosclerotic, and regression. Blood flow to vasa vasorum was measured with microspheres. Blood flow to intima-media (ml/min x 100 g) was 5 +/- 1 (mean +/- SEM) in normal and 47 +/- 7 in atherosclerotic monkeys (p less than 0.05). Infusion of phenylephrine or serotonin did not alter flow through vasa in normal monkeys. In atherosclerotic monkeys, phenylephrine decreased flow through vasa vasorum in intima-media of coronary arteries to 24 +/- 4 (p less than 0.05), and serotonin decreased flow to 27 +/- 5 (p less than 0.05). In regression monkeys, blood flow to intima-media was sixfold less (7 +/- 2 ml/min x 100 g) than in atherosclerotic monkeys (p less than 0.05). During infusion of adenosine, blood flow to vasa was fourfold greater in atherosclerotic monkeys than after regression of atherosclerosis. This finding suggests that loss of vessels, not constriction of existing vessels, accounts for the decrease in flow through vasa in intima-media after regression of atherosclerosis. We conclude that vasa vasorum in atherosclerotic coronary arteries respond to vasoconstrictor stimuli and that there is loss of vasa vasorum and a large decrease in blood flow through vasa to intima-media of coronary arteries after regression of atherosclerosis.

Animals↗