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PubMed1996

Adverse effects of interferon on the cardiovascular system in patients with chronic hepatitis C.

The therapeutic effects of interferon in chronic hepatitis C and many of its adverse effects have been well documented. However, there are only a few reports regarding its adverse effects on the cardiovascular system. The aim of this study was to clarify the clinical features of the adverse effects of interferon on the cardiovascular system in patients with chronic hepatitis C. We monitored 295 patients with chronic active hepatitis C during 312 courses of interferon therapy and for 1 year after the end of treatment for the presence of cardiovascular adverse effects. We found 6 patients with cardiovascular adverse effects during interferon therapy and 4 more patients within 1 year after the end of therapy (10/312, 3.2%). The adverse effects of interferon on the cardiovascular system included arrhythmia (n = 4), ischemic heart disease (n = 4) and myocardial disease (n = 2). None of the clinical factors, including history of cardiovascular disease, were related to these cardiovascular adverse effects. In all instances the patient's condition improved after discontinuation of interferon and adequate therapy. The cardiovascular adverse effects of interferon occurred frequently in patients with chronic hepatitis C, even after the end of therapy and they were unpredictable. Thus, all patients undergoing interferon therapy should be monitored not only during but also after the end of treatment.

Arrhythmias, Cardiac↗
PubMed2005

Physical activity, cardiovascular risk factors, and mortality among Finnish adults with diabetes.

OBJECTIVE: The aim of this study was to examine both single and joint associations of physical activity and conventional cardiovascular risk factors with total and cardiovascular mortality among patients with diabetes. RESEARCH DESIGN AND METHODS: We prospectively followed 3,708 Finnish patients with type 2 diabetes aged 25-74 years. Physical activity, smoking status, blood pressure, height, weight, and serum cholesterol level were determined at baseline. Cox proportional hazard models were used to estimate single and joint effects of physical activity and other cardiovascular risk factors on the risk of mortality. RESULTS: During a mean follow-up of 18.7 years, 1,423 deaths were recorded, 906 of which were due to cardiovascular disease. Moderate or high levels of physical activity were associated with decreased total and cardiovascular mortality, whereas higher levels of BMI and blood pressure and current smoking were associated with increased total and cardiovascular mortality. High serum cholesterol levels also increased cardiovascular mortality. The protective effect of physical activity was consistent in diabetic patients with any levels of BMI, blood pressure, total cholesterol, and smoking. CONCLUSIONS: A moderate or high level of physical activity was associated with a reduced risk of total and cardiovascular mortality among patients with type 2 diabetes. The favorable association of physical activity with longevity was observed regardless of the levels of BMI, blood pressure, total cholesterol, and smoking.

Adult↗
PubMed2000

Isolated Systolic Hypertension Is a Strong Predictor of Cardiovascular and All-Cause Mortality in the Middle-Aged Population: Warsaw Pol-MONICA Follow up Project.

OBJECTIVE: To assess the long-term risk of cardiovascular disease and all-cause mortality associated with various categories of hypertension, particularly isolated systolic hypertension. MATERIALS AND METHODS: Three independent random samples of the general Warsaw population aged 35-64 years (2490 men and 2405 women screened in 1984, 1988, and 1993) were followed for (1) cardiovascular death until 1996 and (2) all-cause death until 1998. Methods of the baseline surveys were consistent with the manual of the WHO MONICA Project. Isolated systolic hypertension was defined as systolic blood pressure greater than or equal to 140 mm Hg and diastolic blood pressure less than 90 mm Hg and was classified into two stages: stage I, when 90 is less than systolic blood pressure is less than 160 mm Hg; and stage II, for subjects with systolic blood pressure greater than or equal to 160 mm Hg. The Cox proportional hazard model was used to calculate the multivariable-adjusted relative risk of cardiovascular disease and all-cause mortality attributed to the particular hypertension category. RESULTS: Compared to normotension, stage I was associated with a 53%-60% increase in age-standardized cardiovascular mortality rates in both genders and with a 70% increase in all-cause mortality in men. A significant and independent association (after multivariable adjustment) was found only for all-cause mortality in men. Stage II was an independent predictor of cardiovascular mortality in men and in women, and of all-cause mortality in men. In both genders, the risks of examined end points associated with stage II were comparable to the risks associated with isolated systolic hypertension. Isolated diastolic hypertension did not significantly increase the risk of all-cause mortality in either gender or of cardiovascular mortality in men. In women the risk of cardiovascular disease associated with isolated diastolic hypertension was almost threefold higher compared with the normotensive group, but the risk was not statistically significant. CONCLUSION: In the middle-aged Polish population, isolated systolic hypertension is a much better predictor of cardiovascular disease and all-cause mortality than isolated diastolic hypertension. The association was stronger for stage II than for stage I. The risk of examined end points associated with stage II were similar to those associated with combined systolic-diastolic hypertension. (c)2000 by Le Jacq Communications, Inc.

Journal Article↗
PubMed1992

Assessment of cardiovascular reflexes is of limited value in predicting maximal +Gz-tolerance.

The importance of +Gz-induced loss of consciousness as a major cause of inflight incapacitation emphasizes the need for predicting +Gz-tolerance and investigating its possible determinants. The cardiovascular changes from +Gz-stress are initially counteracted reflexly by the cardiovascular autonomic system. The integrity of neural cardiovascular reflex control can be assessed by analysing the blood pressure (BP) and heart rate (HR) responses to different maneuvers, such as the Valsalva maneuver, standing and forced respiratory sinus arrhythmia. The aim of the present study was to investigate a possible relation between the cardiovascular responses to these tests and +Gz-tolerance. In 10 healthy subjects continuous Finapres BP and HR responses to the tests have been determined and correlated with their G-levels of peripheral light loss (PLL) during centrifuge-runs (0.1 G/s). Only mean BP recovery during Valsalva maneuver correlated marginally significantly with PLL (r = 0.63, p = 0.049). Cardiovascular findings were within normal range revealing no cardiovascular autonomic dysfunction. These results indicate that intact neural cardiovascular control seems to be a condition for tolerating +Gz-stress without determining maximal +Gz-tolerance. We conclude that assessment of cardiovascular reflexes may only confirm baroreflex integrity. However, they have limited value in predicting +Gz-tolerance.

Acceleration↗
PubMed2005

The cardiovascular continuum and renin-angiotensin-aldosterone system blockade.

A progressive chain of pathophysiological events links cardiovascular risk factors to clinical manifestations of disease and life-threatening cardiovascular events. This chain--the cardiovascular continuum--underlies cardiovascular disease and holds the key to its prevention and treatment. Progressive tissue damage can result in morbidity from congestive heart failure, end-stage heart disease, nephrotic proteinuria and dementia and, eventually, death from cardio- or cerebrovascular causes. The renin-angiotensin-aldosterone system (RAAS) is involved at all stages of the cardiovascular continuum, because the effector molecules of the RAAS, angiotensin II in particular, have direct pathobiological effects on a variety of tissues, including the endothelium, vascular smooth muscle and the renal mesangium. Clinical trials of angiotensin II receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors have demonstrated the essential validity of this hypothesis. Interruption of the RAAS has been shown to reduce cardiovascular morbidity and mortality in patients with left ventricular hypertrophy, heart failure and post-myocardial infarction, as well as renal disease in patients with type 2 diabetes. Key questions remain, however. What are the clinical effects of combination ARB and ACE inhibitor treatment? How will combinations of RAAS blockade with other agents, such as statins, affect the cardiovascular continuum? Answers to these questions will require well-planned, adequately powered clinical trials, such as the Programme of Research tO evaluate Telmisartan End-organ proteCTION (PROTECTION) and the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) programmes. However, it is already clear that RAAS blockade is an essential part of blocking progression along the cardiovascular continuum.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1985

[Statistical study of the risk of cardiovascular disease in hysterectomized patients].

The risk of atherosclerotic or hypertensive cardiovascular disease increases after physiological or surgical menopause, irrespective of whether or not the ovaries are removed. In order to evaluate the direct contribution of the uterus in cutting down the incidence of cardiovascular diseases, the clinical records of 1551 cardiovascular patients and 296 healthy women were examined. All subjects were divided into 8 different groups according to their age. The following data were considered: 1) the incidence of cardiovascular diseases; 2) the number of subjects in physiological or surgical menopause; 3) the number of women hysterectomised in premenopause; 4) the number of women who underwent hysterectomy and bilateral salpingo-oophorectomy in premenopause; 5) the number of women who underwent either operation before or after the menopause. It was found that both in hysterectomised and not hysterectomised women the hypertensive and ischaemic cardiovascular pathologies prevailed in the younger and older groups respectively. Among the patients with cardiovascular diseases the percentage of subjects who had undergone hysterectomy or hysterectomy with bilateral oophorectomy was significantly higher (p less than 0.05) than in the controls. The difference was particularly marked in the younger groups. These data indicate that when the uterus is properly stimulated by the oestrogens, is able to produce a protective factor against cardiovascular diseases. It has been suggested that this factor may be prostacyclin, a potent vasodilator and the most potent inhibitor of platelet aggregation yet discovered. The epidemiological evidence alone that premenopausal hysterectomy increases the risk of cardiovascular disease should be an important consideration in weighing the risks and benefits of the procedure. If the epidemiological data can be supported by a definite mechanism of action via prostacyclin, then current indications for hysterectomy must be carefully reconsidered.

Adult↗
PubMed1984

Opioid analgesics in anesthesia: with special reference to their use in cardiovascular anesthesia.

In this article, an attempt has been made to review the use of receptor stimulating pure agonist opioids in anesthesia, especially in patients with cardiovascular disease. Particular emphasis has been placed on the use of opioids in high doses to produce anesthesia, techniques that recently have become popular in cardiovascular anesthesia. A major benefit of opioid anesthesia is the cardiovascular stability obtained during induction and throughout operation, even in patients with severely impaired cardiac function. There is a considerable body of evidence to support this claim when fentanyl is used. Anesthetic doses of morphine are associated with a higher incidence of cardiovascular disturbances and other problems, and, therefore, more attention to detail is required in order to achieve adequate anesthesia and hemodynamic stability. Although other opioids have been used as sole or principal agents in anesthesia for cardiovascular surgery, none have gained widespread acceptance. Meperidine, for example, which is widely used in lower (nonanesthetic) doses as a supplement to nitrous oxide in cardiac and noncardiac surgery, has proved unsuitable because of severe hemodynamic disturbances when high doses are given. However, initial reports concerning two of the newer agonist opioids, sufentanil and alfentanil, suggest that they may prove to be suitable alternatives and perhaps provide advantages over morphine and fentanyl in patients with or without cardiovascular disease. Although cardiovascular stability usually can be assured in the chronically sick cardiac patient with opioid anesthesia, this is not always so with the healthier patient, particularly those presenting for coronary artery surgery. A frequently occurring problem in these patients is hypertension during or after sternotomy, which can result in myocardial ischemia and infarction. The incidence of severe hypertension (increases in systolic blood pressure greater than 20% of control values) can be reduced drastically by increasing the dose of opioid, e.g., up to 140 micrograms/kg of fentanyl. However, despite such large doses, some patients will continue to need treatment with vasodilators, inhalation anesthetics, or other supplements at certain periods during cardiovascular operations. The use of very large doses of opioids also will prolong postoperative respiratory depression. High doses of opioids can reduce or prevent the hormonal and metabolic responses to the stress of surgery. However, even very large doses of fentanyl or its newer analogues do not prevent marked increases in plasma catecholamine concentrations in response to cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 400 WORDS)

Alfentanil↗
PubMed1997

Specificity of detection of Chlamydia pneumoniae in cardiovascular atheroma: evaluation of the innocent bystander hypothesis.

Chlamydia pneumoniae has been detected in atherosclerotic plaque, raising the question of whether this detection is specific to atheromatous tissue. To evaluate this question, we tested cardiovascular and non-cardiovascular tissue samples from 38 autopsy cases by polymerase chain reaction and immunocytochemistry. We also tested 33 granuloma biopsy specimens, as the organism has been detected in macrophages. C. pneumoniae was detected in coronary artery tissue from 13 (34%), lung from 5 (13%), liver from 4 (10%), and spleen from 2 (5%) of the 38 autopsy cases (P < 0.05 for comparison of proportion of positive coronary arteries with that of each of the other types of tissue). Of the 21 cases with at least one positive tissue sample, 11 had only a positive cardiovascular tissue (coronary artery, venous bypass graft, or myocardium), 7 had both cardiovascular and non-cardiovascular positive tissues, and 3 had only a non-cardiovascular positive tissue. C. pneumoniae was thus detected relatively infrequently in non-cardiovascular tissues, and its detection in these tissues was usually in association with its detection in cardiovascular tissue from the same patient. The organism was also infrequently detected in granulomatous tissue (3/33 specimens). These findings demonstrate that C. pneumoniae is more frequently found in atherosclerotic than normal tissue and support the hypothesis that C. pneumoniae has a role in the pathogenesis of atherosclerosis.

Adolescent↗
PubMed1998

Profile of preparticipation cardiovascular screening for high school athletes.

CONTEXT: Sudden death in young competitive athletes due to unsuspected cardiovascular disease has heightened concern and interest in the preparticipation screening available to high school athletes in the United States. OBJECTIVE: To assess the potential adequacy of the preparticipation screening process for detecting or increasing the suspicion of cardiovascular abnormalities. DESIGN: Current guidelines and requirements for implementation of preparticipation screening from each of the high school jurisdictions in the 50 states and the District of Columbia were analyzed and compared with the 1996 American Heart Association (AHA) consensus panel guidelines on screening. OUTCOME MEASURES: Items contained on preparticipation screening questionnaires; the examiners designated to perform screening. RESULTS: Eight states (16%) have no approved history and physical examination questionnaires to guide examiners, including 1 state without a formal screening requirement. Of the remaining 43 states, several items relevant to cardiac-related problems were frequently omitted from the questionnaires. Exertional dyspnea or chest pain, prior limitation from sports, family history of heart disease, or Marfan syndrome were included in 0% to 56% of the state forms. Specific cardiovascular items on physical examination were included in forms from only 5% to 37% of states, including documentation of a heart murmur, irregular heart rhythm, peripheral pulses, or stigmata of Marfan syndrome. Seventeen (40%) of 43 states had history and physical questionnaires judged to be most adequate with at least 9 of the 13 AHA recommendations, whereas 12 states (28%) were least adequate with 4 or less of these recommended items. Therefore, a total of 20 (40%) of the 51 states have no approved history and physical examination questionnaires, or formal screening requirement, or forms that were judged to be inadequate. In addition to physicians, 21 states also permit nurses or physician assistants to administer examinations, and 11 states specifically provide for practitioners with limited cardiovascular training (such as chiropractors). CONCLUSIONS: Preparticipation athletic screening for cardiovascular disease with standard history and physical examination, as presently employed in US high schools, is highly dependent on the state-approved questionnaires, which frequently are abbreviated and may be inadequate; is implemented by a variety of health care workers with varying levels of expertise; and may be severely limited in its power to detect potentially lethal cardiovascular abnormalities. These observations should represent an impetus for change and improvement in the preparticipation cardiovascular screening process for high school athletes.

Adolescent↗
PubMed2001

The last frontier in cardiovascular health: a landmark lecture for the XVII World Congress of the International Society for Heart Research.

Following World War II, Vannevar Bush described science as an "endless frontier" that should be made accessible to all Americans. Since then, cardiovascular health has improved markedly, largely because substantial investments in biomedical research led to numerous therapies and prevention strategies for cardiovascular disease. Despite these advances, however, science remains an endless frontier and we continue to face an infinite array of opportunities for improving cardiovascular health. A standard definition for "frontier" is the "farthermost limit of knowledge or achievement". The limits of our knowledge are expanding at an ever accelerated pace. Unfortunately, we do not always apply what we know, and therefore fail to achieve all we could. For example, we have known for two decades that heart attack patients benefit from beta-blockers, but even today, the drugs are not always prescribed. And, health disparities continue to exist among races and communities. Therefore, the "last frontier of cardiovascular health" is the translation and application of our knowledge to improve the cardiovascular health of all people. We will not reach the farthermost limit of achievement without new knowledge. But, in our zeal to expand our knowledge of cardiovascular diseases, we must remember to ensure that what we learn is rapidly applied to improve cardiovascular health.

Cardiovascular Diseases↗
PubMed2006

Beta-adrenergic receptors and nitric oxide generation in the cardiovascular system.

Nitric oxide plays a crucial role in cardiovascular homeostasis, with important vasodilatory, anti-thrombotic and anti-atherogenic properties. Beta-adrenergic receptors (betaARs), present on a wide variety of cardiovascular cells, including vascular endothelial cells, platelets, cardiac myocytes and leukocytes, have long been established as key players in maintaining cardiovascular homeostatic control. During the last few years a wealth of evidence has emerged which directly links stimulation of these cardiovascular betaARs to nitric oxide (NO) generation, suggesting a new and important mechanism of adrenergic control of cardiovascular function. This review explores the cardiovascular cell systems in which this coupling of betaARs and NO occurs, the intracellular signalling and regulatory mechanisms involved and the abnormalities in betaAR-NO oxide coupling found in cardiovascular disease states.

Aging↗
PubMed2004

Epicardial coronary artery constriction to cold pressor test is predictive of cardiovascular events in hypertensive patients with angiographically normal coronary arteries and without other major coronary risk factor.

Epicardial coronary endothelial dysfunction independently predicts cardiovascular events in patients with coronary risk factors. This study was designed to evaluate outcome of hypertensive patients on the basis of their epicardial coronary function assessed by cold pressor test (CPT). Control subjects (n = 68, 48.8 +/- 7.6 years) and hypertensive patients (n = 83, 51.3 +/- 7.9 years) with angiographically normal coronary arteries and without other major coronary risk factor underwent epicardial coronary reactivity assessment to CPT using quantitative angiography. Cardiovascular events were recorded with a mean follow-up of 115 months (range 84-132). In control subjects, dilation occurred in 88.2%, no change in 11.8% (mean diameter change: +14.6 +/- 9.3%). In hypertensive patients, dilation occurred in 13.3%, no change in 25.3% (mean diameter change for both: +10.9 +/- 11.2%), and constriction in 61.4% (mean diameter change: -12.7 +/- 3.4%). Endothelium-independent dilation was normal in control subjects and hypertensive patients. In control subjects, there were three cardiovascular events in two subjects (2.9%). In hypertensive patients, there were 17 cardiovascular events in 12 patients (14.5%, P < 0.01 versus control subjects), with 15 cardiovascular events in the 10/51 patients (19.6%) with coronary artery constriction, and two cardiovascular events in the 2/32 patients (6.3%) with no change or dilation (P < 0.05). In conclusion, in hypertensive patients with angiographically normal coronary arteries and without other major coronary risk factors, epicardial coronary artery dysfunction assessed by the cold pressor test is predictive of long-term cardiovascular events.

Adult↗
PubMed2005

Alcohol and the cardiovascular system: research challenges and opportunities.

Excessive alcohol consumption has long been associated with cardiovascular disorders, including cardiomyopathy, hypertension, coronary artery disease, and stroke. However, recent evidence suggests that moderate alcohol intake can actually provide a measure of cardioprotection, particularly against coronary heart disease and ischemia-reperfusion injury. To explore the various dimensions of these opposing actions of alcohol, the National Institute on Alcohol Abuse and Alcoholism and the National Heart, Lung, and Blood Institute sponsored a state-of-the-art workshop on "Alcohol and the Cardiovascular System: Research Challenges and Opportunities" in Bethesda, Maryland, in May 2003. Speakers discussed the following topics: the epidemiology of alcohol and cardiovascular disease, clinical manifestations of alcohol, genetics of alcohol and cardiovascular disease, mechanisms underlying the molecular and cellular effects of alcohol, the application of new and emerging technology, and translation from discovery to therapeutic modalities of treatment. The panel concluded that future studies are needed to: 1) determine the role of genes and the environment in assessing mechanisms underlying the benefits of alcohol use and cardiovascular disease risk; 2) define the biological mechanisms underlying alcohol-induced peripheral vascular damage; 3) clarify the role of genetic variation in alcohol-metabolizing enzymes, genetic susceptibility, and pharmacogenomics in determining cardiovascular disease risk and effective treatment; 4) determine common mechanisms underlying alcohol-induced cardiovascular disease, such as oxidative stress and inflammation; 5) assess the role of insulin resistance, blood clotting, protein kinase C isoforms, and signal transduction mechanisms mediating alcohol's beneficial effects; and 6) explore the potential of stem cells in myocardial regeneration and repair in hearts damaged by alcohol.

Alcohol Drinking↗
PubMed2000

Social support and cardiovascular reactivity.

Recent experimental work on the benefits of social support in buffering cardiovascular stress responses builds on prior epidemiological, psychological, and physiological work. Epidemiological data show that social integration is associated with better health, but cannot unambiguously establish causality (it could be that healthy people attract more friends), nor that the mechanism is psychological (the mechanism could be behavioral; for example, with friends encouraging exercise). Social psychological work suggests that people prefer to be with others, especially in times of stress, and that they evaluate themselves, and their emotional responses, by observing the people around them. This work, while establishing a desire for affiliation, does not show that being with others translates into health benefits. Physiological evidence suggests that exaggerated cardiovascular responses to stress are associated with the development of hypertension and cardiovascular disease, but does not indicate how such potentially damaging stress responses can be reduced. Experimental work on social support and cardiovascular reactivity overcomes many of these limitations. The presence of an ally, especially a female, markedly reduces cardiovascular responses compared both to the presence of an non-supportive other, and to experiencing the stress alone. One fruitful area for further work is the role of social support following stress, both in speeding the cardiovascular return to pre-stress levels, and in limiting rumination-induced cardiovascular responses.

Animals↗
PubMed1998

Circadian variations in cardiovascular function and their relation to the occurrence and timing of cardiac events.

Circadian patterns of risk for cardiac events and their implications for prevention and treatment of cardiovascular conditions are discussed. Sympathovagal tone, a major biological determinant of circadian variation in cardiovascular function, is modulated through circadian patterns of sleep-wake activity. The influence of neurohumoral activity on cardiovascular function is manifested by 24-hour variability in heart rate, blood pressure, and vasomotor tone. Platelet aggregation and plasminogen-activator inhibitor-1 activity peak around the time of awakening. Conversely, endogenous plasminogen activator exhibits a nadir around the time of awakening. Studies of patterns of occurrence of cardiac disorders such as acute myocardial infarction, sudden cardiac death, stroke, and ventricular arrhythmia show an increased occurrence during the period surrounding awakening. These patterns are consistent with observed circadian patterns in cardiovascular function. Diabetes, left ventricular dysfunction, and congestive heart failure may contribute to alterations in patterns of occurrence of cardiac events. Factors such as race, sex, and age may lead to alterations in circadian variation in cardiovascular function. Unusual physical exertion, stress, and anger may act as triggers of an event at any time of day. The circadian patterns of cardiac events follow the natural fluctuations in endogenous physiological processes, with a vulnerable period consistently observed in the early morning; dynamic assessment of markers of cardiovascular function may assist in determining the extent of disease progression and in selecting cardiovascular therapies.

Cardiovascular Diseases↗
PubMedDate not supplied

Gender-specific implications for cardiovascular medication use in the elderly optimizing therapy for older women.

Sex should be considered during the selection of cardiovascular medications and dosages of cardiovascular medications. There is mounting evidence that clinically important differences between the sexes exist in the pharmacokinetic processes that determine drug concentrations and in the pharmacodynamic processes that determine physiologic responses to pharmacologic agents. Although aging also affects these processes, aging does not eliminate the sex-related differences. The major pharmacokinetic differences between the sexes, on average, are lower weight and distribution volumes in women compared with men and lower renal drug clearance in women compared with men. Sex-related differences in hepatic drug clearance are less predictable. Pharmacodynamic responses that differ between the sexes include increased adverse cardiovascular drug effects in women compared with men (torsade de pointes arrhythmias, increased risk of hemorrhagic consequences of anticoagulation or thrombolytic therapy, electrolyte abnormalities with diuretics, myopathy with HMG Co-A reductase inhibitors, cough with ACE inhibitors, and increased incidence of thrombosis). Recommendations for optimizing cardiovascular drug therapy for the older women include individualization of drug selection to minimize the number of medications and side effects; dosage adjustment based on age, size, and sex; close monitoring for side effects; and consideration of cost and access to medications. Optimal care for the older woman with cardiovascular disease will also require investigation of cardiovascular medications in older women and of therapies for cardiovascular diseases that are more common in women than men.

Aged↗
PubMed2003

Ultrasound biomicroscopy-Doppler in mouse cardiovascular development.

The ability to modify the mouse genome has yielded new insights into the genetic control of mammalian cardiovascular development. However, it is far less understood how genetic factors and their consequent structural changes alter cardiovascular function, a void largely due to the lack of effective noninvasive techniques to assess function in the developing mouse cardiovascular system. In this review, we discuss the recent advances in ultrasound biomicroscopy (UBM)-Doppler echocardiography for analyzing cardiovascular function in the embryonic mouse in utero. "Cardiovascular function" encompasses broad aspects of physiology, including systolic and diastolic cardiac function, distribution of blood flow among various embryonic vascular beds, and vascular bed properties (impedance). A wide range of physiological measurements is possible using UBM-Doppler, but it is clear that the limitations of any single measurement warrant a multi-parameter approach to characterizing cardiovascular function. We further discuss the prospects for UBM-Doppler analysis of alternative vertebrate systems increasingly studied in developmental biology. The ability to correlate cardiovascular physiological phenotypes with their corresponding genotypes should lead to the elucidation of mechanisms underlying normal development, as well as embryonic disease and death.

Animals↗
PubMed1992

Hydrogen peroxide-induced cardiovascular reflexes. Role of hydroxyl radicals.

Mesenteric ischemia reflexly activates the cardiovascular system. In addition, mesenteric ischemia and reperfusion generate reactive oxygen species. However, the ability of these short-lived reactive oxygen species to generate cardiovascular reflexes is unknown. We therefore investigated cardiovascular reflexes induced by serosal application of hydrogen peroxide (H2O2) to the gallbladder, stomach, or duodenum in anesthetized cats. Serosal application of hydrogen peroxide (44 mumols) to the gallbladder (n = 14) significantly (p less than 0.05) increased mean arterial blood pressure (MAP) by 37 +/- 6 mm Hg, left ventricular dP/dt by 1,893 +/- 416 mm Hg/sec, heart rate by 6 +/- 1 beats per minute, and systemic vascular resistance from 0.34 +/- 0.01 to 0.42 +/- 0.04 peripheral resistance units. The cardiovascular effects were dose-dependent over a range of 0.4 pmol to 132 mumols H2O2. Celiac and superior mesenteric ganglionectomy abolished H2O2-induced cardiovascular effects. Dimethylthiourea (10 mg/kg), a reactive oxygen species scavenger, significantly (p less than 0.05) attenuated 44 mumols H2O2-induced increases in MAP from 36 +/- 3 to 2 +/- 2 mm Hg. Deferoxamine (10 mg/kg) also significantly attenuated 44 mumols H2O2-induced increases in MAP from 40 +/- 7 to 19 +/- 10 mm Hg, but iron-loaded deferoxamine did not. Aspirin (50 mg/kg) did not attenuate H2O2-induced excitation of the cardiovascular system. These data suggest that H2O2 activates abdominal visceral afferents to reflexly stimulate the cardiovascular system by a mechanism involving hydroxyl radicals. Thus, reactive oxygen species could modulate systemic vascular tone by stimulating abdominal visceral afferents during mesenteric ischemia and reperfusion.

Animals↗