Vasopressin deficiency and pressor hypersensitivity in hemodynamically unstable organ donors.
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BACKGROUND: Solid organ donors often develop hypotension due to vasodilation, and recently we observed that a variety of vasodilatory states are characterized by vasopressin deficiency and hypersensitivity. Thus, we investigated the prevalence of vasopressin deficiency in hypotensive solid organ donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor effect of vasopressin replacement in hypotensive donors. METHODS AND RESULTS: Fifty organ donors were evaluated for hemodynamic instability, (mean arterial pressure [MAP]+info)
Joint effects of an aldosterone synthase (CYP11B2) gene polymorphism and classic risk factors on risk of myocardial infarction.
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BACKGROUND: The -344C allele of a 2-allele (C or T) polymorphism in the promoter of the gene encoding aldosterone synthase (CYP11B2) is associated with increased left ventricular size and mass and with decreased baroreflex sensitivity, known risk factors for morbidity and mortality associated with myocardial infarction (MI). We hypothesized that this polymorphism was a risk factor for MI. METHODS AND RESULTS: We used a nested case-control design to investigate the relationships between this polymorphism and the risk of nonfatal MI in 141 cases and 270 matched controls from the Helsinki Heart Study, a coronary primary prevention trial in dyslipidemic, middle-aged men. There was a nonsignificant trend of increasing risk of MI with number of copies of the -344C allele. However, this allele was associated in a gene dosage-dependent manner with markedly increased MI risk conferred by classic risk factors. Whereas smoking conferred a relative risk of MI of 2.50 (P=0.0001) compared with nonsmokers in the entire study population, the relative risk increased to 4.67 in -344CC homozygous smokers (relative to nonsmokers with the same genotype, P=0.003) and decreased to 1.09 in -344TT homozygotes relative to nonsmokers with this genotype. Similar joint effects were noted with genotype and decreased HDL cholesterol level as combined risk factors. CONCLUSIONS: Smoking and dyslipidemia are more potent risk factors for nonfatal MI in males who have the -344C allele of CYP11B2. (+info)
Correlation between atrial natriuretic peptide and baroreflex sensitivity in patients with congestive heart failure.
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The aim of this study was to investigate the relationship between baroreflex sensitivity (BRS) and humoral factors in patients with congestive heart failure (CHF). BRS was assessed by the phenylephrine method in 16 patients with CHF and in 13 healthy controls. The CHF group was subdivided into 2 groups according to BRS (group A: <6 ms/mmHg, n=9; group B: > or =6 ms/mmHg, n=7). BRS was markedly depressed in CHF than in the controls (4.8+/-2.0 vs 8.3+/-3.6 ms/mmHg, p<0.01), and lower in group A than group B (3.3+/-1.3 vs 6.7+/-0.6 ms/mmHg, p<0.01). The plasma human atrial natriuretic peptide (h-ANP) level in group A was significantly higher than in group B (54.6+/-27.6 vs 18.0+/-7.4 pg/ml, p<0.01), and a significant inverse correlation was observed between plasma h-ANP and BRS (r=-0.635, p<0.01). However, there were no significant differences between the 2 groups in plasma catecholamine concentration, plasma renin activity and cardiac function by echocardiogram. These findings suggest that the elevation of endogenous ANP may also serve to compensate for impaired BRS in patients with CHF, in addition to its principal actions, such as diuresis and vasodilation. (+info)
Reduced baroreflex sensitivity in elderly humans is not due to efferent autonomic dysfunction.
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A progressive decline in baroreflex sensitivity (BRS) is a characteristic feature of human aging, the basis of which is poorly understood. The purpose of the present study was to determine whether alterations in efferent baroreflex function might contribute to the age-related decrease in BRS. We studied 10 healthy young (mean age 30.5 years; age range 22-40 years; six male) and 10 healthy elderly (mean age 70.7 years; age range 67-75 years; five male) volunteers. We tested efferent cardiac vagal function using the bradycardiac response to the cold face test, and efferent sympathetic function using heart rate and blood pressure responses to four stress tests: (i) low-level cognitive stress, (ii) high-level cognitive stress, (iii) hand immersion in ice water (cold pressor test) and (iv) isometric sustained hand-grip. Haemodynamic responses to these stresses are mediated via efferent baroreflex pathways, whereas the afferent components of each reflex response are independent of afferent baroreflex pathways. BRS was measured from simultaneous Finapres-derived continuous blood pressure and digital ECG R-R interval data using the sequence analysis paradigm. As expected, BRS was significantly reduced in the elderly group (7. 29+/-0.74 ms/mmHg; mean+/-S.E.M.) compared with the young group (13. 84+/-1.13 ms/mmHg; P<0.001). However, neither the bradycardiac responses to the cold face test nor the efferent sympathetically mediated heart rate/blood pressure responses to the stress test battery were significantly different between the young and elderly groups. We conclude that the age-related decrease in BRS is not attributable to impairments in the efferent sympathetic or parasympathetic system components of the baroreceptor reflex pathway. (+info)
Altered central nervous system processing of baroreceptor input following hindlimb unloading in rats.
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The effect of cardiovascular deconditioning on central nervous system processing of baroreceptor afferent activity was evaluated following 14 days of hindlimb unloading (HU). Inactin-anesthetized rats were instrumented with catheters, renal sympathetic nerve electrodes, and aortic depressor nerve electrodes for measurement of mean arterial pressure, heart rate, renal sympathetic nerve activity (RSNA), and aortic depressor nerve activity (ADNA). Baroreceptor and baroreflex functions were assessed during infusion of phenylephrine and sodium nitroprusside. Central processing of baroreceptor afferent input was evaluated by linear regression relating RSNA to ADNA. The maximum baroreflex-elicited increase in RSNA was significantly reduced in HU rats (122 +/- 3.8 vs. 144 +/- 4.9% of baseline RSNA), whereas ADNA was not altered. The slope (-0.18 +/- 0.04 vs. -0.40 +/- 0.04) and y-intercept (121 +/- 3.2 vs. 146 +/- 4.3) of the linear regression relating increases in efferent RSNA to decreases in afferent ADNA during hypotension were significantly reduced in HU rats. There were no differences during increases in arterial pressure. Results demonstrate that the attenuation in baroreflex-mediated increases in RSNA following HU is due to changes in central processing of baroreceptor afferent information rather than aortic baroreceptor function. (+info)
Autonomic cardiovascular regulation in obesity.
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Obese persons suffer from an increased mortality risk supposedly due to cardiovascular disorders related to either continuously lowered parasympathetic or altered sympathetic activation. Our cross-sectional correlation study establishes the relationship between obesity and autonomic regulation as well as salivary cortisol levels. Three patient cohorts were sampled, covering ranges of body mass index (BMI) of 27-32 (n=17), 33-39 (n=13) and above 40 kg/m(2)(n=12), and stratified for age, sex and menopausal status. Autonomic cardiovascular regulation was assessed by use of heart rate variability and continuous blood pressure recordings. Spectral analytical calculation (discrete Fourier transformation) yields indices of sympathetic and parasympathetic activation and baroreflex sensitivity. Morning salivary cortisol was concurrently collected. Contrary to expectation, BMI and waist/hip ratio (WHR) were inversely correlated with sympathetic activity. This was true for resting conditions (r=-0.48, P<0.001; r=-0.33, P<0.05 for BMI and WHR respectively) and for mental challenge (r=-0.42, P<0.01 for BMI). Resting baroreflex sensitivity was strongly related to the degree of obesity at rest (BMI: r=-0.35, P<0.05) and for mental challenge (r=-0.53, P<0.001). Salivary cortisol correlated significantly with waist circumference (r=-0.34, P=0.05). With increasing weight, no overstimulation was found but a depression in sympathetic and parasympathetic activity together with a significant reduction in baroreflex functioning and in salivary cortisol levels. (+info)
Diagnosis of carotid sinus hypersensitivity in older adults: carotid sinus massage in the upright position is essential.
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OBJECTIVE: To assess the diagnostic value of supine and upright carotid sinus massage in elderly patients. DESIGN: Prospective controlled cohort study. SETTING: Three inner city accident and emergency departments and a dedicated syncope facility. PATIENTS: 1375 consecutive patients aged > 55 years presenting with unexplained syncope and drop attacks; 25 healthy controls. INTERVENTIONS: Bilateral supine carotid sinus massage, repeated in the 70 degrees head up tilt position if the initial supine test was not diagnostic of cardioinhibitory and mixed carotid sinus hypersensitivity. MAIN OUTCOME MEASURES: Diagnosis of cardioinhibitory or mixed carotid sinus hypersensitivity; clinical characteristics of supine v upright positive groups. RESULTS: 226 patients were excluded for contraindications to carotid sinus massage. Of 1149 patients undergoing massage, 223 (19%) had cardioinhibitory or mixed carotid sinus hypersensitivity; 70 (31%) of these had a positive response to massage with head up tilt following negative supine massage (95% confidence interval, 25.3% to 37.5%). None of the healthy controls showed carotid sinus hypersensitivity on erect or supine massage. The initially positive supine test had 74% specificity and 100% sensitivity; these were both 100% for the upright positive test. The clinical characteristics of the supine v upright positive subgroups were similar. CONCLUSIONS: The diagnosis of carotid sinus hypersensitivity amenable to treatment by pacing may be missed in one third of cases if only supine massage is performed. Massage should be done routinely in the head up tilt position if the initial supine test is negative. (+info)
Centrally produced neuronal nitric oxide in the control of baroreceptor reflex sensitivity and blood pressure in normotensive and spontaneously hypertensive rats.
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We studied the effect of chronic nitric oxide synthase (NOS) blockade in the brain on mean arterial pressure [MAP (mmHg)], heart rate [HR (bpm)] and baroreceptor reflex sensitivity [BRS (mean slope: bpm/mmHg)] in Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Intracerebroventricular (i.c.v.) infusion of the nonselective NOS inhibitor N-Nitro-L-arginine-methylester (L-NAME) (50 microg/kg per day, 11-12 days) increased MAP in WKY and SHR (125+/-2.1 vs 118+/-1.1 controls, P<0.01 and 179+/-3.59 vs 156+/-4.0 controls, P<0.001, respectively) without affecting HR. In L-NAME-treated WKY, BRS to bradycardia was suppressed (-0.79+/-0.09 vs -1.76+/-0.17 controls, P=0.001), whereas in SHR, L-NAME did not affect BRS to bradycardia. BRS to tachycardia remained unaffected in either strain. In WKY, 7-nitroindazole (7-NI x Na+) (34 microg i.c.v./kg per day, 11-12 days), a selective nNOS inhibitor, did not affect MAP or HR, but BRS to bradycardia and tachycardia was decreased (-0.37+/-0.20 vs -0.97+/-0.41 controls, P<0.01 and -1.78+/-0.20 vs -2.52+/-0.40 controls, P=0.05, respectively). In SHR, the same dose of 7-NI x Na+ increased resting MAP (171+/-5.00 vs 150+/-7.00 controls, P<0.05) without affecting HR or BRS to bradycardia or tachycardia. Thus in WKY, BRS to acute changes in systemic blood pressure (BP) is regulated by NO produced by nNOS in the brain, serving as a neurotransmitter in sympathetic and parasympathetic efferent pathways. In SHR, systemic BP is regulated in part by NO released by the type I NOS isoenzyme in the brain. (+info)