(1/1429) Phasic right coronary artery blood flow in conscious dogs with normal and elevated right ventricular pressures.
We studied phasic right coronary blood flow in well trained normal dogs and dogs with pulmonic stenosis. We installed electromagnetic flow transducers and pressure tubes under anesthesia to monitor right coronary blood flow, cardiac output, central aortic blood pressure, and right ventribular pressure. In normotensive dogs, systolic flow amplitude equaled early diastolic flow levels. The ratio of systolic to diastolic flow at rest was substantially greater in the right coronary bed (36+/-1.3%) than in the left circumflex bed (13+/-3.6%). Right diastolid flow runoff, including the cove late in diastole, resembled left circumflex runoff. Blood flow to the normotensive right (37+/-1.1 ml/min 100(-1) g) and the left (35+/-1.0 ml/min(-1) g) ventricular myocardium indicated equal perfusion of both cardiac walls. Throttling of systolic flow was related directly to the right ventricular systolic pressure level in the dogs with pulmonic stenosis. Retrograde systolic flow occurred in severe right ventricular hypertension. The late diastolic runoff pattern in dogs with pulmonic stenosis appeared the same as for the normotensive dogs. We obtained systolic to diastolic flow ratios of 1/3 the value of normotensive hearts in high and severe pulmonic hypertension. Electrocardiograms and studies of pathology suggested restricted blood flow to the inner layers of the right myocardium in the dogs with severe and high right ventricular hypertension. Normotensive and hypertensive peak hyperemic flow responses were similar, except for an increased magnitude of diastolic flow, with proportionately less systolic flow in hypertensive states. (+info)
(2/1429) Reduction in baroreflex cardiovascular responses due to venous infusion in the rabbit.
We studied reflex bradycardia and depression of mean arterial blood pressure (MAP) during left aortic nerve (LAN) stimulation before and after volume infusion in the anesthetized rabbit. Step increases in mean right atrial pressure (MRAP) to 10 mm Hg did not result in a significant change in heart rate or MAP. After volume loading, responses to LAN stimulation were not as great and the degree of attenuation was propoetional to the level of increased MRAP. A change in responsiveness was observed after elevation of MRAP by only 1 mm Hg, corresponding to less than a 10% increase in average calculated blood volume. after an increase in MRAP of 10 mm Hg, peak responses were attenuated by 44% (heart rate) and 52% (MAP), and the initial slopes (rate of change) were reduced by 46% (heart rate) and 66% (MAP). Comparison of the responses after infusion with blood and dextran solutions indicated that hemodilution was an unlikely explanation for the attenuation of the reflex responses. Total arterial baroreceptor denervation (ABD) abolished the volume-related attenuation was still present following bilateral aortic nerve section or vagotomy. It thus appears that the carotid sinus responds to changes inblood volume and influences the reflex cardiovascular responses to afferent stimulation of the LAN. On the other hand, cardiopulmonary receptors subserved by vagal afferents do not appear to be involved. (+info)
(3/1429) Ventricular pressure-volume curve indices change with end-diastolic pressure.
Many indices have been proposed to describee the diastolic pressure-volume curve mathematically and permit quantification of the elastic properties of the myocardium itself in hopes that changes in the muscle caused by disease would b.e reflected in the diastolic pressure-volume curve. To date, none of the proposed indices has been shown convincingly to discriminate one group of patients from another. While this situation in part arises from the relatively large amount of noise introduced by the technical difficulties of measuring synchronous pressures and volumes during diastole in man, ther is a more fundamental difficulty. In practice, one can measure only a short segment of the entire pressure-volume curve, and the values of all diastolic pressure-volume curve parameters investigated change significantly when one uses different segments of the same pressure-volume curve to compute them. These results were derived from relatively noise-free pressure-volume curves obtained by filling nine excised dog left ventricles at a known rate and monitoring pressure-volume curve used to compute the parameter. Merely increasing measurement fidelity will not resolve this problem, because none of these parameters accurately characterizes the entire diastolic pressure-volume curbe from a segment like that which one can reasonably expect to obtain from humans. (+info)
(4/1429) 'Home hypertension': exploring the inverse white coat response.
BACKGROUND: The classical 'white coat response' to blood pressure measurement has been studied thoroughly. However, little is known about patients showing a reverse pattern, i.e. who have lower blood pressure readings at the clinic than outside healthcare facilities. AIM: To estimate the proportion of patients whose blood pressure levels as determined by self-measurements at home are higher than those taken at the clinic and to explore possible associations with demographic, clinical, and psychological variables. METHOD: Patients consecutively attending (n = 214) an academic family medicine department in Toronto, Canada, were eligible. Subjects aged below 16 years and those on psychotropic or blood pressure-lowering agents were excluded. The clinic-home blood pressure difference (CHBPD) was calculated for each participating subject by subtracting home blood pressure from clinic blood pressure. Those who had negative values were compared with the rest of the sample. RESULTS: A considerable proportion of patients had lower blood pressure at the clinic than at home (systolic, 34.6%; diastolic, 23.8%). These subjects did not differ from the rest of the sample with regard to age, sex, levels of education attained, immigration status, body mass index, experience of current symptoms, blood pressure levels, or psychological distress. However, in patients with a 'negative CHBPD', i.e. lower blood pressure at the clinic than at home, readings taken by an automatic, self-inflating device when still at the clinic were higher than in the rest of the sample. CONCLUSION: The results point to measurement bias being at least partly responsible for higher blood pressure readings outside the clinic. Automatic measurement devices used for self/home blood pressure measurement seem to cause an alerting reaction analogous to the well-described 'white coat response'. (+info)
(5/1429) Energy cost of sport rock climbing in elite performers.
OBJECTIVES: To assess oxygen uptake (VO2), blood lactate concentration ([La(b)]), and heart rate (HR) response during indoor and outdoor sport climbing. METHODS: Seven climbers aged 25 (SE 1) years, with a personal best ascent without preview or fall (on sight) ranging from 6b to 7a were assessed using an indoor vertical treadmill with artificial rock hand/foot holds and a discontinuous protocol with climbing velocity incremented until voluntary fatigue. On a separate occasion the subjects performed a 23.4 m outdoor rock climb graded 5c and taking 7 min 36 s (SE 33 s) to complete. Cardiorespiratory parameters were measured using a telemetry system and [La(b)] collected at rest and after climbing. RESULTS: Indoor climbing elicited a peak oxygen uptake (VO2climb-peak) and peak HR (HRpeak) of 43.8 (SE 2.2) ml/kg/min and 190 (SE 4) bpm, respectively and increased blood lactate concentration [La(b)] from 1.4 (0.1) to 10.2 (0.6) mmol/l (p < 0.05). During outdoor climbing VO2 and HR increased to about 75% and 83% of VO2climb-peak and HRpeak, respectively. [La(b)] increased from 1.3 (0.1) at rest to 4.5 mmol/l (p < 0.05) at 2 min 32 s (8 s) after completion of the climb. CONCLUSIONS: The results suggest that for elite climbers outdoor sport rock climbs of five to 10 minutes' duration and moderate difficulty require a significant portion of the VO2climb-peak. The higher HR and VO2 for outdoor climbing and the increased [La(b)] could be the result of repeated isometric contractions, particularly from the arm and forearm muscles. (+info)
(6/1429) Ankle-arm index as a predictor of cardiovascular disease and mortality in the Cardiovascular Health Study. The Cardiovascular Health Study Group.
Peripheral arterial disease (PAD) in the legs, measured noninvasively by the ankle-arm index (AAI) is associated with clinically manifest cardiovascular disease (CVD) and its risk factors. To determine risk of total mortality, coronary heart disease, or stroke mortality and incident versus recurrent CVD associated with a low AAI, we examined the relationship of the AAI to subsequent CVD events in 5888 older adults with and without CVD. The AAI was measured in 5888 participants >/=65 years old at the baseline examination of the Cardiovascular Health Study. All participants had a detailed assessment of prevalent CVD and were contacted every 6 months for total mortality and CVD events (including CVD mortality, fatal and nonfatal myocardial infarction, congestive heart failure, angina, stroke, and hospitalized PAD). The crude mortality rate at 6 years was highest (32.3%) in those participants with prevalent CVD and a low AAI (P<0.9), and it was lowest in those with neither of these findings (8.7%, P<0.01). Similar patterns emerged from analysis of recurrent CVD and incident CVD. The risk for incident congestive heart failure (relative risk [RR]=1.61) and for total mortality (RR=1.62) in those without CVD at baseline but with a low AAI remained significantly elevated after adjustment for cardiovascular risk factors. Hospitalized PAD events occurred months to years after the AAI was measured, with an adjusted RR of 5.55 (95% CI, 3.08 to 9.98) in those at risk for incident events. A statistically significant decline in survival was seen at each 0.1 decrement in the AAI. An AAI of <0.9 is an independent risk factor for incident CVD, recurrent CVD, and mortality in this group of older adults in the Cardiovascular Health Study. (+info)
(7/1429) Anthropometric, lifestyle and metabolic determinants of resting heart rate. A population study.
AIM: To clarify the determinants of resting heart rate at the population level in a random sample of the Belgian population. METHODS AND RESULTS: Data of 5027 men and 4150 women aged 25-74 years obtained from a Belgian nationwide survey were analysed. In multivariate analysis, blood pressure strongly correlated with heart rate in men (t = 12.4 for systolic; t = 8.8 for diastolic) and women (t = 12.0 for systolic; t = 7.7 for diastolic). Age (t = -3.4 in men; t = -8.1 in women) and height (t = -3.7 in men; t = -3.1 in women) correlated negatively with heart rate. Smoking raised heart rate in men (1-19 cigarettes.day-1, t = 6.1; > or = 20 cigarettes.day-1, t = 10.3) and women (> or = 20 cigarettes.day-1, t = 3.5). Serum phosphorus correlated negatively with heart rate (t = -3.5 in men; t = -8.3 in women). Serum log alkaline phosphatase (t = 6.7 in men; t = 7.2 in women) and serum protein (t = 5.3 in men; t = 4.4 in women) correlated positively with heart rate. CONCLUSION: At the population level, blood pressure, cigarette smoking, serum alkaline phosphatase and serum protein correlate independently, significantly and positively with heart rate, and age, height and serum phosphorus negatively. (+info)
(8/1429) Resistance to remnant nephropathy in the Wistar-Furth rat.
The Wistar-Furth rat, an inbred strain resistant to actions of mineralocorticoids, was used to study the concept that mineralocorticoids contribute to progressive renal injury. It was postulated that if chronic nephropathy depends on aldosterone and if Wistar-Furth rats are resistant to aldosterone, remnant nephropathy would be attenuated in Wistar-Furth rats. Wistar-Furth rats and control Wistar rats were subjected to 5/6 nephrectomy or a sham procedure and then followed for 4 wk. Renal ablation resulted in hypertension at 4 wk in both strains (164+/-5 [Wistar-Furth] versus 184+/-7 [Wistar] mm Hg mean arterial pressure), with sham animals remaining normotensive (134+/-6 mm Hg). Renal damage in response to 5/6 nephrectomy was greatly decreased in Wistar-Furth rats compared with Wistar rats. Albuminuria was markedly less in Wistar-Furth rats (12.7+/-4.2 [Wistar-Furth] versus 97.4+/-22.6 [Wistar] mg/d per 100 g body wt, P<0.01). Glomerular damage, consisting of mesangial proliferation, mesangial lysis, and segmental necrosis, was observed in 42% of glomeruli from Wistar rats but in 0% of glomeruli from Wistar-Furth rats (P<0.01). To address the possibility that higher BP in partially nephrectomized Wistar rats mediated the greater renal damage, the study was repeated, with Wistar rats (not Wistar-Furth rats) being treated with a hydralazine-reserpine-hydrochlorothiazide regimen. Although this antihypertensive regimen equalized BP (conscious systolic) (144+/-8 mm Hg [Wistar] versus 157+/-7 mm Hg [Wistar-Furth] at 4 wk), albuminuria remained more than 10-fold greater in Wistar rats. In summary, renal damage upon 5/6 nephrectomy was markedly reduced in Wistar-Furth rats, a finding not attributable to reduced systemic BP. Since Wistar-Furth rats have been shown previously to be resistant to the actions of mineralocorticoids, the data from the present study support the hypothesis that aldosterone mediates, at least in part, the renal injury attendant to renal mass reduction. (+info)