Changes In Diastolic Pressure Research Articles

Baroreflex resetting during exercise: mechanisms and meaning

the cardiovascular adjustments to exercise constitute well- coordinated responses throughout the body. Virtually every organ system is required to do more (e.g., skeletal muscle, the respiratory pump, and the cardiac pump) or to do the same as at rest while receiving less blood flow. Of all the

Ventricular‐Arterial Coupling Deteriorates with Sedentary Aging but is Restored by Endurance Training in Healthy Seniors

We tested the hypotheses that dynamic properties of ventricular-arterial coupling deteriorate with healthy but sedentary aging and that endurance training preserve it in seniors. In 9 healthy sedentary seniors (71±3 yrs, mean±SD), 12 age-matched Masters athletes (68±3 yrs), and 9 young healthy controls (30±7 yrs), transfer function gain (Gain) between beat-to-beat changes in pulmonary artery diastolic pressure (Swan-Ganz catheter, approximating LV end-diastolic pressure, LVEDP) and systemic arterial systolic pressure (SBP, Finapres) were estimated during 6 min fixed rate (0.2 Hz) respiration to evaluate the transmission properties of changes in the LVEDP to the SBP. In addition, the transmission properties were determined after completion of 1-year endurance training (70–95% HRmax, 25–60 min/day, 3–6 days/wk) in the seniors. At baseline, Gain at high frequency (0.15–0.25 Hz) was decreased with age but preserved by chronic endurance training (Seniors, 0.7±0.3; Masters, 1.1±0.8, Young, 1.2±0.3 mmHg/mmHg). Moreover, 1-year training in the seniors normalized Gain (1.3±0.8 mmHg/mmHg). Thus, dynamic ventricular-arterial coupling deteriorates with sedentary aging but is preserved and restored by endurance training. We speculate that with healthy but sedentary aging, ventricular and vascular stiffening results in impaired ventricular-arterial coupling, while exercise training normalizes these abnormalities of the circulation.

Ventricular‐arterial coupling and arterial‐baroreflex function in patients with heart failure and normal ejection fraction

Changes in ventricular-arterial coupling may lead to diastolic dysfunction with aging. Arterial-baroreflex function is impaired in heart failure. It is unknown whether these characteristics are more or less impaired in patients with heart failure but a normal ejection fraction (CHF-nlEF). Methods Five CHF-nlEF subjects (74±8 yrs, mean±SD) were compared with 6 age- and gender-matched controls (68±3 yrs). High frequency (0.15–0.25 Hz) transfer function gains between beat-to-beat changes in the pulmonary artery diastolic pressure (Swan-Ganz catheter, approximating beat-to-beat changes in LV end-diastolic pressure, LVEDP) and systemic arterial systolic pressure (SBP, Finapres) (Gain LVEDP-SBP), and between the SBP and R-R interval (RR, 3-lead ECG) (Gain SBP-RR) were estimated during 6 min fixed rate (0.2 Hz) respiration. Results Gain LVEDP- SBP (ventricular-arterial coupling) was decreased in CHF-nlEF compared with control (CHF-nlEF, 0.56±0.31; Control, 0.97±0.30 mmHg/mmHg). However, Gain SBP-RR (arterial-baroreflex function) was not different (CHF-nlEF, 4.9±3.8; Control, 5.4±3.2 msec/mmHg) both of which are substantially reduced compared to young subjects in our lab (21.1±14.4 msec/mmHg, N=5). Conclusion The combination of abnormal ventricular-arterial coupling and impaired baroreflex function may represent the substrate which leads to CHF-nlEF in the elderly.

How to characterize daily profile of pulse blood pressure?

The aim of this work is studying of double-phase rhythm characteristics of pulse pressure (PP) at untreated patients AH. The absent of night reduce of PP can be the consequent of night incommensurable change of systolic and diastolic pressure at night in comparison with day change. It was revealed two types of incommensurable double-phase rhythm of pulse pressure ( PP) on the basis of database analysis: Type 1 - with night increase of SHP (type 1a with night decrease DBP, type 1b with gap of increase DBP from SBP at night). Type 2 - with decrease of SBP and DBP at night. Ratio of daily index SBP and DBP ≥ 0,70 provide for decrease PP at night in comparison of day hours with probability ≥ 96 %. Accepting k = 0,70 as bench mark allow us to insert quantitative characteristics of double-phase rhythm of pulse pressure (PP), without using the traditional measure scale of daily index, the usage opportunity of which by BP demands more precise definition The presence of incommensurable daily rhythm of BP was associated with more expressed abnormalities from the point of target organs even with normal daily rhythm of SHP. Thus, I he estimation of proportionality of daily rhythm of SHP and DBP against their daily index is very important additional characteristic of daily profile of HP, allowing to identify patients in dipper and non-dipper groups, whose target organs condition can't be explained by the character of double-phase rhythm of SHP.

One-Year Observation of Kidney Allograft Recipients Converted From Cyclosporine Microemulsion to Tacrolimus

The results from previous trials suggested that tacrolimus-based treatment in kidney transplantation was associated with a significantly lower incidence of acute rejection, and that cyclosporine microemulsion (CsA-Me)-treated patients converted to tacrolimus had numerically better 6-year graft survival than those remaining on CsA-Me. Death with a functioning graft and chronic graft nephropathy are the leading causes of late allograft loss. While standard cardiovascular risk factors are relevant, renal function itself becomes an important risk factor for cardiovacular morbidity and mortality in kidney transplantation patients. Expected benefits of the conversion from CsA-Me to tacrolimus with respect to renal function and cardiovascular status were the rationale for this observational study. Twenty one patients underwent conversion due to nephrotoxicity of cyclosporine ( n = 18) or side effects ( n = 3). Two out of 21 patients did not complete the study. The patient survival after 1 year was 100% in this group of patients; graft survival 94.7%. No cases of de novo diabetes mellitus were identified. Mean serum creatinine fell from 2.13 ± 0.4 to 1.84 ± 0.3 mg/dL ( P < .02) and calculated glomerular filtration rate increased from 49.6 ± 14.4 to 56.2 ± 15.5 mL/min ( P < .01). Total cholesterol decreased from 229.4 ± 50.1 to 195.9 ± 28.5 mg/dL ( P < .005) and, low-density lipoprotein cholesterol from 125.7 ± 37.3 to 104.4 ± 22.6 mg/dL ( P < .02). No significant changes in mean systolic or diastolic pressure or blood glucose levels were observed. The results of this observational study showed that in a group of patients with raised creatinine levels at entry, conversion to tacrolimus resulted in improved graft function and a more favorable cardiovascular risk profile.

Cross-sectional and longitudinal relationships between alcohol consumption and lipids, blood pressure and body weight indices.

Serum lipids, blood pressure and body mass may mediate the U-shaped relationship of alcohol consumption with type 2 diabetes mellitus and coronary heart disease. This study examines the cross-sectional and long-term longitudinal relationships of (changes in) alcohol consumption with (changes in) serum lipids, blood pressure and body mass indices. In this prospective, observational cohort study, two measurements of alcohol consumption, serum total and high-density lipoprotein cholesterol, triglycerides, blood pressure, body weight, the thickness of four skinfolds and waist circumference were performed 4 years apart in healthy volunteers (143 men and 174 women, 32 years old at the first measurement). Alcohol consumption from beer, wine and distilled spirits was assessed using an extensive dietary history interview. Linear regression analyses were performed to study the cross-sectional relationships between the amount of alcohol consumed at the age of 32 years and the levels of the lipids, blood pressure and body weight indices, and to study the longitudinal relationships between the changes in the amount of alcohol consumed over the 4 years of follow-up and the concurrent changes in the lipids, blood pressure and body weight indices. Nonlinearity was investigated for the cross-sectional relationships. A 10-g/day difference in alcohol consumption was positively related with a 0.05 mmol/L (1.9 mg/dl) difference in high-density lipoprotein cholesterol in both cross-sectional (p = .004), and longitudinal (p < .0001) analyses. This relationship did not differ for men and women or for the consumption of beer, wine or distilled spirits. Relationships with changes in total cholesterol, triglycerides, systolic, diastolic, and pulse pressure, body weight and the sum of four skinfolds were not significant. A borderline significant inverse longitudinal relationship was found with waist circumference. The other lifestyle behaviors (tobacco smoking, physical activity and dietary habits) were major confounders of most cross-sectional relationships between alcohol and serum lipids, blood pressure and body mass indices. The longitudinal relationships, however, were not confounded by changes in the other lifestyle behaviors. A significant nonlinear relationship was found for systolic blood pressure, in which drinkers of about 30 g/day had the lowest values. Moderate alcohol consumption and moderate long-term changes in alcohol consumption are positively related with the levels and changes in high-density lipoprotein cholesterol in healthy adult men and women. A moderate inverse association between alcohol and waist circumference may be expected. No relationships were found with triglycerides, blood pressure, body weight and the sum of the thickness of four skinfolds. Other lifestyle behaviors confound the cross-sectional, but not the longitudinal, relationships between alcohol consumption and serum lipids, blood pressure and body mass indices. Gender and type of beverage do not modify the relationships between alcohol consumption and these indices.

Salt Restriction in the Treatment of Isolated Systolic and Combined Hypertension

The most recent recommendations of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) have emphasized dietary sodium (salt) restriction as a major lifestyle intervention with which to reduce blood pressure in those with “prehypertension” and as adjunctive therapy in combination with antihypertensive drugs in those with established hypertension.1 The benefit of a reduction in salt intake in lowering blood pressure in many, but not all hypertensive subjects, is well known and widely accepted on the basis of numerous trials.2 Nonetheless, debate continues regarding the extent of restriction required and whether all forms of hypertension benefit. He et al, in this issue of Hypertension , provide new insight into the impact of modest salt restriction on blood pressure in those with isolated systolic hypertension, as well as those with combined systolic–diastolic hypertension by reanalyzing data from 4 previous trials that they conducted.3 Among 24 subjects with isolated systolic hypertension and an average age of 63 years, a mean reduction of urinary sodium excretion from 175 to 87 mmol/d for 1 month resulted in an average decrease of 10/1 mm Hg (systolic/diastolic) (baseline 166/86; intervention 156/85) in blood pressure. These findings are similar to much larger drug intervention studies in such subjects demonstrating significant decreases in systolic pressure without appreciable changes in diastolic pressure. Among 88 younger (average age, 55 years) subjects with systolic/diastolic hypertension, a reduction from 175 to 98 mmol/d in average sodium excretion resulted in an …

Effects of bupivacaine used with sevoflurane on the rhythm and contractility in the isolated rat heart.

The effects of sevoflurane on bupivacaine cardiotoxicity are mainly attributed to systemic effects. The purpose of this study was to investigate the direct myocardial effects of sevoflurane on bupivacaine toxicity. Hearts of 30 Wistar albino rats were isolated and mounted on a Langendorff apparatus perfused by modified Tyrode solution. Experimental groups were: a sevoflurane group (Group S, n = 10)--following baseline and 20 min (Stage 1) recordings, sevoflurane was added in doses of 1.4% (1 MAC) and 2.8% (2 MAC). In the two bupivacaine groups, bupivacaine 5 micromol (Group B5, n = 10) and bupivacaine 10 micromol (Group B10, n = 10) was added to the solution at Stage 1, and sevoflurane was added to the system as in Group S. Haemodynamic variables, i.e. heart rate, PR interval, QRS duration, left ventricular systolic pressure, contractility (+dp/dtmax), relaxation, time to reach peak systolic pressure, change in left ventricular diastolic pressure from baseline, and rate-pressure product were recorded. In Group S, there was no change in cardiac rhythm. In bupivacaine groups, severe rhythm disturbances occurred and both the PR intervals and QRS complexes were prolonged significantly. All contractility variables deteriorated and the rate-pressure product decreased by 67-90% with the addition of bupivacaine. In all groups, 2 MAC sevoflurane lowered +dp/dtmax further. Sevoflurane does not have any untoward effect on bupivacaine-induced cardiotoxicity in clinically relevant doses in the isolated rat heart.

Immediate effects of atrial contribution loss in sequentially paced patients demonstrated by non-invasive hemodynamic monitoring using the Finometer device.

was to find out which of the output parameters of a noninvasive finger arterial pressure evaluation device (Finometer®) is most sensitive to abrupt changes in systolic output of the left ventricle induced by loss of atrial contribution. A total of 15 hemodynamically stable patients aged 67±15 years were enrolled. All patients had dual chamber pacemakers enabling alternation between an atrioventricular delay (AVD) 170ms (period A) to an AVD 50ms (period B), while maintaining a constant heart rate and constant RR intervals. Beat-to-beat changes in systolic (sBP), diastolic (dBP) and mean (MP) arterial pressure and cardiac output (CO – calculated by the device from the shape of the individual pressure waves) were analyzed in a period of seven minutes in each setting. After the switchover, an average drop in CO (22%), sBP (15%), dBP (7%) and MP were recorded (period B). At the end of the seven-minute period (period C) all parameters returned to initial values apart from CO (lower by 9.4%, P &#60; 0.001). The abrupt fall in atrial contribution causes a drop in arterial pressure and CO. While the CO remains decreased, arterial pressure returns to the control level within 7 minutes. The Finometer device enables very sensitive analysis of hemodynamic changes induced by manipulation of the systolic output of the left ventricle.

EFFECTS OF WEAK EXTERNAL MECHANICAL FORCE STIMULATION ON THE HEART RATE VARIABILITY OF RATS

Motivation: The heartbeat is driven by electric signals generated inside the heart, the cardiac conducting system plays an important role. Although there are pharmacological and electrical methods working on this conducting system, effect of mechanical stimulation has rarely been discussed. Methods: We used waterbed (size 60×40×10 cm) as a media to study the heart rate variability (HRV) affected by beating the bed with weak mechanical force with 0.5-mm-Hg amplitude. The waterbed is specially designed to raise the transmission efficiency for sound wave. Results: Among 7 studies on 5 rats, there were almost no changes in diastolic pressure, systolic pressure and heart rate, but average of CV (coefficient of variance) of 15-minute heart rate sequences increased from the control value 0.0098±0.0023 (mean±SD) to 0.0119±0.0032 (mean±SD) during the stimulation and decreased to 0.0078±0.0020 (mean±SD) in 15 minutes after the stimulation [p values (paired t-test, both compared with the control) &lt; 0.006 and &lt; 0.0007 respectively]. Discussion: Here we show that such a weak mechanical stimulation was sufficient to affect the circulatory system. Since the effect is not directly acting on the conducting system, this small power may influence the arterial system through resonance mechanism.

Relations of Serum Uric Acid to Longitudinal Blood Pressure Tracking and Hypertension Incidence

Serum uric acid (UA) has been implicated in the pathogenesis of hypertension. We investigated the relationship of serum UA to hypertension incidence and blood pressure (BP) progression in 3329 Framingham Study participants (mean age 48.7 years; 55.6% women) free of hypertension, myocardial infarction, heart failure, renal failure, or gout. At follow-up 4 years from baseline, 458 persons (13.8%) had developed hypertension, and 1201 persons (36.1%) had experienced progression to a higher BP stage. Age- and sex-adjusted rates of hypertension incidence increased progressively from 9.8% for the lowest quartile to 15.6% for the top quartile of serum UA; BP progression rates increased from 32.8% (lowest quartile) to 39.6% (top quartile). In multivariable analyses adjusting for age, sex, body mass index, diabetes, smoking, alcohol intake, serum creatinine, proteinuria, glomerular filtration rate, baseline BP, and interim weight change, a 1 SD higher serum UA was associated with an odds ratio (OR) of 1.17 (95% confidence interval [CI], 1.02 to 1.33) for developing hypertension, and an OR of 1.11 (95% CI, 1.01 to 1.23) for BP progression. In analyses of a subsample of 3157 individuals not on antihypertensive treatment at the follow-up examination, serum UA was positively associated with changes in systolic (P=0.02) and diastolic pressure 4 years later (P=0.04). In summary, serum UA level was an independent predictor of hypertension incidence and longitudinal BP progression at short-term follow-up in our community-based sample.

Do Pulmonary Hemodynamics Change After Effective Lung Volume Reduction Surgery for Emphysema?

The improvement in lung function, exercise test, blood gas levels, and symptoms in emphysema patients after volume reduction surgery is a result of improvements in breathing mechanics. The question is, is the improvement in the condition related to pulmonary hemodynamics? Few studies have examined pre- and postoperative pulmonary pressure. This paper examines whether there is any significant change in systolic and diastolic pulmonary pressure after effective volume reduction surgery. From October 1999 to October 2002, 12 emphysema patients who underwent volume reduction surgery were studied. Systolic and diastolic pulmonary pressures were measured 2 days before surgery through cardiac catheterization and 2 days after removal of the chest tubes through Swan Ganz catheters placed in the operating room just before surgery. Patients were stable and breathed without assistance during the postoperative pressure measurement. Blood gas analysis, lung function tests, and a 6-minute walk test were performed preoperatively and 3 months postoperatively. The two sets of data were compared using the Wilcoxon signed rank test. There was no significant change in pulmonary hemodynamics, although pulmonary function improved. The improvement in pulmonary function after volume reduction surgery is not related to pulmonary hemodynamics.

Acute β-Blockade Increases Muscle Sympathetic Activity and Modifies Its Frequency Distribution

The possible mechanisms by which beta-adrenergic antagonists may act on the neural regulation of the cardiovascular system are still elusive. Recent studies reported a marked increase of postganglionic muscle sympathetic nerve activity (MSNA) after acute beta-blockade associated with unchanged values of arterial blood pressure and baroreflex sensitivity. We tested the hypothesis that acute beta-blockade might also alter the oscillatory characteristics of MSNA, thus decreasing its effectiveness on peripheral vasoconstriction. In 11 healthy volunteers, ECG, MSNA, arterial pressure, and respiration were recorded before and after atenolol (0.05 mg/kg IV bolus) administration. The frequency distribution of RR interval, MSNA, systolic arterial pressure (SAP), and respiratory variability was assessed by spectrum and cross-spectrum analysis. Spontaneous baroreflex sensitivity (alpha-index) and plasma catecholamines (high-performance liquid chromatography) were measured. Atenolol induced a significant increase in RR interval (14.3+/-1.6%) with no changes in systolic and diastolic arterial pressure. MSNA increased (42+/-13% from 18+/-2 bursts per minute). The low-frequency (LF) component of RR and MSNA variability decreased (-44+/-7% and -24+/-5%, respectively), whereas the high-frequency (HF) component increased (163+/-55% and 34+/-11%, respectively), expressed in normalized units. Spectral coherence, an index of oscillatory coupling, decreased between LF(RR) and LF(MSNA), whereas it increased between HF(MSNA) and HF(Resp). SAP variability, alpha-index, and plasma catecholamines remained unchanged. Atenolol induced a change in MSNA frequency distribution reflecting a stronger respiratory coupling. This shift toward high frequency, despite an increase in MSNA, may lead to a less efficient sympathetic vasomotor modulation.

Effects of coil closure of patent ductus arteriosus on left anterior descending coronary artery blood flow using transthoracic Doppler echocardiography

Transthoracic Doppler echocardiography provides noninvasive measurements of coronary blood flow in the left anterior descending coronary artery (LAD). This method has the potential to show the effects of acute changes in loading conditions on blood flow. Coil closure of patent ductus arteriosus (PDA) is a model of acute changes in blood pressure and left ventricular (LV) preload that influences coronary blood flow. We applied this technique to assess the coronary blood flow changes for patients with PDA before and immediately after PDA coil closure. We examined 9 patients (1.8 ± 1.1 years) with simple PDA and 8 age-matched healthy children. LV dimensions and LV mass were measured. Maximum peak flow velocity and flow volume in the LAD were measured. Pulmonary to systemic flow ratios (Qp/Qs) were obtained by cardiac catheterization. After PDA coil closure, LV end-diastolic dimension decreased, and systolic and diastolic blood pressures increased significantly. The maximum peak flow velocity, LAD flow volume, and the ratio of LAD flow volume to LV mass increased significantly. The changes in maximum peak flow velocity and the ratio of LAD flow volume to LV mass (F/M) correlated positively with the changes in diastolic pressure and Qp/Qs. In 5 patients who had Qp/Qs > 1.5, the mean F/M was significantly lower compared with control subjects, but they increased to normal values after coil closure of PDA. PDA coil closure increases diastolic pressure and decreases Qp/Qs, resulting in improvement of myocardial perfusion. These findings provide new insights into the relationship between cardiac function and coronary circulation in pediatric patients with heart diseases associated with PDA.

Regression of electrocardiographic left ventricular hypertrophy predicts regression of echocardiographic left ventricular mass: the LIFE study

The electrocardiogram (ECG) is widely used for detection of left ventricular hypertrophy (LVH). However, whether changes in ECG LVH during antihypertensive therapy predict changes in LV mass remains unclear. Baseline and year-1 ECGs and echocardiograms were assessed in 584 hypertensive patients with ECG LVH by Sokolow-Lyon or Cornell voltage-duration product criteria at entry into the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. A >/=25% decrease in Cornell product defined regression of ECG LVH; a <25% decrease defined no significant regression; and an increase defined progression of ECG LVH. Regression of echocardiographic LVH was defined by a >/=20% reduction in LV mass. After 1 year of therapy, 155 patients (27%) had regression of ECG LVH, 286 (49%) had no significant change, and 143 (25%) had progression of ECG LVH. Compared with patients with progression of ECG LVH, patients with no significant decrease and patients with regression of ECG LVH had stepwise greater absolute decreases in LV mass (-16+/-33 vs -29+/-37 vs -32+/-41 g, P<0.001), greater percent reductions in LV mass (-5.7+/-14.6 vs -11.3+/-13.6 vs -12.3+/-15.6%, P<0.001), and were more likely to decrease LV mass by >/=20% (11.2 vs 24.8 vs 36.1%, P<0.001), even after adjusting for possible effects of baseline and change in systolic and diastolic pressures. Compared with progression of ECG LVH, regression of the Cornell product ECG LVH is associated with greater reduction in LV mass and a greater likelihood of regression of anatomic LVH.

Familial and genomic analyses of postural changes in systolic and diastolic blood pressure.

The physiological adaptation to the erect posture involves integrated neural and cardiovascular responses that might be determined by genetic factors. We examined the familial- and individual-specific components of variance for postural changes in systolic and diastolic blood pressure in 767 volunteer nuclear adult families from the Victorian Family Heart Study. In 274 adult sibling pairs, we made a genome-wide scan using 400 markers for quantitative trait loci linked with the postural changes in systolic and diastolic pressures. Overall, systolic pressure did not change on standing, but there was considerable variation in this phenotype (SD=8.1 mm Hg). Familial analyses revealed that 25% of the variance of change in systolic pressure was attributable to genetic factors. In contrast, diastolic pressure increased by 6.3 mm Hg (SD=7.0 mm Hg) on standing and there was no evidence of contributory genetic factors. Multipoint quantitative genome linkage mapping suggested evidence (Z=3.2) of linkage of the postural change in systolic pressure to chromosome 12 but found no genome-wide evidence of linkage for the change in diastolic pressure. These findings suggest that genetic factors determine whether systolic pressure decreases or increases when one stands, possibly as the result of unidentified alleles on chromosome 12. The genetics of postural changes in systolic blood pressure might reflect the general buffering function of the baroreflex; thereby, the predisposition to sudden decreases or increases in systolic pressure might cause postural hypotension or vessel wall disruption, respectively.

Decreased cardiac output in humans during laparoscopic antireflux surgery: direct measurements.

In a porcine model, we demonstrated that laparoscopic Nissen fundoplication causes a significant drop in cardiac output (30%) because it exposes both the peritoneal cavity and the mediastinum to CO(2) under pressure. To determine if this occurs in humans, we examined cardiovascular physiology during laparoscopic Nissen fundoplication. Because of invasiveness required in this pilot trial, only six patients were studied. The arterial blood pressure (via radial arterial catheter) and the pulmonary artery diastolic pressure and cardiac index (via pulmonary artery thermodilution catheter) were measured at seven points in time during each laparoscopic Nissen fundoplication. The systolic blood pressure decreased in all patients, and the cardiac index decreased in all but one patient. The exception was a patient with Huntington disease, in whom the cardiac output did not decrease. In four of the five patients, the cardiac output was lowest during hiatal dissection, and in the fifth, it was lowest after reverse Trendelenburg positioning. No significant change in the pulmonary artery diastolic pressure was noted. All patients received adequate intravenous fluid replacement (average, 58 +/- 16 mL/kg) to support blood pressure. In one patient, with a particularly large paraesophageal hernia, profound hypotension (40/25 mm Hg) developed during the mediastinal phase of the procedure, and this patient required alpha-adrenergic support followed by laparotomy to eliminate a surgical cause (none found). Although it is a tremendous advance for patients, laparoscopic Nissen fundoplication can be associated with a significant reduction in cardiac output and blood pressure. Surgeons and anesthesiologists must be alert to changes reflecting these decreases during procedures, which violate both the peritoneal cavity and the mediastinum. We propose careful hemodynamic monitoring during these procedures, especially in patients with coronary artery disease or significant left ventricular dysfunction.

Effects of bupivacaine used with sevoflurane on the rhythm and contractility in the isolated rat heart

Background and objective: The effects of sevoflurane on bupivacaine cardiotoxicity are mainly attributed to systemic effects. The purpose of this study was to investigate the direct myocardial effects of sevoflurane on bupivacaine toxicity. Methods: Hearts of 30 Wistar albino rats were isolated and mounted on a Langendorff apparatus perfused by modified Tyrode solution. Experimental groups were: a sevoflurane group (Group S, n = 10) - following baseline and 20 min (Stage 1) recordings, sevoflurane was added in doses of 1.4% (1 MAC) and 2.8% (2 MAC). In the two bupivacaine groups, bupivacaine 5 μmol (Group B5, n = 10) and bupivacaine 10 μmol (Group B10, n = 10) was added to the solution at Stage 1, and sevoflurane was added to the system as in Group S. Haemodynamic variables, i.e. heart rate, PR interval, QRS duration, left ventricular systolic pressure, contractility (+dp/dtmax), relaxation, time to reach peak systolic pressure, change in left ventricular diastolic pressure from baseline, and rate-pressure product were recorded. Results: In Group S, there was no change in cardiac rhythm. In bupivacaine groups, severe rhythm disturbances occurred and both the PR intervals and QRS complexes were prolonged significantly. All contractility variables deteriorated and the rate-pressure product decreased by 67-90% with the addition of bupivacaine. In all groups, 2 MAC sevoflurane lowered +dp/dtmax further. Conclusions: Sevoflurane does not have any untoward effect on bupivacaine-induced cardiotoxicity in clinically relevant doses in the isolated rat heart.

Effect of human urotensin-II infusion on hemodynamics and cardiac function.

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by +/-dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.

Blood pressure and pulse pressure development in a population sample of women with special reference to basal body mass and distribution of body fat and their changes during 24 years.

To study blood pressure and pulse pressure longitudinally and their association with basal and change of body mass index (BMI) and waist to hip ratio (WHR). A prospective population study of 1462 women in Gothenburg, Sweden, aged 38-60 y at baseline, with a longitudinal follow-up of 24 y. Incidence of hypertension, systolic and diastolic blood pressure, and pulse pressure at baseline and after 12 and 24 y of follow-up. Systolic and diastolic blood pressure as well as pulse pressure increased with age and turned down again at high age. BMI and WHR at baseline were each independently associated with baseline systolic and diastolic blood pressure, but only BMI with pulse pressure. However, baseline BMI and WHR were not associated with change of systolic, diastolic or pulse pressure during 12 or 24 y of follow-up. Increase in BMI during the follow-up period was associated with increase in systolic and diastolic blood pressure but not with increase in pulse pressure. There were no such associations with WHR changes which, were either unrelated or in one analysis inversely related with blood pressure changes. When considering incidence of hypertension during the first 12 y of follow-up, BMI and change in BMI were significant predictors, independent of WHR. Age, BMI and increments in BMI seem to be strong predictors for hypertension and increased systolic and diastolic blood pressure in women. In contrast, WHR plays a lesser and uncertain role in the development of hypertension in middle-aged women. Changes in BMI seem not to be accompanied by changes in pulse pressure during a long time follow-up.