The effect of ephedrine and phenylephrine on BIS values during propofol anaesthesia.

BACKGROUND: The purpose of this study was to evaluate the effect of ephedrine and phenylephrine on propofol concentrations and bispectral index during propofol anesthesia. METHODS: General anaesthesia was induced with propofol and was maintained with propofol (4 mg kg-1 h-1) and fentanyl. Vecuronium was used to facilitate the artificial ventilation of the lungs. Patients with systolic blood pressure > 90 mmHg were defined as the control group (n = 16). Patients who had to be treated for larger decreases in arterial blood pressure (systolic blood pressure 60, whereas no patient in the control or phenylephrine groups had bispectral index >60. There were no significant differences in propofol concentrations or cardiac output relative to baseline at 3 or 10 min after the administration of ephedrine or phenylephrine. CONCLUSIONS: Ephedrine increases bispectral index values without decreasing propofol concentrations during general anesthesia.

Slow rewarming improves jugular venous oxygen saturation during rewarming.

BACKGROUND: There have been many studies regarding the etiology of postoperative cognitive dysfunction after coronary artery bypass graft (CABG) surgery. Although its etiology remains unresolved, one possible factor related to postoperative cognitive dysfunction is a reduced internal jugular venous oxygen hemoglobin saturation (SjvO2) during the rewarming period. The purpose of this study was to examine the effect of rewarming rates on SjvO2 during rewarming. METHODS: One-hundred patients scheduled for elective CABG surgery were randomly divided into two groups; control group (0.48 +/- 0.09 degrees C, n = 50), slow rewarming group (0.24 +/- 0.09 degrees C, n = 50). After the induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor SjvO2 continuously. Hemodynamic parameters, arterial and jugular venous blood gases were measured at nine time-points. RESULTS: Cerebral desaturation (defined as a SjvO2 value below 50%) during rewarming was more frequent in the control group than in the slow group. Cerebral desaturation time (duration when SjvO2 was less than 50%) and the ratio of the cerebral desaturation time to the total CPB time in the control group differed significantly from those in the slow group (control group: 17 +/- 11 min, 12 +/- 4%, slow group: 10 +/- 8 min, 7 +/- 4%, respectively, P < 0.05). There was no significant difference in mini-mental state examination on the day before the operation nor at 1 month after the surgery among four values (the day before the operation: control group; 48 +/- 8, slow group; 48 +/- 7, at one month after the surgery: control group; 46 +/- 7, slow group; 45 +/- 9). CONCLUSIONS: A slow rewarming rate could reduce the chance of a decrease in SjvO2 during rewarming.

Inhibition by docosahexaenoic acid of receptor-mediated Ca(2+) influx in rat vascular smooth muscle cells stimulated with 5-hydroxytryptamine.

The effect of docosahexaenoic acid treatment on intracellular Ca(2+) dynamics in rat vascular smooth muscle cells stimulated with 5-hydroxytryptamine (5-HT) has been investigated in order to elucidate one of the mechanisms for its beneficial effect on cardiovascular disorders. The treatment of cells with 30 microM docosahexaenoic acid for 2 days inhibited an increase in intracellular Ca(2+) concentration induced by 5-HT (10 microM) and a depolarizing concentration of KCl (80 mM). Docosahexaenoic acid treatment significantly inhibited divalent cation influx stimulated by 5-HT and KCl, as measured by Mn(2+) quenching method, whereas had no effect on 5-HT-induced Ca(2+) release from the internal stores. Docosahexaenoic acid treatment also significantly inhibited 5-HT receptor-mediated Ca(2+) influx through Ni(2+)-insensitive channels that were distinct from store-operated channels. These results suggest that the specific inhibition of intracellular Ca(2+) dynamics in vascular smooth muscle cells may contribute to the beneficial properties of docosahexaenoic acid on cardiovascular disorders.

HPLC determination of cyanuric acid in swimming pool waters using phenyl and confirmatory porous graphitic carbon columns.

The chlorinated salts of cyanuric acid have found an important role in recreational swimming pool waters across the United States. Upon application to pool water, they can (1) release disinfectant chlorine or (2) stabilize the free available chlorine by acting as chlorine reservoirs in the form of cyanuric acid, preventing the photolytic destruction of residual chlorine by sunlight. Recommended levels of the cyanuric acid stabilizer are in the 10-100 mg/L concentration range according to the National Swimming Pool Foundation (San Antonio, TX). Two isocratic HPLC methods with UV detection (213 nm) employing phenyl and porous graphitic carbon (PGC) columns and phosphate buffer eluents (pH 6.7 and pH 9.1, respectively) were developed to accurately measure cyanuric acid in swimming pools. The two methods allowed fast separation and detection of the stabilizer in 4 (phenyl) and 8 (PGC) min. Both methods offered practical sensitivities with method detection limits of 0.07 (phenyl) and 0.02 mg/L (PGC). Neither one of the two methods required the use of sample cleanup cartridges. They exhibit chromatograms with excellent baseline stability enabling low-level quantitation. Most important, the PGC column had a useful lifetime of five months and 500 sample analyses/column. Eleven pool water samples were fortified with 4.8-50.0 mg/L stabilizer, and the average recovery was 99.8%. Finally, statistical analysis on the relative precisions of the two methods indicated equivalence at the 0.05 critical level.

An HPLC method with UV detection, pH control, and reductive ascorbic acid for cyanuric acid analysis in water.

Every year over 250 million pounds of cyanuric acid (CA) and chlorinated isocyanurates are produced industrially. These compounds are standard ingredients in formulations for household bleaches, industrial cleansers, dishwasher compounds, general sanitizers, and chlorine stabilizers. The method developed for CA using high-performance liquid chromatography (HPLC) with UV detection simplifies and optimizes certain parameters of previous methodologies by effective pH control of the eluent (95% phosphate buffer: 5% methanol, v/v) to the narrow pH range of 7.2-7.4. UV detection was set at the optimum wavelength of 213 nm where the cyanuric ion absorbs strongly. Analysis at the lower pH range of 6.8-7.1 proved inadequate due to CA keto-enol tautomerism, while at pHs of <6.8 there were substantial losses in analytical sensitivity. In contrast, pHs of >7.4 proved more sensitive but their use was rejected because of CA elution at the chromatographic void volume and due to chemical interferences. The complex equilibria of chlorinated isocyanurates and associated species were suppressed by using reductive ascorbic acid to restrict the products to CA. UV, HPLC-UV, and electrospray ionization mass spectrometry techniques were combined to monitor the reactive chlorinated isocyanurates and to support the use of ascorbic acid. The resulting method is reproducible and measures CA in the 0.5-125 mg/L linear concentration range with a method detection limit of 0.05 mg/L in water.

Left ventricular aneurysm without coronary artery disease, incidence and clinical features: clinical analysis of 11 cases.

OBJECTIVE: To examine the incidence, underlying disease and clinical features of left ventricular aneurysm (LVA) not related to coronary artery occlusion. METHODS: Retrospective review of consecutive patients who underwent both left ventriculography and coronary angiography. PATIENTS: LVA was confirmed in 11 of 2,348 consecutive patients (0.47%). RESULTS: The location of LVA was mainly in the apical region (81.8%). In five of the 11 patients (45.5%), the underlying heart disease was hypertrophic cardiomyopathy (HCM), including 4 patients of dilated phase and one patient of midventricular type. The serial ECG changes from left ventricular hypertrophy to abnormal Q wave and endomyocardial biopsy were useful for the differential diagnosis of these cases against myocardial infarction. The underlying disease of the remaining patients was: myocarditis (2 patients), arrhythmogenic right ventricular dysplasia (1 patient), Chagas' disease (1 patient), glycogen storage disease (1 patient), and sarcoidosis (1 patient). Ventricular tachycardia appeared in 9 of 11 cases (81.8%) including 2 patients with sustained ventricular tachycardia. CONCLUSION: LVA formation without coronary artery disease was a rare phenomenon. The underlying disease was varied but the incidence of hypertrophic cardiomyopathy in the dilated phase was comparatively high. Ventricular tachycardia was a significant complication in these patients.

Jugular venous bulb oxygen saturation in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass.

BACKGROUND: The authors hypothesized that patients with cerebrovascular abnormalities or metabolic disorders may experience abnormality in cerebral circulation more frequently than patients without these risks. The current study attempted to assess jugular venous bulb oxygen saturation (SjvO2) in patients with preexisting diabetes mellitus or stroke undergoing normothermic cardiopulmonary bypass. METHODS: Thirty-nine patients undergoing elective coronary artery bypass graft surgery were studied, including 19 age-matched control patients, 10 diabetic patients, and 9 patients with preexisting stroke A 4.0-French fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor internal SjvO2. Hemodynamic parameters and arterial and jugular venous blood gases were measured at seven time points: (1) after the induction of anesthesia and before the start of surgery, (2) just after the beginning of cardiopulmonary bypass, (3) 20 min after the beginning of bypass, (4) 40 min after the beginning of bypass, (5) 60 min after the beginning of bypass, (6) just after the cessation of bypass, and (7) at the end of the operation. RESULTS: No significant differences were seen in mean arterial pressure, arterial carbon dioxide tension (PaCO2), or hemoglobin concentration among the three groups during the study. The SjvO2 value did not differ among the three groups after anesthesia induction and before surgery, just after the beginning of cardiopulmonary bypass, 60 min after the beginning of bypass, just after the end of bypass, or at the end of the operation. Significant differences between the control group and the diabetic and stroke groups were observed, however, at 20 min and 40 min after the beginning of bypass (at 20 min: control group 62.2 +/- 6.8%, diabetes group 48.4 +/- 5.1%, stroke group 45.9 +/- 6.3%; at 40 min: control group 62.6 +/- 5.2%, diabetes group 47.1 +/- 5.2%, stroke group 48.8 +/- 4.1% [values expressed as the mean +/- SD]; P < 0.05). Also, values in the diabetes and stroke groups were decreased at 20 min and 40 min after the beginning of bypass compared with before the start of surgery. CONCLUSIONS: A reduced SjvO2 value was observed more frequently in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass. It is possible that cerebral circulation during normothermic bypass is altered in patients with risk factors for cerebrovascular disorder.

[Malfunctioning of cerebral function monitors in three cases of carotid endarterectomy].

In three patients, EEG, jugular venous oxygen saturation (Sjvo2) and near infrared spectroscopy (NIRS) were monitored to detect cerebral ischemia during carotid endarterectomy. In all cases, no changes in Sjvo2 and NIRS were observed during carotid artery occlusion, but in two patients EEG showed changes when carotid artery was clamped. It is important to know the precise mechanism of cerebral monitors to assess the cerebral ischemia in patients with preexisting neurological disorder during carotid endarterectomy.

Activation of matrix metalloproteinase-2 in human breast cancer cells overexpressing cyclooxygenase-1 or -2.

Human breast cancer cell line Hs578T was stably transfected with cDNA for cyclooxygenase-1 or -2. When the cells overexpressing cyclooxygenase-1 or -2 were stimulated with concanavalin A, the processing of matrix metalloproteinase-2 was observed with the aid of gelatin zymography. This processing was not seen in mock-transfected and original cells which did not express detectable cyclooxygenase activity. Furthermore, Northern blotting showed 8-13 fold induction of membrane-type 1 matrix metalloproteinase which processed matrix metalloproteinase-2 in the cells expressing cyclooxygenases. These findings suggest that both isoforms of cyclooxygenase mediate the processing of matrix metalloproteinase-2 through induction of membrane-type I metalloproteinase in breast cancer cells.

Chronic Chagas' heart disease in a Japanese-Brazilian traveler. A case report.

A 57-year-old Japanese-Brazilian man, visiting Japan for only 9 days, was admitted to our hospital due to syncope and frequent ventricular premature beats. He grew up in a rural area of Brazil and moved to Sao Paulo in 1959 when he was 20 years old. We suspected chronic Chagas' heart disease, i.e., dilated cardiomyopathy with apical ventricular aneurysm, right bundle branch block with left anterior fascicular block, and various arrhythmias including supraventricular premature beats, ventricular premature beats and non-sustained ventricular tachycardia because he showed typical echo- and electrocardiographic features of the disease. Coronary arteriograms were normal, and left ventriculogram confirmed the existence of apical ventricular aneurysm. A left ventricle biopsy specimen showed hypertrophic cardiac muscle with mild fibrosis. The diagnosis of chronic Chagas' disease was finally confirmed by the demonstration of Trypanosoma cruzi itself in the blood as well as Trypanosoma cruzi antibodies.

5-hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells.

The effects of Ni2+, a non-selective cation channel inhibitor, on 5-hydroxytryptamine (5-HT)- and angiotensin II (Ang II)-induced intracellular Ca2+ dynamics in rat aortic smooth muscle cells were investigated. Ni2+ (1 mM) significantly inhibited the transient increase in intracellular Ca2+ concentration ([Ca2+]i) induced by Ang II (100 nM) in aortic smooth muscle cells, as measured using fura-2. However, Ni2+ did not suppress the transient increase in Ca2+ influx induced by 5-HT (10 microM), while significantly suppressed the sustained increase. Ca2+ influx evoked by high KCl (80 mM), thapsigargin (TG) (1 microM) or depletion of intracellular Ca2+ store was almost completely suppressed by Ni2+. Ni2+ had no effect on 5-HT-induced inositol triphosphate production and Ca2+ release from the intracellular store(s). These results suggest that 5-HT, but not Ang II, induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels, which are distinguishable from the voltage-dependent or store-operated Ca2+ channels.

Effects of hypothermic and normothermic cardiopulmonary bypass on brain oxygenation.

BACKGROUND: In this study, we assessed the effects of normothermia and hypothermia during cardiopulmonary bypass (CPB) both on internal jugular venous oxygen saturation (SjvO2) and the regional cerebral oxygenation state (rSO2) estimated by near infrared spectroscopy (NIRS). METHODS: Thirty patients scheduled for elective coronary artery bypass graft surgery (CABG) were randomly divided into two groups. Group 1 (n = 15) underwent surgery for normothermic (> 35 degrees C) CPB, and group 2 (n = 15) underwent surgery for hypothermic (30 degrees C) CPB, and alpha-stat regulation was applied. A 4.0-French fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor the SjvO2 value. To estimate the rSO2 state, a spectrophotometer probe was attached to the mid-forehead. SjvO2 and rSO2 values were then collected simultaneously using a computer. RESULTS: Neither the cerebral desaturation time (duration during SjvO2 value below 50%), nor the ratio of the cerebral desaturation time to the total CPB time significantly differed (normothermic group: 18+/-6 min, 15+/-6%; hypothermic group: 17+/-6 min, 13+/-6%, respectively). The rSO2 value in the normothermic group decreased during the CPB period compared with the pre-CPB period. The rSO2 value in the hypothermic group did not change throughout the perioperative period. CONCLUSIONS: These findings suggest that near infrared spectroscopy might be sensitive enough to detect subtle changes in regional cerebral oxygenation.

Balloon pump-induced pulsatile perfusion during cardiopulmonary bypass does not improve brain oxygenation.

BACKGROUND: Whether pulsatile flow offers substantial advantages for brain protection during cardiopulmonary bypass is controversial. The purpose of this study is to determine whether differences exist between pulsatile and nonpulsatile bypass concerning the effects on internal jugular venous saturation and on the state of regional cerebral oxygenation during normothermia. METHODS: Twenty-two patients undergoing elective coronary artery bypass grafting were randomly divided into 2 groups: group 1 (n = 11) received nonpulsatile perfusion during cardiopulmonary bypass and group 2 (n = 11) received pulsatile perfusion during bypass. We used an intra-aortic balloon pump to generate pulsatility. A spectrophotometric probe (INVOS 3100R, Somanetics, Troy, Mich) was used to assess the state of regional cerebral oxygenation. A 4F fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor jugular venous oxygen saturation. Hemodynamic variables, arterial and jugular venous blood gases, and regional cerebral oxygenation were measured at 7 times points. RESULTS: In both groups, jugular venous oxygen saturation decreased at the early stage of the cardiopulmonary bypass (P =.03). Five patients in group 1 and 6 in group 2 had a jugular venous oxygen saturation of less than 50%. In both groups, the regional cerebral oxygenation value decreased during cardiopulmonary bypass (P =.04). CONCLUSIONS: The present results showed that pulsatility generated through the use of intra-aortic balloon pumping did not produce any beneficial effects on jugular venous oxygen saturation and regional cerebral oxygenation at normothermia.

Sentinel lymphadenectomy in breast cancer: identification of sentinel lymph node and detection of metastases.

Sentinel lymphadenectomy is a useful way of assessing axillary status and obviating axillary dissection in patients with node-negative breast cancer. However, controversies remain concerning the optimal method to identify the sentinel lymph node (SLN) and detect micrometastases in this lymph node. We reviewed the literature concerning sentinel lymphadenectomy in breast cancer and reached the following conclusions: (a) A combination of preoperative lymphoscintigraphy with intraoperative dye-guided and gamma probe-guided methods achieves a higher rate of identification of SLN than any of these techniques alone. (b) Immediate and reliable intraoperative assessment of sentinel node status is vital to the technique's success. However, the reliability of sentinel node diagnosis using frozen sections is questionable, because micrometastatic foci cannot always be identified. (c) Hematoxylin and eosin (H&E) staining and/or immunohistochemistry on permanent sections are useful for the detection of micrometastases in the sentinel node. Although a reverse transcriptase-polymerase chain reaction (RT-PCR) method is more sensitive than H&E staining and immunohistochemistry, it would not distinguish benign from malignant epithelial cells in the SLN. Therefore, further study is required before sentinel lymphadenectomy gains general acceptance for patients with primary breast cancer.

Adjuvant chemotherapy with a combination of mitoxantrone, methotrexate, 5-fluorouracil for node-positive breast cancer: phase II pilot study.

A phase II pilot study was carried out on 30 patients to ascertain the toxicity and efficacy of combination chemotherapy with mitoxantrone, methotrexate, 5-fluorouracil (NMF) in the adjuvant setting for axillary lymph node-positive breast cancer. The NMF regimen was mitoxantrone 10 mg/m2, methotrexate 40 mg/m2, and 5-fluorouracil 600 mg/m2 administered i.v. on day 1, repeated every 3-4 weeks for 6 cycles. The median nadir WBC count was 2,000/microl; grade 4 leukocytopenia occurred only in 1 patient. Nausea and vomiting appeared as grade 0 and 1 severity in 26/30 patients. Alopecia was extremely mild, appeared as grade 0 and 1 in 29/30 patients. The overall and relapse-free survival rates were 67.8% and 68.4% at the 82-month follow-up, respectively. The overall survival rate in premenopausal patients was significantly better than that in postmenopausal patients (P<0.05). NMF is a well-tolerated combination regimen, suitable as adjuvant chemotherapy for node-positive breast cancer.

Cerebral oxygenation during prostaglandin E1 induced hypotension.

PURPOSE: To evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E1 (PGE1) during fentanyl-oxygen anaesthesia. METHODS: Ten patients who underwent elective cardiac surgery received infusion of PGE1. After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO2) estimated by INVOS 3100R, PGE1 was continuously infused at 0.25-0.65 microgram.kg-1.min-1 (mean dosage: 410 +/- 41.4 mg.kg-1.min-1) intravenously. Ten, 20 and 30 minutes after the start of drug infusions, blood gases described above were obtained simultaneously with the measurement of systemic haemodynamics and rSO2. Thirty minutes from the start of drug infusions, administration of PGE1 was stopped. The same parameters were measured again 10, 30 minutes after the stop of drug infusion. RESULTS: PGE1 decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE1 increased mixed venous saturation, but in contrast did not affect internal jugular pressure, internal jugular oxygen saturation and rSO2. CONCLUSIONS: These results suggest that PGE1 is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.

Effect of 5-hydroxytryptamine on intracellular calcium dynamics in cultured rat vascular smooth muscle cells.

The present study elucidated the precise mechanism of 5-hydroxytryptamine (5-HT)-induced increase of intracellular Ca2+ concentration ([Ca2+]i) in cultured vascular smooth muscle cells isolated from rat aortic media. [Ca2+]i was measured using fluorescent Ca2+ indicator, fura-2. 5-HT caused a dose-dependent increase in [Ca2+]i, which was completely inhibited by ketanserin. alpha-Methyl-5-HT had an equipotent effect to 5-HT. Diltiazem at 10 microM partially suppressed the 5-HT-induced increase in [Ca2+]i. 5-HT also augmented Mn2+ influx, when monitored by Mn2+ quenching of fura-2 fluorescence. When extracellular Ca2+ (1.3 mM) was removed, a decrease in resting level and a small, transient increase in [Ca2+]i were observed. 5-HT stimulation also induced an increase in the production of inositol triphosphate. 5-HT-induced increase in [Ca2+]i was significantly, but partially inhibited by staurosporin and H-7. Phorbol 12-myristate 13-acetate induced an increase in [Ca2+]i, which was abolished by removal of extracellular Ca2+. 5-HT-induced increase in [Ca2+]i was not affected by the pretreatment with pertussis toxin (PTX), and was not accompanied by a change in cyclic AMP content. These results suggest that, in cultured rat aortic smooth muscle cells, 5-HT increases [Ca2+]i via 5-HT2 receptor subtype by inducing influx of extracellular Ca2+ partially through L-type voltage-dependent Ca2+ channel, as well as by mobilizing Ca2+ from its intracellular stores. Activation of protein kinase C may be positively involved in the regulatory mechanism of Ca2+ influx, but PTX-sensitive G protein and cyclic AMP seem to be not involved.

Effect of docosahexaenoic acid on smooth muscle cell functions.

There is increasing evidence that fish oil-enriched diets attenuate the progression of several types of human and experimental renal, intestinal and cardiovascular disorders, including hypertension. Docosahexaenoic acid (DHA), may be one of the active biological component. We previously reported that dietary DHA suppressed the progression of hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). The purpose of this study is to clarify the in vitro effect of DHA on cultured smooth muscle cell functions such as cell growth, hypertrophy, NO release, and intracellular Ca2+ metabolism, which are involved in the regulatory mechanisms of vascular tone. Addition of DHA to the culture medium of aortic smooth muscle cells isolated from SHRSP and normotensive Wistar Kyoto rats (WKY) had no significant effects on cell growth or on cell hypertrophy induced by angiotensin II as measured by flow cytometry. DHA had no stimulatory effect on interleukin-1beta (10 ng/ml)-induced nitric oxide release from smooth muscle cells of SHRSP, but rather slightly inhibited it. However, the treatment of smooth muscle cells with DHA (30 microM) for 2 days significantly suppressed the increase in intracellular Ca2+ concentration induced by angiotensin II, but not by thapsigargin. This was due to the suppression of Ca2+ influx, as determined by Mn2+ influx experiment. These results indicate that DHA specifically suppresses Ca2+ mobilization into smooth muscle cells. This may be one of the mechanisms by which dietary DHA prevents the development of hypertension in SHRSP.

Effect of docosahexaenoic acid on intracellular calcium dynamics in vascular smooth muscle cells from normotensive and genetically hypertensive rats.

The effects of DHA treatment on intracellular Ca2+ dynamics in aortic smooth muscle cells isolated from young stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched normotensive Wistar Kyoto rats (WKY) were investigated. The resting intracellular Ca2+ concentration ([Ca2+]i) before stimulation and the peak [Ca2+]i induced by 5-HT, angiotensin II and depolarizing concentration of KC1 were higher in SHRSP than in WKY. When added to the culture medium for 2 days, DHA at a concentration of 30 microM significantly suppressed the peak [Ca2+]i induced by these stimulants in aortic smooth muscle cells isolated from WKY, whereas smooth muscle cells of SHRSP were refractory to the suppression. DHA had no suppressive effect on the 5-HT-induced increase in the inositol triphosphate production. The present study indicates that DHA can suppress receptor-mediated Ca2+ influx, at least, through the voltage-dependent channel, in vascular smooth muscle cells. Since the intracellular Ca2+ plays an important role in regulating vascular tone, the suppressive effect of DHA on [Ca2+]i in vascular smooth muscle cells may be contributed to the beneficial properties of DHA on cardiovascular disorders. The precise mechanisms of action remain to be elucidated.

Influence of mild to moderate obesity on left ventricular stress filling pattern in hypertension.

In resting condition, obese subjects are described as having impaired diastolic filling. To examine the effect of mild to moderate obesity on left ventricular diastolic performance during stress in hypertension, we determined the filling responses to dynamic submaximal exercise in 19 obese hypertensive patients (body mass index, 26 to 30 kg/m2) with a normal left ventricular structure, 19 age- and sex-matched, non-obese hypertensive patients, and 19 age- and sex-matched, non-obese normotensive controls (mean age, 55+/-3 yr). Doppler echocardiographic studies were performed at baseline and 1 min after exercise on a supine ergometer bicycle. At rest, systolic function and filling indices, peak velocities of early (E) and late (A) filling, and their ratio (E/A), were similar in the two hypertensive groups, while normotensive controls had higher peak velocities of E and E/A. At a maximum workload of 75 W, blood pressure and heart rate increased similarly in the two hypertensive groups. Peak velocities of E and A increased significantly after exercise. The percentage change in the peak velocity of E was greater in obese hypertensive patients than in non-obese hypertensive patients and normotensive controls (23+/-4 vs. 12+/-3 and 14+/-3%, p < 0.05). Percentage changes in A and E/A were similar in the three groups. Our study suggests that mild to moderate obesity does not further worsen left ventricular diastolic filling at rest and mitigates diastolic filling abnormalities after exercise in hypertensive patients.