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Biomedical subjects

M Safar

Publications and source records attributed to M Safar.

At least 91 records · Page 5Linked to original sources
PubMed1998

Further study on the carotid baroreflex system in the cardiovascular deconditioning induced by head-down tilt.

HYPOTHESIS: The responses of the carotid baroreflex and of the peripheral sympathetic system to stimulations induced by either lower body negative pressure (LBNP -40 mmHg) or cold pressor test were investigated in eight volunteers before and after 48 h in the -6 degrees head-down tilt (HDT). METHODS: Geometry (diastolic diameter and pulsatile distention) and dynamics (cross-sectional compliance and tangential tension) of the bulb and the common carotid artery were investigated using ultrasonic devices, echotracking and aplanation tonometry. The activity of the sympathetic system was evaluated through measurements of plasma concentrations of catecholamines (CAs) and 3,4-dihydroxyphenyl glycol (DHPG). RESULTS: During LBNP -40 mmHg, the pulsed tangential tension was decreased and the pressure amplification, induced by the reflexion of the pressure wave, was increased with no difference between before and after HDT. Since cross-sectional compliance and distensibility coefficient remained unchanged and the carotid contour of the waveform unaltered, it is concluded that the carotid reflexogenic area reads the same message during LBNP whether the cardiovascular system was deconditioned or not. Nonetheless, during LBNP after 48 h HDT, the heart rate accelerated faster and CAs and DHPG concentrations increased out of proportion, suggesting that the peripheral sympathetic activity was more reactive after HDT than before. Finally, forearm vascular resistances were measured in response to cold pressor test; they increased in the same proportion after HDT when compared with before. CONCLUSION: Results indicate that the carotid baroreflex and the peripheral sympathetic system were not deficient after 48 h HDT.

Adolescent↗
PubMed1998

[Arterial hypertension, non-drug treatment and cardiovascular risk].

Four non-drug measures have been shown to be effective on reduction of blood pressure: low-salt diet, weight loss, reduction of alcohol consumption and sports activity. Other measures, mainly dietary (increased potassium intake, DASH diet), may also be effective. The two limits to non-drug treatment of HT are the absence of demonstrated benefit in terms of cardiovascular morbidity-mortality, and the difficulty to ensure good patient compliance with this type of often constraining measure. However, these non-drug measures could probably decrease the overall level of cardiovascular risk. The main drawback, related to the required modification of the patient's lifestyle, is poor compliance with these measures. Compliance can be improved by various methods which share in common their time-consuming nature.

Alcohol Drinking↗
PubMed1997

[Conn's syndrome. Study of systemic cardiovascular hemodynamics after medical treatment with spironolactone and after surgical treatment].

OBJECTIVES: Assess hemodynamic effect of Conn's syndrome in order to better prepare patients for surgical resection of their adenoma. PATIENTS AND METHODS: Hemodynamic investigations were conducted before any treatment in 13 patients with Conn's syndrome. Results were compared with those in 13 control subjects with permanent primary hypertension. In the 13 patients with Conn's syndrome, the same hemodynamic parameters were studied in 13 after drug therapy using spironolactone and in 8 after surgery. RESULTS: Hypertension was associated with a significant increase in stroke volume and a non-significant increase in cardiac index. Blood pressure normalized after sprironolactone and after surgery in parallel with a significant decrease in blood volume. DISCUSSION: These hemodynamic disorders in Conn's disease patients suggest that the increase in stroke volume is a consequence of increased venous return and more likely, in myocardium contractility or a combination of both. CONCLUSION: These hemodynamic characteristics of Conn's disease should be useful in guiding monitoring schemes for these patients in the perioperative period.

Adolescent↗
PubMed1997

Improvement of internal jugular vein cannulation using an ultrasound-guided technique.

OBJECTIVE: To determine whether ultrasound guidance can help operators to improve the results of jugular vein access in the ICU. DESIGN: Prospective, randomized study. SETTING: General Intensive Care Unit of a University Hospital. PATIENTS: Seven-nine patients were assigned to internal jugular vein cannulation using anatomical landmarks alone (control group, n = 42) or with ultrasound guidance (ultrasound group, n = 37). INTERVENTION: All cannulations were performed by junior house staff under the direct supervision of a senior physician. In the ultrasound group, an ultrasonography (7.5 MHz) was used and the transducer was covered by a sterile sheath. The placement and direction of the cannulating needle were determined on the ultrasound image. MEASUREMENTS AND RESULTS: Internal jugular vein cannulation was successful in 37/37 (100%) patients in the ultrasound group and in 32/42 patients (76%) in the control group (p < 0.01). Average access time was longer in the control group (235 +/- 408 s vs 95 +/- 174 s, p = 0.06) and carotid artery puncture occurred in five patients in each group (p = 0.83). Jugular cannulation was successful at the first attempt in 26% in the control group and 43% in the ultrasound group (p = 0.11). Thirty-two patients (86%) in the ultrasound group and 23 patients (55%) in the control group (p < 0.05) were cannulated within 3 min. The cannula could therefore not be inserted within 3 min in 19 patients (45%) in the control group. Failure was explained by thrombosis (n = 1), small caliber of the internal jugular vein (< 5 mm, n = 3), abnormal vascular relations (n = 3). Among the ten primary failures of cannulation, an internal jugular vein catheter was able to be inserted in four cases by an experienced physician on the side initially selected and with ultrasound guidance in two cases. The catheter was inserted into the contralateral internal jugular vein under ultrasound guidance in the remaining four cases. CONCLUSION: Ultrasound guidance improved the success rate of jugular vein cannulation in ICU patients. Our results suggest that ultrasound guidance should be used when the internal jugular vein has not been successfully cannulated within 3 min by the external landmark-guided technique.

Aged↗
PubMed1997

Red blood cells participate in the metabolic clearance of catecholamines in the rat.

The aim of the present study was to investigate the possible role of erythrocytes in the metabolic clearance of catecholamines (CAs) in the rat. Intravenous infusion of exogenous CAs (dopamine -DA-, norepinephrine -NE-, or epinephrine -Epi-) was carried out at increasing doses to cover a range of plasma concentrations from the lower to the upper physiological and to pharmacological levels. Whatever the mechanism(s) underlying the CAs erythrocyte/plasma balance: 1. it seemed more efficient at lower concentrations of CAs; 2. it reached an apparent plateau where plasma and erythrocyte concentrations were not statistically different; 3. finally, saturation was suggested when further increase in plasma concentration was associated with a lower response in erythrocytes. This series of experiments confirms previous reported results with human erythrocytes and suggests that rat erythrocytes could transport CAs from their sites of release to their sites of elimination. In a second series of experiments, the intra-erythrocyte metabolism of CAs was investigated. DA was strikingly increased in plasma and in erythrocytes 2 hours after 1,2-dimethyl-3-hydroxy-4-pyridone (CP20), 100 mg/kg i.p., known to inhibit catechol-O-methyl transferase. Our data demonstrate an increase in glucuro-conjugated DA in vivo (24 hours after CP20 injection) as well as in vitro (3 hours incubation at 37 degrees C), suggesting activation of the glucuroconjugating pathway. Increased glucuroconjugated DA after in vitro incubation demonstrates intra-erythrocyte synthesis while increased concentration in Ringer-Hepes medium demonstrates an inside-out transport of glucuro-conjugate. These data are the first evidence in favour of an intra-erythrocyte glucuro-conjugation of CAs in the rat.

Animals↗
PubMed1997

Role of endothelium in the endothelin-1-mediated potentiation of the norepinephrine response in the aorta of hypertensive rats.

OBJECTIVE: To investigate the role of the endothelium in the functional interaction between endothelin-1 and norepinephrine in the contractile response of aortas from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: Thoracic aorta rings with and without endothelium from SHR and from WKY rats were suspended in an organ bath to record the isometric tension. After an equilibration period of 120 min, the preparations with and without endothelin-1 were subjected to single and cumulative additions of norepinephrine in different experiments. To characterize the mechanisms involved in the interaction between endothelin-1 and norepinephrine, the aortic rings were pretreated with a cyclooxygenase pathway inhibitor (piroxicam, SO29548), an inhibitor of NO synthase [NG-nitro-L-arginine (NLA)], or selective endothelin receptor blockers (BQ-123 or BQ-788). In some experiments we examined the contractile responses to norepinephrine in aortas pretreated either with angiotensin II (AII) or with U46619, an agonist of prostaglandin H2-thromboxane A2 receptors. Finally, we examined the effect of the combination of calcium-entry blockade by administration of nifedipine and treatment with either endothelin-1 or U46619 on the norepinephrine reactivity. RESULTS: Administration of 3 x 10(-10) mol/l endothelin-1 potentiated the contractile response to norepinephrine in SHR aortas with endothelium, irrespective of whether they had been treated with NLA. No endothelin-1-mediated enhancement of the response to norepinephrine was observed in SHR denuded rings and in untreated and NLA-treated WKY rat aortas. All did not affect the response to norepinephrine in SHR rings with endothelium. The amplification by endothelin-1 of the response to (1-100) x 10(-9) mol/l norepinephrine was abolished by blockade of the cyclooxygenase pathway with piroxicam or SO29548. In WKY rat and SHR denuded aortas, 10(-8) mol/l U46619 potentiated the contractile responses to norepinephrine. Administration of 3 x 10(-6) mol/l BQ-123 abolished the increase in reactivity to norepinephrine evoked by endothelin-1 in intact SHR aorta, whereas 3 x 10(-6) mol/l BQ-788 failed to modify this potentiating effect. Administration of 10(-8) mol/l nifedipine inhibited the potentiation of the norepinephrine-induced contractions evoked both by endothelin-1 in SHR aortic rings with endothelium and by U46619 in SHR denuded rings. CONCLUSION: Our results show that a low concentration of endothelin-1 induced potentiation of the contractile response to norepinephrine in SHR aortas but not in WKY rat aortas. This response was endothelium-dependent. Furthermore, our study affords functional arguments that both endothelial and smooth muscle pathways are involved in the potentiating interaction. We propose that endothelin-1 stimulates the production of endothelium- and cyclooxygenase-generated vasoconstrictor factors, which in turn may serve directly as priming stimuli at the vascular smooth muscle level, to activate the Ca(2+)-signal pathway and consequently to increase locally the vascular sensitivity to norepinephrine.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Effects of clonidine and flesinoxan on blood pressure variability in conscious spontaneously hypertensive rats.

The effects of two centrally acting antihypertensive agents, clonidine (0.1 mg/kg/day s.c.) and flesinoxan (1 mg/kg/day s.c.), on short-term blood pressure variability (BPV) were investigated in conscious spontaneously hypertensive rats (SHRs). The drugs were infused subcutaneously during 24 h and 4 weeks by osmotic minipumps. BPV was characterized by spectral analysis. In conscious SHRs, clonidine significantly and preferentially reduced the low frequency (LF; 0.25-0.75 Hz) oscillations of mean arterial pressure (MAP) in short-term (24 h) and long-term (4 weeks) treatments but significantly decreased MAP level only in short-term treatments. In contrast, flesinoxan significantly reduced MAP level whatever the duration of infusion but decreased LF-MAP only in short-term treatments. These results show that centrally mediated inhibition of sympathetic tone by stimulation of either alpha2-adrenoceptors or 5-HT1A (serotonin) receptors can reduce BPV. This effect is independent of the modifications in BP level. The effects of the drugs on baroreceptors may also contribute to the decrease in BPV. The dual properties of clonidine (alpha2-adrenoceptors and imidazoline receptors) may account for its differential effects on BP level and BPV.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1997

In vivo/in vitro comparison of rat abdominal aorta wall viscosity. Influence of endothelial function.

Arterial wall viscosity (AWV) is a potential source of energy dissipation in circulation. That arteries, which are known to be markedly viscous in vitro, have lower viscosity in vivo has been suggested but not demonstrated under similar pressure conditions. Endothelium, which may modulate AWV through smooth muscle tone, could contribute to the low level of viscosity in vivo. Our objectives were first to compare AWV of the rat abdominal aorta, in vivo and in vitro, with similar pulse-pressure waves, and second, to determine whether endothelial function influences AWV in vivo and in vitro. The diameter of the abdominal aorta and distending pressure were measured in vivo and in vitro with a high-resolution echotracking system and a micromanometer, respectively. AWV was calculated as the area of the pressure-volume curve hysteresis. After in vivo examination, the arterial segments were isolated in vitro and submitted to resynthesized pressure waves identical to those recorded in vivo. Deendothelialization was performed in vivo by balloon rubbing; then arteries were examined either in vivo or in vitro. AWV was markedly lower in vivo than in vitro (6.6 +/- 0.7 versus 22.7 +/- 3.7 J.m-1.10(-5), respectively; P < .001). After deendothelialization, a sustained 40% increased AWV was observed during a 15-minute follow-up (P < .01). In vitro, deendothelialized arteries have a 64% higher AWV than segments with endothelium (P < .01). Our results indicate that the physiological effective viscosity, measured in vivo in intact animals, is threefold lower than the intrinsic viscosity of the arterial wall, measured in vitro. Endothelium removal determines a sustained increase in AWV, either in vivo or in vitro. These results suggest that active mechanisms compensate for intrinsic viscosity under physiological conditions. One of these energy-saving mechanisms might be dependent on normal endothelial function.

Animals↗
PubMed1997

Pulse pressure: a predictor of long-term cardiovascular mortality in a French male population.

Studies on the usefulness of blood pressure as a prognostic factor in cardiovascular disease have more often involved investigations of the levels of diastolic or systolic blood pressure. However, blood pressure may be divided into two other components: steady (mean pressure) and pulsatile (pulse pressure). In this study, the relationship of pulse pressure to cardiovascular mortality was investigated in 19 083 men 40 to 69 years old who were undergoing a routine systematic health examination and were being followed up after a mean period of 19.5 years. Subjects were divided into four groups according to age (40 to 54 and 55 to 69 years) and mean arterial pressure (<107 and > or =107 mm Hg). Each group was further divided into four subgroups according to the pulse pressure level. A wide pulse pressure (evaluated according to the quartile group or as a continuous quantitative variable) was an independent and significant predictor of all-cause, total cardiovascular, and, especially, coronary mortality in all age and mean pressure groups. No significant association between pulse pressure and cerebrovascular mortality was observed. In conclusion, in a large population of men with a relatively low cardiovascular risk, a wide pulse pressure is a significant independent predictor of all-cause, cardiovascular, and, especially, coronary mortality.

Adult↗
PubMed1997

Increased stiffness of radial artery wall material in end-stage renal disease.

The incremental elastic modulus (Einc), which is the slope of the relationship between stress and strain of arteries, is a marker of vascular wall material stiffness. Isobaric Einc is reduced at the site of the radial artery in patients with essential hypertension and increased at the site of the common carotid artery in subjects with end-stage renal disease (ESRD). Whether the changes in Einc are influenced by the topography of the vessels, the composition of the arterial wall, and/or by the presence of ESRD is largely ignored. Radial artery Einc was measured in 19 patients with ESRD and compared with the Einc of 89 subjects with essential hypertension and 20 normotensive control subjects. Transcutaneous measurements of radial artery internal diameter and wall thickness (echo-tracking device) and digital pulse pressure (Finapres) were allowed to calculate Einc under operational (ie, at the mean arterial pressure of each group) and isobaric (100 mm Hg) conditions, as well as for a given wall stress. Internal diameter and pulsatile changes in diameter were identical in the three groups. Wall thickness and mean blood pressure were significantly elevated in subjects with hypertension but not in ESRD patients. Circumferential wall stress was identical in the three groups. For the same operational wall stress, and therefore at the operational mean arterial pressure of each group, Einc (kPa x 10[3]) was increased in patients with ESRD (5.53+/-4.0 versus 3.3+/-2.4 in control subjects; P<.05) and normal in subjects with essential hypertension (3.87+/-4.0). Under isobaric conditions, Einc was also significantly lower in subjects with hypertension and elevated in patients with ESRD. Thus, at the site of a medium-sized muscular artery constantly devoid of atherosclerosis, the stiffness of wall material is increased in patients with ESRD. The demonstrated alterations of the arterial wall are independent of the level of blood pressure and tensile stress and should be related to the status ESRD.

Blood Pressure↗
PubMed1996

[First intention treatment of arterial hypertension using a combination of two drugs].

The limited efficacy of single-drug regimens in the treatment of high blood pressure has led to an evaluation of combination regimens for first intention treatment. Two-drug regimens favor the hypotensive efficacy and reduce the frequency of certain side effects. Medications combining two drugs in a single formulation would allow use as first line treatment although marketing authorizations have not yet been obtained. In addition, current good clinical practice recommendations do not allow combination therapy in this situation. A complete assessment based on medical results and cost effectiveness will undoubtedly confirm the usefulness of two-drug therapies as first line treatment for moderate hypertension.

Antihypertensive Agents↗
PubMed1996

Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema.

BACKGROUND: Converting enzyme inhibitors meet most of the criteria required to be used in acute pulmonary edema. However, they could also induce deleterious effects on renal function and electrolytes. The purpose of this study was to evaluate the efficacy and safety of a single intravenous 2-hour infusion of enalaprilat (1 mg) after an acute pulmonary edema. METHODS AND RESULTS: This was a placebo-controlled, randomized, double-blind study performed in 20 congestive heart failure patients (New York Heart Association class III or IV). Systemic and regional hemodynamic parameters, biological parameters, and blood gases were measured before and repeatedly after the onset of infusion. Compared with placebo, enalaprilat decreased pulmonary capillary wedge pressure (-37% versus -10%, P = .001), diastolic and mean systemic blood pressures (-21% versus 0%, P = .009, and -18% versus -1%, P = .026, respectively), diastolic and mean pulmonary blood pressures (-21% versus -8%, P = .040; -18% versus -9%, P = .046), and brachial and renal resistances (-44% versus -14%, P = .017, and -22% versus -2%, P = .014, respectively); increased brachial and renal blood flows (+77% versus +8%, P = .036, and +12% versus 0%, P = .043, respectively), arterial oxygen tension (+2% versus -16%, P = .041), and arterial oxygen saturation (+1% versus -2%, P = .045); and tended to decrease rate-pressure product (-19% versus -7%, P = .076), increase brachial artery diameter (+13% versus 0%, P = .081), and improve intrapulmonary shunt (-18% versus +16%, P = .080). Enalaprilat did not affect cardiac output or carotid or hepatosplanchnic hemodynamics. CONCLUSIONS: Early administration of enalaprilat is effective and well tolerated in acute pulmonary edema.

Acute Disease↗
PubMed1996

Influence of angiotensin-converting enzyme and angiotensin II type 1 receptor gene polymorphisms on aortic stiffness in normotensive and hypertensive patients.

BACKGROUND: Clinical and experimental studies have demonstrated a major role of the renin-angiotensin system in the functional and structural changes of the large arteries in hypertension. Because genetic studies may help us to understand the mechanisms underlying the involvement of this system in arterial regulation, the present study was designed to assess the contribution of polymorphisms of the ACE insertion/deletion (I/D) and angiotensin II type 1 receptor (AGTR1 A 1166C) genes on aortic stiffness regulation. METHODS AND RESULTS: This study included 311 untreated hypertensive and 128 normotensive subjects. Aortic stiffness was evaluated by measurement of the carotid-femoral pulse-wave velocity (PWV). In normotensive subjects, the two polymorphisms did not influence any of the studied parameters. In hypertensive subjects, there was a decreasing trend of mean PWV with the number of ACE D alleles, but this association became significant only after adjustment for blood pressure (P < .05). Conversely, the AGTR1 A 1166C polymorphism was independently associated with aortic stiffness. Mean values of PWV were 11.6 +/- 2.7 m/s in AGTR1 AA homozygotes, 13.3 +/- 3.3 m/s in AC heterozygotes, and 15.3 +/- 4.3 m/s in CC homozygotes (P < .0001 and P < .00001 after adjustment for age and mean blood pressure, respectively). The percentage of variance of PWV explained by AGTR1 A 1166C polymorphism (11.6%) was much larger than that of ACE I/D polymorphism (1.7%). CONCLUSIONS: These results suggest that in hypertensive but not normotensive subjects, the AGTR1 and ACE genotypes are involved in the regulation of aortic rigidity. The presence of the AGTR1 C allele is a strong independent determinant of aortic stiffness, whereas presence of the ACE 1 allele is weakly associated with increased stiffness.

Adolescent↗
PubMed1996

Prevalence and circadian variations of ST-segment depression and its concomitant blood pressure changes in asymptomatic systemic hypertension.

Coronary artery disease is a major complication of hypertension; one of its manifestations is silent ischemia. The aim of this study was to assess the prevalence and circadian distribution of ST-segment depression together with concomitant blood pressure (BP) and heart rate variations. One hundred patients (male:female ratio 1:1) with a mean age (+/- SD) of 51 +/- 8 years underwent ambulatory monitoring using the combined AMP 5600 monitor which simultaneously records a continuous Holter electrocardiogram and intermittent noninvasive BP measurements at 15-minute intervals, with extra measurements triggered by detection of a horizontal or downsloping ST depression (> 1 mm and >60 seconds). Cardiovascular risk factors were fully evaluated in all patients; accurate and reliable echocardiogram enabled left ventricular mass index to be calculated in 52 patients. Twenty-three patients (15 men and 8 women) experienced a total of 72 episodes of ST depression. Duration of such episodes (mean +/- SD) was 132 +/- 65 seconds and amplitude was 1.51 +/- 0.55 mm. Circadian distribution showed 2 peaks: on awakening and in the late afternoon periods. The mean ambulatory BP load was greater in the patients with than without ST-segment depression for both systolic and diastolic BP (135 +/- 14 vs 129 +/- 15 and 84 +/- 8 vs 79 +/- 10 mm Hg, respectively; p < 0.01). Plasma glucose (5.83 +/- 0.70 vs 5.46 +/- 0.71 mmol/L; p = 0.04) and self-related work-related stress levels (22% vs 13%; p = 0.03) were also higher in patients with ST-segment depression. There were no significant differences between groups for clinical parameters, left ventricular mass index, and other cardiovascular risk factors. During ST depression episodes, systolic BP increased by 9 +/- 15 mm Hg, diastolic BP by 7 +/- 11 mm Hg, and heart rate by 5 +/- 17 beats/min. Thus, 24-hour Holter electrocardiographic monitoring showed ST depression episodes in 23 of 100 hypertensive patients (23%); ambulatory BP load was greater in these patients. BP variations, and mainly its elevation, may trigger such episodes of ST-segment depression.

Adult↗
PubMed1996

Diagnostic and therapeutic implications of transesophageal echocardiography in medical ICU patients with unexplained shock, hypoxemia, or suspected endocarditis.

OBJECTIVE: To evaluate the diagnostic and therapeutic implications of transesophageal echocardiography (TEE) in intensive care patients. DESIGN: Comparative study. SETTING: A 10-bed general intensive care unit. PATIENTS: Between 1 January 1992 and 31 May 1993, 61 patients prospectively identified with shock (n = 14), severe, unexplained hypoxemia (Partial pressure of oxygen in arterial blood/fractional inspired oxygen < 200) (n = 31), or suspected endocarditis (n = 16) underwent a TEE examination to supplement transthoracic echocardiography (TTE) examination. INTERVENTIONS: The results of each TEE examination were compared with the clinical findings and TTE data. TEE examinations were classified as follows: 0, TEE results were similar to TTE results; 00, TEE examination resulted in exclusion of suspected abnormalities; 1, TEE revealed a new but minor diagnosis compared to the TTE diagnosis; 2, TEE revealed a new major diagnosis not requiring a change of treatment; 3, TEE results revealed a new major diagnosis requiring an immediate change of treatment. RESULTS: Intraobserver reliability of the TEE classification was confirmed by a 100% concordance and interobserver reliability was evaluated as an 84% concordance. Results of the TEE classification were: class 0, n = 21 (34%); class 00, n = 13 (21%); class 1, n = 7 (12%); class 2, n = 8 (13%); class 3, n = 12 (20%). Therapeutic implications of TEE in class 3 patients were cardiac surgery in 5 patients (2 cases of acute mitral regurgitation, 2 valvular abscesses, and 1 hematoma compressing the left atrium), discontinuation of positive end-expiratory pressure in 1 ventilated patient with an atrial septal defect, weaning off mechanical ventilation in 1 patient with an atrial septal defect, prescription of antimicrobial therapy in 3 patients with endocarditis, and prescription of anticoagulant therapy in 2 patients with left atrial thrombus. No difficulty inserting the transducer was observed in any of the 61 patients studied. The only noteworthy complication was a case of spontaneously resolving atrial fibrillation. CONCLUSION: TEE is safe and well tolerated and is useful in the management of patients in the intensive care unit with shock, unexplained and severe hypoxemia, or suspected endocarditis when TTE is inconclusive.

Aged↗
PubMed1996

A dopamine transporter in human erythrocytes: modulation by insulin.

Red blood cells are capable of transport and accumulation of catecholamines. The aim of this paper is to characterize the catecholamine transport system in the human red blood cell and in particular that of dopamine. Dopamine, noradrenaline and adrenaline enter the red blood cell by a similar process, which shows saturation kinetics with Vmax values of 0.54 +/- 0.12, 0.48 +/- 0.08 and 0.63 +/- 0.13 mumol (1 cells)-1 min-1, respectively, and K(m) values of 15.62 +/- 1.19, 5.81 +/- 1.19 and 12.00 +/- 2.97 nM, respectively. Observations based on the dependence of dopamine influx on the transmembrane H+ gradient, and the effect of transport inhibitors such as DMA (dimethyl-amiloride), DIDS (4,4'-diisothiocyanatostilbene 2,2'-disulphonic acid), reserpine, GBR 12909 (1-(2-(di(4-fluoro-phenyl)-methoxy)-ethyl)-4-(3-phenylpropyl)piperazine) , GBR 12935 (1-(2-(diphenyl-methoxy)-ethyl)-4-(3-phenyl-propyl)piperazine), and cyanine suggest that catecholamine transport is not mediated by the Na(+)-H+ exchanger, the anion exchanger or a system similar to that responsible for dopamine uptake in either synaptosomes or the proximal tubule. However, choline inhibits the influx of dopamine with an IC50 value of 17 microM and stimulates the efflux of dopamine with a K(m) value of 8.20 microM. These results strongly suggest that dopamine is transported by the choline exchanger previously reported to be present in red blood cells. Probenecid inhibits dopamine uptake with an IC50 of 0.63 microM. The presence of insulin receptors in human red blood cells, and the relationship between insulin and catecholamine levels in the plasma led us to investigate the effect of insulin on catecholamine transport. In fasting subjects, dopamine, adrenaline and noradrenaline influxes were higher than in fed subjects. Furthermore, the addition of exogenous insulin to red blood cells from fasting subjects significantly reduced the influx of catecholamines while no effect was observed when insulin was added to red blood cells obtained from fed subjects. The present study shows that catecholamines, and in particular dopamine, are transported in red blood cells via an exchanger which is possibly the choline transport system. The activity of this transporter is regulated by insulin. These results support a role for red blood cells as a storage pool for circulating catecholamines.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗