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Biomedical subjects

M Seyfarth

Publications and source records attributed to M Seyfarth.

At least 19 recordsLinked to original sources

[Reduced radioiodine uptake at increased iodine intake and 131I-induced release of "cold" iodine stored in the thyroid].

AIM: The extent of urinary iodine excretion (UIE) provides information about iodine supply and release. In the present study we investigated correlations between UIE and radioiodine uptake (RIU) as well as effects of radioiodine therapy on UIE in patients with autonomous goitre. PATIENTS, METHODS: In 197 consecutive patients with thyroid autonomy, UIE was measured twice during radioiodine test (RITe) and correlated with RIU. In 98 of these patients, thyroglobulin and thyroid volume (V) were determined prior to therapy. Individual changes in urinary iodine excretion (DeltaUIE) and TG (DeltaTG) could be investigated four weeks (4W) and six months (6M) after radioiodine therapy. Additionally, DeltaV was determined 6M after therapy. DeltaUIE, DeltaTG and DeltaV were correlated with target dose and target volume. RESULTS: Patients with higher iodine excretion exhibited significantly lower thyroidal radioiodine uptake values. Twofold increased UIE prior to therapy decreased radioiodine uptake by 25%. Compared with pretherapeutic values, UIE and TG were significantly increased four weeks after radioiodine therapy (p < 0.001). Median values of both parameters were found to be doubled. The product of target dose and target volume was not only correlated with a decrease of thyroid volume 6M after therapy, but also with an increase of UIE and TG in the early phase after therapy. CONCLUSIONS: It was confirmed that UIE during RITe is a measure for iodine intake and can be used to investigate the competition between stable iodine and radioiodine. The increase of UIE and TG four weeks after therapeutic administration of radioiodine can be explained by disintegrated thyroid follicles. The therapy-induced iodine release may be one important cause for the development of hyperthyroidism in some patients during the first weeks after radioiodine therapy. It may contribute to the known decrease of radioiodine uptake after preapplications of 131I in various thyroid diseases.

Humans↗

[Right ventricular involvement in acute myocardial infarction].

Within the course of an acute posterior wall myocardial infarction there may be involvement of the right ventricle leading to right ventricular infarction. The long-term prognosis of patients with right ventricular infarction is not meaningfully compromised provided that the left ventricular function is preserved. However, in the acute phase, there may be a threefold increase in mortality if the right ventricular infarction leads to substantial right ventricular dysfunction. Consequently, right ventricular involvement should be detected as early as possible. In addition to the clinical presentation, the ECG and echocardiogram can provide decisive information. In addition to reperfusion, specific measures are employed to address the hemodynamic derangement of right ventricular dysfunction. These include administration of fluids for volume expansion to increase filling pressure and avoidance of vasodilators and diuretics.

Comorbidity↗

Blocking caspase-activated apoptosis improves contractility in failing myocardium.

Cardiac myocyte apoptosis has been demonstrated in end-stage failing human hearts. The therapeutic utility of blocking apoptosis in congestive heart failure (CHF) has not been elucidated. This study investigated the role of caspase activation in cardiac contractility and sarcomere organization in the development of CHF. In a rabbit model of heart failure obtained by rapid ventricular pacing, we demonstrate, using in vivo transcoronary adenovirus-mediated gene delivery of the potent caspase inhibitor p35, that caspase activation is associated with a reduction in contractile force of failing myocytes by destroying sarcomeric structure. In this animal model gene transfer of p35 prevented the rise in caspase 3 activity and DNA-histone formation. Genetically manipulated hearts expressing p35 had a significant improvement in left ventricular pressure rise (+dp/dt), decreased end-diastolic chamber pressure (LVEDP), and the development of heart failure was delayed. To better understand this benefit, we examined the effects of caspase 3 on cardiomyocyte dysfunction in vitro. Microinjection of activated caspase 3 into the cytoplasm of intact myocytes induced sarcomeric disorganization and reduced contractility of the cells. These results demonstrate a direct impact of caspases on cardiac function and may lead to novel therapeutic strategies via antiapoptotic regimens.

Adenoviridae↗

Previous cytomegalovirus infection and restenosis after coronary stent placement.

BACKGROUND: Reactivated cytomegalovirus may promote neointima formation after percutaneous coronary interventions by facilitating cell cycle progression through inhibition of the eukariotic tumor suppressor protein p53. This prospective study sought to investigate the effect of previous cytomegalovirus infection on restenosis after coronary stenting. METHODS AND RESULTS: In 551 consecutive patients with successful stent placement, we determined cytomegalovirus IgG titers. Primary and secondary end points were the rate of angiographic restenosis at 6 months and the rate of target vessel reintervention at 1 year, respectively. Three hundred forty patients (62%) had a positive cytomegalovirus IgG titer. We obtained angiographic follow-up in 82% of all patients. Angiographic restenosis rate was 28.7% in patients with positive cytomegalovirus titers and 34.6% in patients with negative titers (P=0.18). Between the groups with and without positive cytomegalovirus titers, there were no significant differences in late lumen loss (1.16+/-0.90 mm and 1.23+/-0.86 mm, respectively, P=0.44). Target vessel reintervention was performed in 16.8% of the patients with positive cytomegalovirus titers and in 17.5% of those without (P=0.82). Even after correction for potential confounding variables by multivariate analysis, positive cytomegalovirus titers did not manifest as a predictor of angiographic restenosis (adjusted odds ratio [95% confidence interval], 0.78 [0.52 to 1.19]). CONCLUSIONS: Previous cytomegalovirus infection does not carry an increased risk of restenosis after stenting.

Aged↗

Intracoronary stenting and angiographic results: strut thickness effect on restenosis outcome (ISAR-STEREO) trial.

BACKGROUND: Increased thrombogenicity and smooth muscle cell proliferative response induced by the metal struts compromise the advantages of coronary stenting. The objective of this randomized, multicenter study was to assess whether a reduced strut thickness of coronary stents is associated with improved follow-up angiographic and clinical results. METHODS AND RESULTS: A total of 651 patients with coronary lesions situated in native vessels >2.8 mm in diameter were randomly assigned to receive 1 of 2 commercially available stents of comparable design but different thickness: 326 patients to the thin-strut stent (strut thickness of 50 microm) and 325 patients to the thick-strut stent (strut thickness of 140 microm). The primary end point was the angiographic restenosis (>/=50% diameter stenosis at follow-up angiography). Secondary end points were the incidence of reinterventions due to restenosis-induced ischemia and the combined rate of death and myocardial infarctions at 1 year. The incidence of angiographic restenosis was 15.0% in the thin-strut group and 25.8% in the thick-strut group (relative risk, 0.58; 95% CI, 0.39 to 0.87; P=0.003). Clinical restenosis was also significantly reduced, with a reintervention rate of 8.6% among thin-strut patients and 13.8% among thick-strut patients (relative risk, 0.62; 95% CI, 0.39 to 0.99; P=0.03). No difference was observed in the combined 1-year rate of death and myocardial infarction. CONCLUSIONS: The use of a thinner-strut device is associated with a significant reduction of angiographic and clinical restenosis after coronary artery stenting. These findings may have relevant implications for the currently most widely used percutaneous coronary intervention.

Aged↗

Restenosis after coronary placement of various stent types.

Coronary stent implantation is being performed in an increasing number of patients with a wide spectrum of clinical and lesion characteristics. A variety of stent designs are now available and continuous efforts are being made to improve the stent placement procedure. The objective of this study was to perform a comprehensive analysis of the relation between clinical, lesion, and procedural factors, and restenosis after intracoronary stenting in a large and unselected population of patients. A consecutive series of 4,510 patients with coronary stent placement was analyzed. Exclusion criteria were only a failed procedure and an adverse outcome within the first month after the intervention. Follow-up angiography was performed in 80% of patients at 6 months. Clinical, lesion, and procedural data from all 3,370 patients (4,229 stented lesions) with follow-up angiography were analyzed in a logistic regression model for restenosis (> or =50% diameter stenosis). Clinical factors contributed to the predictive power of the model much less than lesion and procedural factors. The strongest risk factor for restenosis was a small vessel size, with a 79% increase in the risk for a vessel of 2.7 mm versus a vessel of 3.4 mm in diameter. Stent design was the second strongest factor; the incidence of restenosis ranged from 20.0% to 50.3% depending on the stent type implanted. In conclusion, this study demonstrates the predominant role of lesion and procedural factors in determining the occurrence of restenosis after coronary stent placement. Among these factors, stent design appears to play a particularly important role in the hyperplastic response of the vessel wall.

Analysis of Variance↗

Adenosine inhibits norepinephrine release in the postischemic rat heart: the mechanism of neuronal stunning.

OBJECTIVE: Numerous studies support the concept of impaired postischemic sympathetic neurotransmission in the heart. We hypothesized that postischemic neuronal dysfunction (neuronal stunning) is caused by a transient suppression of exocytotic norepinephrine (NE) release from sympathetic nerve terminals. Furthermore, we assessed the role of presynaptic adenosine-receptors and alpha2-adrenoceptors in neuronal stunning. METHODS AND RESULTS: Exocytotic NE release was induced by two electrical field stimulations (S(1) and S(2)) in isolated perfused rat hearts. S(1) was performed under baseline conditions and S(2) either during or following intervention. Results are expressed as mean S(2)/S(1) ratios+/-S.E.M. Stepwise increase of global ischemic periods (10, 20, and 30 min) induced a progressive suppression of NE release in the postischemic hearts, which was reversible during reperfusion. Both the degree and duration of NE suppression was dependent on the extent of the preceding ischemic period. Following 10-min ischemia complete recovery of NE release was achieved after 5-min reperfusion (1.07+/-0.12), whereas 5-min reperfusion did not restore NE release after 30 min (0.36+/-0.07) of ischemia. The adenosine-receptor antagonists 8-phenyltheophylline (8-PT; non-selective) and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; adenosine A1-receptor subtype selective) significantly increased NE release after 30-min ischemia and 5-min reperfusion (0.78+/-0.06 and 0.64+/-0.07), while in the same experimental protocol blockade of alpha2-adrenoceptors by yohimbine failed to restore the postischemic release (0.24+/-0.06). In non-ischemic hearts the adenosine analogue R(-)N(6)-(2-phenylisopropyl)adenosine (R-PIA) resulted in a marked suppression of NE release (0.61+/-0.07). The inhibitory effect of R-PIA and 2-chloro-N(6)-cyclopentyladenosine (CCPA; adenosine A1-receptor subtype selective agonist) persisted 5 min after cessation of R-PIA (0.62+/-0.05) and CCPA (0.58+/-0.04). Activation of alpha2-adrenoceptors by 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (UK 14,304) also caused a reduction of NE release (0.50+/-0.02), but the release increased to control levels 5 min after cessation of UK 14,304 (0.90+/-0.06). CONCLUSIONS: The results establish the phenomenon of neuronal stunning in terms of a postischemic suppression of exocytotic NE release and provide evidence that neuronal stunning is mediated by endogenous adenosine through activation of presynaptic adenosine A1-receptors.

Adenosine↗

Inter-individual differences in cytokine release in patients undergoing cardiac surgery with cardiopulmonary bypass.

Cardiac surgery with cardiopulmonary bypass (CPB) leads to a systemic inflammatory response with secretion of cytokines (e.g. IL-6, TNF-alpha, IL-1 beta and sIL-2R). The objective of the following study was to investigate in vitro and in vivo cytokine responses and white blood cell counts (WBC) of patients with high versus low cytokine secretion after a coronary artery bypass grafting (CABG) procedure. Twenty male patients undergoing elective CABG surgery with CPB under general anaesthesia were enrolled in the study. On the day of surgery (postoperatively), serum levels of TNF-alpha and IL-1 beta were significantly higher in patients of the high IL-6 level group compared to the respective values in the patient group with low IL-6 levels. The inter-individual differences in IL-6 release in patients undergoing CABG surgery with CPB were accompanied by differences in the release of other cytokines, such as TNF-alpha, IL-1 beta and sIL-2R. To understand whether genetic background plays a role in influencing cytokine plasma levels under surgical stress, we examined the distribution of polymorphic elements within the promoter regions of the TNF-alpha and IL-6 genes, and determined their genotype regarding the BAT2 gene and TNF-beta intron polymorphisms. Our preliminary data suggests that regulatory polymorphisms in or near the TNF locus, more precisely the allele set 140/150 of the BAT2 microsatellite marker combined with the G allele at -308 of the TNF-alpha gene, could be one of the genetic constructions providing for a less sensitive response to various stimuli. Our results suggest: (1) close relationships between cytokine release in the postoperative period, and (2) inter-individually varying patterns of cytokine release in patients undergoing CABG surgery with CPB.

Cardiopulmonary Bypass↗

Enhanced cardiac contractility after gene transfer of V2 vasopressin receptors In vivo by ultrasound-guided injection or transcoronary delivery.

BACKGROUND: Systemic levels of arginine vasopressin (AVP) are increased in congestive heart failure, resulting in vasoconstriction and reduced cardiac contractility via V(1) vasopressin receptors. V(2) vasopressin receptors (V2Rs), which promote activation of adenylyl cyclase, are physiologically expressed only in the kidney and are absent in the myocardium. Heterologous expression of V2Rs in the myocardium could result in a positive inotropic effect by using the endogenous high concentrations of AVP in heart failure. METHODS AND RESULTS: We tested gene transfer with a recombinant adenovirus for the human V2R (Ad-V2R) to stimulate contractility of rat or rabbit myocardium in vivo. Ultrasound-guided direct injection or transcoronary delivery of adenovirus in vivo resulted in recombinant receptor expression in the myocardial target area, leading to a substantial increase in [(3)H]AVP binding. In 50% of the cardiomyocytes isolated from the directly injected area, single-cell shortening measurements detected a significant increase in contraction amplitude after exposure to AVP or the V2R-specific desmopressin (DDAVP). Echocardiography of the target myocardial area documented a marked increase in local fractional shortening after systemic administration of DDAVP in V2R-expressing animals but not in control virus-treated hearts. Simultaneous measurement of global contractility (dP/dt(max)) confirmed a positive inotropic effect of DDAVP on left ventricular function in the Ad-V2R-injected animals. CONCLUSIONS: Adenoviral gene transfer of the V2R into the myocardium increases cardiac contractility in vivo. Heterologous expression of cAMP-forming receptors in the myocardium could lead to novel strategies in the therapy of congestive heart failure by bypassing the desensitized beta-adrenergic receptor-signaling cascade.

Adenoviridae↗

Effect of glycoprotein IIb/IIIa receptor blockade with abciximab on clinical and angiographic restenosis rate after the placement of coronary stents following acute myocardial infarction.

OBJECTIVES: In the Intracoronary Stenting and Antithrombotic Regimen-2 trial (ISAR-2), we sought to investigate the effect of abciximab on angiographic and clinical restenosis after stenting following acute myocardial infarction (AMI). We also intended to assess the impact of abciximab on clinical outcome in this setting. BACKGROUND: It is unclear whether abciximab reduces neointima formation after stenting. Such an effect may be particularly prominent in thrombus-containing lesions. METHODS: Patients undergoing stenting within 48 h after onset of AMI were randomly assigned to receive either standard-dose heparin or abciximab plus reduced-dose heparin. Of 401 patients randomized, 366 without 30-day adverse events were eligible for six-month angiographic follow-up. Scheduled angiography was performed in 80% of these patients. RESULTS: By 30 days, the composite clinical end point of death, reinfarction, and target lesion revascularization (TLR) was reached in 5.0% of the abciximab group and in 10.5% of the control group (p = 0.038). At one year, absolute reduction in the composite clinical end point by abciximab was still 5.7% but had lost its statistical significance. Our primary end point, late lumen loss, was 1.26+/-0.85 mm with abciximab and 1.21+/-0.74 mm with standard heparin (p = 0.61), and binary angiographic restenosis rates were 31.1% and 30.6%, respectively (p = 0.92). CONCLUSIONS: In patients undergoing stenting following AMI, abciximab exerted beneficial effects by substantially reducing the 30-day rate of major adverse cardiac events. During one-year follow-up, there was no additional benefit from a reduction in TLR nor did abciximab reduce angiographic restenosis.

Abciximab↗

Quality of salivary tears following autologous submandibular gland transplantation for severe dry eye.

BACKGROUND: This study aimed to characterise the composition of the pre-ocular fluid after transplantation of the autologous submandibular gland (SMG) for patients with severe dry eye. METHODS: Stimulated and unstimulated pre-ocular fluid from 15 patients (17 eyes) with a viable SMG graft ("SMG-salivary tears"), as well as normal tears and SMG saliva (20 normal subjects/ 20 eyes), was sampled. As global tear parameters, fern pattern analysis and SDS gel electrophoresis were performed. As specific quality parameters, total protein content, secretory immunoglobulin A (SIgA), lysozyme, amylase, sodium, potassium and osmolality were measured using routine laboratory methods. The flow rate of SMG-salivary tears was determined in 5 patients by means of sequential scintillography. RESULTS: The fern pattern of SMG-salivary tears was coarse and thus more similar to normal SMG saliva than tears. SDS gel electrophoresis of the SMG-salivary tears showed albumin and two unidentified proteins in addition to the normal tear pattern. Osmolality and total protein content of SMG-salivary tears were higher than in normal SMG saliva, but still lower than in normal tears. High activities of normal tear antibacterial proteins (SIgA, lysozyme and amylase) were detected in the salivary tears. Stimulation of the secretion did not alter the composition of SMG-salivary tears. The flow rate of SMG-salivary tears was closer to that of normal tears than normal SMG saliva. CONCLUSION: Salivary tears resulting from SMG-transplantation represent condensed SMG saliva. Thus their quality is intermediate between normal tears and normal SMG saliva. High levels of secretory proteins demonstrate that the gland maintains an active function. Surgical denervation and residual tear components from the ocular surface are the most likely factors to cause the complex differences between normal SMG saliva and SMG-salivary tears. The effects of this secretion on the ocular surface are currently being evaluated in a clinical and laboratory study.

Adolescent↗

Is there an analytical or diagnostic advantage from including trisialo transferrin into the fraction of carbohydrate-deficient transferrin? Lessons from a comparison of two commercial turbidimetric immunoassays with the carbohydrate-deficient transferrin determination by high-performance liquid chromatography.

OBJECTIVES: Carbohydrate-deficient transferrin CDT has originally been defined as the sum of isotransferrins exhibiting isoelectric point values > or = 5.7 asialo, monosialo, and disialo transferrin but may also include at least in part trisialo transferrin when measured by modern commercial immunoassays. To examine the effects of divergently defining the analyte CDT, we compared two commercial assays yielding differently composed CDT fractions with a high-performance liquid chromatography HPLC assay commonly regarded as a reference method of CDT determination. METHODS: Relative CDT levels (CDT concentrations expressed as percent of total transferrin) were determined in 142 sera by (i) a turbidimetric immunoassay (ChronAlco I.D.) reportedly detecting asialo to disialo transferrin as CDT, (ii) an analogous assay (CDT Turbidimetric ImmunoAssay [TIA]) said to additionally include part of trisialo transferrin into the CDT fraction measured, and (iii) an anion-exchange HPLC method. Isotransferrins separated by the two commercial assays were also investigated by isoelectric focusing. RESULTS: Data from HPLC and isoelectric focusing indicate that the ChronAlco assay detects major parts of asialo, monosialo, and disialo transferrin as CDT while the CDT TIA yields CDT as the total of asialo, monosialo, disialo, and trisialo transferrin. When relative CDT concentrations obtained by both assays were classified as either normal or elevated according to reference ranges cited by the manufacturer and then were compared to analogously classified HPLC data, there were clearly more discrepancies between corresponding results from CDT TIA and HPLC (22%) than between ChronAlco and HPLC results (9%). CONCLUSION: Including trisialo transferrin into the CDT fraction enlarges the analytical signal and therefore slightly improves assay precision but also results in a significant number of pathologic results in samples exhibiting physiologic levels of the classical CDT components asialo to disialo transferrin. As long as the diagnostic information of the trisialo transferrin concentration is largely unknown, we strongly recommend not to include this isotransferrin into the determination of CDT.

Adolescent↗

G protein beta3 subunit polymorphism and risk of thrombosis and restenosis following coronary stent placement.

C825T polymorphism in the G protein beta3 subunit gene (GNB3) has been associated with arterial hypertension, coronary artery disease and myocardial infarction. On the cellular level, C825T polymorphism is associated with altered transmembrane signaling via adenylyl cyclase inhibiting (G(i)) G proteins. This study was designed to test whether C825T polymorphism has an impact on the processes leading to restenosis and thrombosis following coronary stenting. The primary endpoint of the study was angiographic restenosis (> or =50% diameter stenosis) at 6-month follow-up. Secondary endpoint was angiographically proven stent thrombosis within 30 days of implantation. In the 562 consecutive patients C825T genotype was CC, 46.1%, CT, 45.2% and TT, 8.7%. The incidence of angiographic restenosis was 32.7% in homozygous carriers of the C allele, 28.2% in CT patients and 33.3% in homozygous carriers of the T allele (P = 0.563). C825T genotype distribution in 34 consecutive patients with subacute stent thrombosis (44.0% CC, 50.0% CT, and 6.0% TT) was not different from that of 451 patients with angiographically patent stented vessel (45.4% CC, 44.6% CT, 10.0% TT; P = 0.644). In conclusion, C825T polymorphism has no appreciable impact on the mechanisms leading to thrombosis and restenosis following coronary stent placement.

Aged↗

The immune-endocrine interaction varies with the duration of the inflammatory process in cardiac surgery patients.

The present study investigated the perioperative course of cytokine release and hypothalamic-pituitary-adrenal (HPA) axis activation in relation to the duration of the inflammatory response in cardiac surgery patients. Twelve male patients scheduled for elective coronary artery bypass grafting surgery with cardiopulmonary bypass and general anaesthesia were divided into two study groups: group 1 (n=6) underwent surgery at 13.00 h+/-30 min, group 2 (n=6) at 08.30 h+/-50 min. Blood samples were collected preoperatively and up to the first postoperative day. Postoperatively, on the day of surgery, serum concentrations of the proinflammatory cytokines interleukin (IL)-6, IL-1beta and tumour necrosis factor (TNF)-alpha were not significantly different between the two groups, while blood concentrations of cortisol, adrenocorticotrophic hormone (ACTH) and beta-endorphin in group 2 patients were significantly higher than in group 1 patients. Postoperatively, on the day of surgery, ACTH and cortisol concentrations in group 1 patients were positively correlated to the blood concentrations of IL-1beta, IL-6 and TNF-alpha. By contrast, group 2 patients showed no significant relationship between cytokine release and activation of HPA axis at this time. Our results suggest that in patients undergoing cardiac surgery, the cytokine response is initiated before the HPA axis is fully activated. In the early postoperative period, cytokines appear to be involved in the activation of the HPA axis, while in the later postoperative period, high cortisol concentrations may inhibit the release of IL-6.

Adrenocorticotropic Hormone↗

Why is urological laparoscopy minimally invasive?

OBJECTIVES: Laparoscopic procedures have been developed and established with the view that a similar operative effect can be achieved with less traumatization, especially as far as systemic stress response is concerned. We report a prospective, controlled, nonrandomized animal and patient study to determine the systemic response to laparoscopic and open surgical procedures. METHODS: In the animal study, 26 female pigs underwent either a laparoscopic bilateral varix ligation followed by bilateral nephrectomy (group I), sole introduction of trocars (group II) or sole establishment of an open surgical approach (group III). In the patient study, 145 patients underwent various laparoscopic procedures (nephrectomy, renal cyst marsupialization, varix ligation), open surgical procedures (nephrectomy, inguinal orchiectomy) or extracorporeal shockwave lithotripsy (ESWL). The serum parameters interleukin (IL)-6, IL-10 and C-reactive protein (CRP) were measured before, during and after the operative procedure. RESULTS: In animals and patients, laparoscopy resulted in significantly lower serum levels of CRP during and after the operative procedure. Animals in group I showed a 5-fold elevation, in group II a 3-fold elevation and in group III a 9-fold elevation of CRP. In patients, the increase of CRP was twice as high after open unilateral nephrectomy than after laparoscopic unilateral or bilateral nephrectomy. IL-6 showed less marked elevation during laparoscopy, ESWL and minor operative procedures like laparoscopic varix ligation or inguinal orchiectomy when compared to an open unilateral nephrectomy. The parameter IL-10 showed no significant differences among the patient groups. CONCLUSIONS: The extent of the acute phase reaction to the operative trauma correlates much more convincingly to the approach than to the extent of the procedure. Only larger operations like nephrectomy trigger a systemic acute phase reaction, which can be limited by the laparoscopic access. For minor operative procedures like varix ligation or exploration of cryptorchidism, laparoscopy offers technical advantages rather than minimal invasiveness.

Acute-Phase Reaction↗

On-line analysis of electrolytes in extracorporeally circulating blood: application of a rat model to examine the effect of a single pharmacological dose of melatonin on electrolyte levels in blood.

An experimental model was developed to study the kinetics of electrolytes under different physiological and/or pathological conditions. The model was applied to investigate in vivo the effect of a pharmacological dose of melatonin on the concentrations of Ca2+, K+, Na+, and pH in the anticoagulated blood of anaesthetized male Wistar rats (250-350 g). After the application of 0.25 mg melatonin/kg body weight, injected intraperitoneally into each of 8 rats, the electrolytes were measured by a flow-through system with highly sensitive ion-selective electrodes. The results were compared to a control group (n=8) which was treated with diluent (saline). The electrolytes were monitored continuously via an extracorporeal circulation, on-going for at least 60 min. Melatonin induced a significant increase of blood Ca2+ (p<0.02) by an average of 9.9% after 60 min. However, total calcium concentration did not increase significantly. The extracorporeal circulation provoked an elevation of K+ by hemolysis. This K+ increase was slightly diminished by melatonin (p<0.06). No melatonin effects were seen on Na+, pH and magnesium in blood and plasma, respectively. Also, the urine concentrations of the electrolytes were not altered by melatonin. The mechanism by which melatonin influences the blood concentrations of ionized calcium and potassium is not yet understood.

Animals↗