Prolonged increase in micturition threshold volume by anogenital afferent stimulation in the rat

Neuroendocrine components exist in the human nasal mucosa. However, the pathophysiological and neuroimmunological roles of the regulatory peptides in allergic rhinitis (AR) require further investigation. To analyse the functional morphology and quantify the tissue concentration of regulatory peptides in the nasal mucosa of AR subjects, human inferior turbinate mucosa specimens from 25 patients with AR, 20 patients with non-allergic rhinitis and 10 patients without any nasal diseases were investigated. Using immunohistochemistry and radioimmunoassays, we detected the presence, distribution and concentrations of various neuropeptides [vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), substance P (SP) and calcitonin gene-related peptide (CGRP)] and general neuroendocrine markers (neuron-specific enolase and chromogranin A). Quantitative analysis of the stained fibres and cells was performed using a graphic AutoCAD program. The presence and distribution of NPY, CGRP and SP nerve fibres and neuroendocrine cells were similar among the three subject groups. AR subjects had significantly higher tissue concentrations of VIP and SP. AR subjects had increased numbers of VIP fibres which predominantly innervated vessels. Thus, VIP and SP play important neuroimmunological roles in the pathogenesis of AR.     

Amitriptyline metabolism in elderly depressed patients and normal controls in relation to hypothalamic-pituitary-adrenal system function

The pharmacokinetics of amitriptyline (AMI) have been extensively studied, and a large interindividual variability between oral dose and concentration of the drug in plasma has been documented. The aim of this study was twofold: first, to compare AMI kinetics in depressed patients with those of healthy controls and, second, to describe the relationship between AMI levels in plasma and hypothalamic-pituitary-adrenal (HPA) system changes during depression. Thirty-eight patients with a DSM-III-R diagnosis of major depression and 13 healthy control persons received 75 mg of AMI daily for 6 weeks. Levels of AMI and nortriptyline in plasma were determined, and neuroendocrine testing with the combined dexamethasone-suppression/CRH-stimulation test (DST) was done before AMI administration and after weeks 1, 3, and 6 of medication. AMI levels in plasma were significantly higher in the patient group compared with controls during the entire treatment period, whereas nortriptyline levels did not differ between the two groups. Drug levels correlated significantly with age, but gender had no effect on the concentration of the drug in plasma. Twenty-two patients remitted after treatment. There was no difference in drug levels between responders and nonresponders. Fifteen patients were DST nonsuppressors before treatment; 23 patients and all controls suppressed cortisol after dexamethasone. DST suppressors had significantly higher AMI levels in plasma at weeks 3, 5, and 6 compared with DST nonsuppressors. In comparison to patients with high AMI levels in plasma, those with low drug concentration had higher postdexamethasone cortisol and adrenocorticotropic hormone levels and an increased hormone release after additional CRH.(ABSTRACT TRUNCATED AT 250 WORDS)     

A bioluminescent method of determining antibiotic sensitivity of microbial cells in septic blood]

Previous studies have shown that adhesion molecules play a crucial role in leukocyte-endothelium interactions that occur during myocardial ischemia and reperfusion. We assessed the plasma levels of the soluble form of E-selectin (sE-selectin) and intercellular adhesion molecule-1 (sICAM-1) in 15 patients with acute myocardial infarction (AMI) and in 15 controls with chronic stable angina. In patients with AMI, the levels of sE-selectin and sICAM-1 increased significantly during the first 8 h after infarction and subsequently decreased. Soluble E-selectin levels were inversely related to the peak plasma levels of creatine kinase-MB (CK-MB), and the time course of their appearance in plasma correlated with that of neutrophil count and plasma D-dimer. In individual patients, peak and mean sICAM-1 levels correlated respectively with plasma D-dimer concentrations and monocyte count, but no correlation were found when their time courses were analyzed. Eight hours after symptom onset, the mean plasma sE-selectin levels were higher in patients with AMI than in those with stable angina, whereas no significant differences were found in mean plasma sICAM-1 levels between the two groups at every time analyzed. In the acute phase of MI (a) sE-selectin and sICAM-1 levels increase during the first 8 h and subsequently decrease; (b) the increase in sE-selectin probably reflects activation of endothelial cells, correlates with other inflammatory and coagulation parameters, and is inversely related to the degree of myocardial damage; and (c) sICAM-1 plasma levels do not represent a good marker of "cell activation" because they reflect activation of different cells and may be affected by different conditions.     

Serum magnesium, serum potassium and arrhythmia profile in patients with acute myocardial infarct

In 176 patients with acute myocardial infarction (AMI) serum magnesium concentration (MGK) and serum potassium concentration (KK) were analysed during the first 48 hours after AMI. The patients rhythm was continuously recorded. In a subgroup of 70 patients a signal averaging-ECG was performed. 4.5% of the patients had a low, 55.7% a normal and 39.8% a high MGK. 14.8% of the patients had a low, 80.1% a normal and 5.1% a high KK. Ventricular arrhythmias > or = Lown IV b were found in 25% of the patients with low MGK, in 38.8% with normal and in 52.9% with high MGK. 50% of the patients with low, 62.2% with normal and 61.3% with high MGK had late potentials. There was no relation between hypomagnesemia and ventricular arrhythmias as between hypomagnesemia and late potentials. Thus, hypomagnesemia in AMI patients is rare and does not correlate with ventricular arrhythmia or delayed ventricular potentials.     

Intractable diarrhea in a boy with vasoactive intestinal peptide-producing ganglioneuroblastoma

A 1-year-old boy had intractable diarrhea and symptoms of the watery-diarrhea-hypokalemia-achlorhydria (WDHA) syndrome, a well-known entity in adults. Resection of a ganglioneuroblastoma situated in the neck caused prompt relief of symptoms. The ganglioneuroblastoma in this instance contained the enterohormone vasoactive intestinal peptide (VIP); blood levels of this peptide were elevated preoperatively. After tumor resection, the VIP level returned to normal, and the diarrhea ceased on the day of the operation. The genesis of the diarrhea in relation to the production of polypeptides from neuroendocrine origin is discussed (APUD-cell concept). VIP may be the mediator of the WHDA syndrome in ganglioneuroblastoma.     

Metabolic modulation of acute myocardial infarction. The ECLA (Estudios Cardiológicos Latinoamérica) Collaborative Group

BACKGROUND: Several trials have been performed in the past using glucose, insulin, and potassium infusion (GIK) for the treatment of acute myocardial infarction (AMI). Because of continuing uncertainty about the potential role of this therapeutic intervention, we conducted a randomized trial to evaluate the impact of a GIK solution during the first hours of AMI. METHODS AND RESULTS: Four hundred seven patients with suspected AMI admitted within 24 hours of symptoms onset were enrolled. In a ratio of 2:1, 268 patients were allocated to receive GIK (high- or low-dose) and 139 to receive control. Phlebitis and serum changes in the plasma concentration of glucose or potassium were observed more often with GIK. A trend toward a nonsignificant reduction in major and minor in-hospital events was observed in patients allocated to GIK. In 252 patients (61.9%) treated with reperfusion strategies, a statistically significant reduction in mortality (relative risk [RR] 0.34; 95% CI: 0.15 to 0.78; 2P=0.008) and a consistent trend toward fewer in-hospital events in the GIK group were observed. CONCLUSIONS: Our results confirm that a metabolic modulation strategy in the first hours of an AMI is feasible, applicable worldwide, and has mild side effects. The statistically significant mortality reduction in patients who underwent a reperfusion strategy might have important implications for the management of AMI patients. It is now essential to perform a large-scale trial to reliably determine the magnitude of benefit.     

Induction of cytokine expression in leukocytes by binding of thrombin-stimulated platelets

BACKGROUND: Activated platelets tether and activate myeloid leukocytes. To investigate the potential relevance of this mechanism in acute myocardial infarction (AMI), we examined cytokine induction by leukocyte-platelet adhesion and the occurrence of leukocyte-platelet conjugates in patients with AMI. METHODS AND RESULTS: We obtained peripheral venous blood samples in 20 patients with AMI before and daily for 5 days after direct percutaneous transluminal coronary angioplasty (PTCA) and in 20 patients undergoing elective PTCA. Throughout the study period, CD41 immunofluorescence of leukocytes (flow cytometry) revealed increased leukocyte-platelet adhesion in patients with AMI compared with control patients (mean +/- SE of fluorescence [channels] before PTCA: 77 +/- 16 versus 35 +/- 9; P = .003). In vitro, thrombin-stimulated fixed platelets bound to neutrophils and monocytes. Within 2 hours, this resulted in increased mRNA for interleukin (IL),1 beta, IL-8, and monocyte chemoattractant protein (MCP)-1 in unfractionated leukocytes. After 4 hours, IL-1 beta and IL-8 concentration of the cell-free supernatant had increased by 268 +/- 36% and 210 +/- 7%, respectively, and cellular MCP-1 content had increased by 170 +/- 8%. Addition of activated platelets to adherent monocytes had a similar effect and was associated with nuclear factor-kappa B activation. Inhibition of binding by anti-P selectin antibodies reduced the effect of activated platelets on cytokine production. CONCLUSIONS: In patients with AMI, leukocyte-platelet adhesion is increased. Binding of activated platelets induces IL-1 beta, IL-8, and MCP-1 in leukocytes. Our findings suggest that leukocyte-platelet adhesion contributes to the regulation of inflammatory responses in AMI.     

Discrimination between myocardial and skeletal muscle injury by assessment of the plasma ratio of myoglobin over fatty acid-binding protein

BACKGROUND: Myoglobin and fatty acid-binding protein (FABP) each are useful as early biochemical markers of muscle injury. We studied whether the ratio of myoglobin over FABP in plasma can be used to distinguish myocardial from skeletal muscle injury. METHODS AND RESULTS: Myoglobin and FABP were assayed immunochemically in tissue samples of human heart and skeletal muscle and in serial plasma samples from 22 patients with acute myocardial infarction (AMI), from 9 patients undergoing aortic surgery (causing injury of skeletal muscles), and from 10 patients undergoing cardiac surgery. In human heart tissue, the myoglobin/FABP ratio was 4.5 and in skeletal muscles varied from 21 to 73. After AMI, the plasma concentrations of both proteins were elevated between approximately 1 and 15 to 20 hours after the onset of symptoms. In this period, the myoglobin/FABP ratio was constant both in subgroups of patients receiving and those not receiving thrombolytics and amounted to 5.3 +/- 1.2 (SD). In serum from aortic surgery patients, both proteins were elevated between 6 and 24 hours after surgery; the myoglobin/FABP ratio was 45 +/- 22 (SD), which is significantly different from plasma values in AMI patients (P < .001). In patients with cardiac surgery, the ratio increased from 11.3 +/- 4.7 to 32.1 +/- 13.6 (SD) during 24 hours after surgery, indicating more rapid release of protein from injured myocardium than from skeletal muscles. CONCLUSIONS: The ratio of the concentrations of myoglobin over FABP in plasma from patients with muscle injury reflects the ratio found in the affected tissue. Since this ratio is different between heart (4.5) and skeletal muscle (20 to 70), its assessment in plasma allows the discrimination between myocardial and skeletal muscle injury in humans.     

Location of a VIPoma by iodine-123-vasoactive intestinal peptide scintigraphy

A major problem in patients with small endocrine tumors is the difficulty in localizing the primary tumor site. Many endocrine tumors possess larger amounts of high affinity vasoactive intestinal peptide (VIP) binding sites compared with normal tissue or blood cells. We used radiolabeled VIP to localize the tumor site in a patient with Verner-Morrison syndrome (VMS). Under octreotide therapy, the VIP levels had declined in this patient, but a tumor site could not be detected by conventional techniques or by radiolabeled octreotide. However, using 123I-VIP, the tumor was detectable in the pancreatic tail. Surgical resection of the tumor was followed by complete remission of the VMS. Expression of VIP binding sites in the tumor was confirmed by a radioreceptor assay and showed cross-competition between VIP and octreotide. The identity of the VIP binding site in the tumor was analyzed by Northern blotting and revealed the expression of somatostatin receptor subtype 3, which binds both somatostatin-14 and VIP with higher affinity than octreotide. Iodine-123-VIP scintigraphy would be an effective tracer to identity the tumor site in VMS patients.     

Thrombolytic therapy in acute myocardial infarction: comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the kallikrein system and plasmin

BACKGROUND: Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI. METHODS AND RESULTS: Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01). CONCLUSIONS: The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.     

Biochemical markers of myocardial damage for early diagnosis and prognosis in patients with acute coronary syndromes. Minireview based on a doctorial thesis

In patients with suspected AMI. Monitoring of a combination of myoglobin and CK-MB or tn-T allowed ruling-in AMI within 2-3 hours and ruling-out AMI within 3-6 hours in almost all patients admitted with chest pain and a nondiagnostic ECG. This might have a large impact on the early handling and treatment of these patients. The neural network methodology, with monitoring of myoglobin, CK-MB and tn-T allowed, within the first three hours, reliable diagnosis/exclusion of AMI/MMD and prediction of infarct size in patients admitted with suspicion of AMI. The computer system was faster than clinicians. Thus, neural network methodology might be a useful support for the early assessment of patients with suspected myocardial infarction. In patients with unstable CAD. The risk of subsequent cardiac events is increased by increasing maximal levels of tn-T obtained during the initial 24 hours. Thereby a normal, a slightly elevated and a clearly elevated tn-T level identified a low, intermediate and high risk group, respectively, for MI or death. The tn-T level was an independent prognostic variable for MI or death in a multivariate analysis comparing other early available risk indicators. Furthermore, tn-T seemed to be superior to CK-MB (mass) for risk stratification. In patients able to perform a predischarge ET both the tn-T level and the ET response were independent prognostic indicators for MI or death. The combination of tn-T and the ET response allowed a further improved risk stratification. In patients with tn-T elevation at inclusion, prolonged dalteparin treatment was beneficial. However, in patients without tn-T elevation, long term dalteparin treatment had no protective effect. Thus, tn-T determination provides independent and important prognostic information in unstable CAD. In the selection of treatment strategy for the individual patient, this simple, inexpensive and early available biochemical test might be useful.     

Vasoactive intestinal peptide stimulation of human trabecular meshwork cell growth

PURPOSE: To demonstrate that vasoactive intestinal peptide (VIP), a 28-amino acid neuropeptide, is a growth factor of human trabecular meshwork (TM) cells in culture and in a corneoscleral explant organ culture treated with laser trabeculoplasty (LTP). METHODS: Proliferating human TM cells in cell cultures were incubated with VIP for 20 hours, followed by total cell number determination, using a Coulter counter. The percentage of proliferating TM cells was assessed, using an antibody against the proliferating cell nuclear antigen (PCNA). To test the growth effect of VIP on TM cells in situ, corneoscleral explants in organ cultures were first treated with argon LTP to initiate TM-cell proliferation and then were exposed to VIP for 48 hours. The mitotic TM cells were demonstrated immunocytochemically, using anti-PCNA in paraffin sections of the explants; and the total number of TM cells was determined after paraffin sections were counterstained by hematoxylin. RESULTS: Vasoactive intestinal peptide dose-dependently stimulated the proliferation of TM cells in cell culture. Treatment with 5 x 10(-10) M VIP resulted in a maximal increase of 40% in cell number. The effect of VIP was blocked by a VIP antagonist. The number of PCNA-stained TM cells and the total cell number in the TM in LTP-treated corneoscleral explants were increased by VIP. CONCLUSIONS: Exogenously applied VIP stimulated the proliferation of human TM cells in subconfluent cultures and in LTP-treated corneoscleral explants. In that LTP has been shown to increase the number of TM cells in situ, the growth stimulatory effect of VIP may help enhance this therapy.     

All prepro-VIP-derived peptides, except PHI/PHV, are expressed in the female rat anterior pituitary and increased by estrogen

The expression of VIP precursor products: prepro-VIP(22-79), peptide histidine isoleucine (PHI), peptide histidine valine (PHV), prepro-VIP(111-122), VIP, prepro-VIP(156-170), and prepro-VIP mRNA in the anterior pituitary of estrogen-treated, ovariectomized rats, of ovariectomized controls, and of sham-operated controls was examined. Using radioimmunoassays based on antisera against each of the prepro-VIP sequences, we found that all sequences were expressed and markedly induced by estrogen, except PHI and PHV, which both were undetectable. By immunohistochemistry, it appeared that the number of cells immunoreactive for each of these sequences was increased in the estrogen-treated animals. However, PHI/PHV-immunoreactive cells could not be detected, despite the use of four different PHI antisera with different specificities. Estrogen treatment increased the prepro-VIP mRNA as judged by Northern blotting. In situ hybridization signals for both VIP mRNA and PHI mRNA were observed in few pituitary cells from control animals whereas strong positive signals were observed in a larger number of cells after estrogen treatment. The findings show that estrogen causes activation of the VIP gene expression in anterior pituitary cells, and that the absence of PHI and PHV probably is due to translational or posttranslational events.     

Effect of puerarin on plasma endothelin, renin activity and angiotensin II in patients with acute myocardial infarction

OBJECTIVE: To study the changes of endothelin (ET), renin activity (RA) and angiotensin II (AT-II) before and after puerarin treatment in patients with acute myocardial infarction (AMI). METHODS: Forty-three patients with AMI were divided into two groups, and were given puerarin and glucose-insulin-kalium (GIK) treatment respectively. Plasma ET, RA and AT-II were measured by radioimmunoassay (RIA) before and after treatment in different phases. RESULTS: It showed that plasma ET and RA, AT-II levels in AMI were higher than those in control group (P < 0.01). ET level was conversely correlated with RA and AT-II (P < 0.01). After treatment with puerarin, plasma levels of ET, RA and AT-II were recovered to normal in 3 days, but these data recovered to nearly normal until 7-14 days in group with GIK treatment. CONCLUSION: Puerarin might play an important role in regulating the imbalance of ET, RA and AT-II of patients with AMI.     

Role of VIP, PACAP, and related peptides in the regulation of the hypothalamo-pituitary-adrenal axis

Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are members of a family of regulatory peptides that are widely distributed in the body and share numerous biologic actions. The two peptides display a remarkable amino acid-sequence homology, and bind to a class of G protein-coupled receptors, named PACAP/VIP receptors (PVRs), whose signaling mechanism mainly involves the activation of adenylate-cyclase and phospholipase-C cascades. A large body of evidence suggests that VIP and PACAP play a role in the control of the hypothalamo--pituitary-adrenal (HPA) axis, almost exclusively acting in a paracrine manner, since their blood concentration is very low. VIP and PACAP are contained in both nerve fibers and neurons of the hypothalamus, and VIP, but not PACAP, is also synthesized in the pituitary gland. Both peptides are expressed in the adrenal gland, and especially in medullary chromaffin cells. All the components of the HPA axis are provided with PVRs. VIP and PACAP enhance pituitary ACTH secretion, VIP by eliciting the hypothalamic release of CRH and potentiating its secretagogue action, and PACAP by directly stimulating pituitary corticotropes. Through this central mechanism, VIP and PACAP may increase mineralo- and glucocorticoid secretion of the adrenal cortex. VIP but not PACAP also exerts a weak direct secretagogue action on adrenocortical cells by activating both PVRs and probably a subtype of ACTH receptors. VIP and PACAP raise aldosterone production via a paracrine indirect mechanism involving the stimulation of medullary chromaffin cells to release catecholamines, which in turn enhance the secretion of zona glomerulosa cells via a beta-adrenoceptor-mediated mechanism. PACAP appears to be able to evoke a glucocorticoid response through the activation, at least in the rat, of the intramedullary CRH/ACTH system. The relevance of these effects of VIP and PACAP under basal conditions is questionable, although there are indications that endogenous VIP is involved in the maintenance of the normal growth and steroidogenic capacity of rat adrenal cortex. However, indirect evidence suggests that these peptides might play a relevant role under paraphysiological conditions (e.g., in the mediation of HPA axis responses to cold and inflammatory stresses) or may be somehow involved in the pathogenesis of Cushing disease or some case of hyperaldosteronism associated with secreting pheochromocytomas.     

The neuropeptides, VIP and NPY, that are present in the thyroid nerves are not released into the thyroid vein

In the present study, we tested the hypothesis that the neuropeptides, vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY), which are present in the thyroid nerves, act as physiological neurotransmitters involved in the regulation of thyroid hormone secretion and thyroid blood flow. Specifically, we examined whether these neuropeptides can be released into thyroid blood vessels by electrical stimulation of the major thyroid nerves or whether their expression is altered by changes in iodine intake. Sprague-Dawley rats were used in this study. The cervical sympathetic trunk or the superior laryngeal nerve was stimulated by bipolar electrodes in anesthetized rats. During nerve stimulation, blood samples were withdrawn from the thyroid vein. Thyroid blood flow was monitored by laser Doppler blood flowmetry. Sympathetic stimulation caused a marked decrease in thyroid blood flow, which was associated with a significant increase in release of norepinephrine. However, these effects were not accompanied by any change in NPY release into the thyroid vein. Stimulation of the superior laryngeal nerve was not associated with changes in thyroid blood flow or VIP release into the thyroid vein. In a separate experiment, rats were fed a diet containing low-, high-, or normal iodine concentrations. Triiodothyronine (T3) and thyroxine (T4) levels in thyroid venous plasma were significantly reduced in rats fed a low-iodine diet but not in a separate group of rats fed a high iodine diet. However, these treatments had no effect on VIP or NPY concentrations in thyroid venous plasma or in thyroid ganglia. Thus, our results indicate that VIP and NPY, which are present in the thyroid nerves, may not be directly involved in the regulation of thyroid function.     

The changes of vasoactive intestinal peptide somatostatin and pancreatic polypeptide in blood and CSF of acute cerebral infarction patients and the effect of acupuncture on them

VIP, SS and PP which exist in gastrointestinal tract and CNS might be to play an important role in nervous system as neurotransmitters of neuromediaters. There have been a few of reports about their changes in plasma and CSF in ICVD. The effects of acupuncture, which was used in treatment of ICVD with good efficiency, on VIP, SS and PP have not been known. For researching their changes in ICVD and effects of electro-acupuncture on them, and finding the mechanism of acupuncture in treatment of ICVD, the study was performed. The levels of VIP, SS and PP in 64 patients with acute cerebral infarction were determined. The points of acupuncture were Quchi (LI 12), Waiguan (SJ 5), Huantiao (BG 30), and Zusanli (ST 36). The routine treatment included dextran, nicotinic acid, aspirin, dipyridamole and radix salviae miltiorrhizae composita. The CSF and blood were taken before the begining of treatments and after a course of treatment. The level of VIP, SS and PP were measured by radiommunoassay. Results showed the level of CSF VIP in the patients was significantly lower as compared with controls. The level of plasma SS in the patients was lower, but the difference was not significant as compared with controls, and level of plasma PP in the patients was significantly increased when it was compared with controls. After electro-acupuncture treatment, in patients with good efficiency, CSF VIP recovered to normal level and the levels of plasma and CSF SS were significantly increased, while the level of plasma PP had no significant change. The results suggest that acupuncture might regulate the disturbances of metabolism of VIP and SS in CNS.     

Determination of cardiac troponin-I in prediction of thrombolysis

Acute myocardial infarction (AMI) is a disease with high morbidity and mortality. Diagnosis of AMI using common methods (classical biochemistry, ECG) fails even in the fifth part of patients so that other noninvasive diagnostic methods are preferred. Recently, the biochemical analysis has been restored in the case of AMI diagnostics and also in prediction of coronary reperfusion after administration of a fibrinolytic agent. A suitable markers of AMI diagnostics is a combination of myoglobin and cardial troponin-I which is reported as a marker with high specificity and sensitivity. To determine coronary reperfusion, the examination of cardial troponin-T and CK-MB mass is recommended. In the literature, there exist isolated papers dealing with dynamics of cTn-I suitable for prediction of coronary revascularization. However, these papers do not report any adequate algorithm and subsequently mathematical differences between successful thrombolysis and failing thrombolysis. Therefore the aim of our study was to describe dynamics of cTn-I changes in AMI patients treated by thrombolysis. The study comprised of 8 AMI patients with delay from the occurrence of pains to fibrinolysis application under 4 hours (delay 4 hrs). These probands were examined for concentration of cTn-I and CK-MB mass in 3-hour intervals in the first 48 hours after admission to the clinic and further in 6-hour intervals from the hour 48 to the hour 90 after admission. All probands had a successful reperfusion (estimated using CK-MB peak, in 4 patients reperfusion was verified by subsequent coronarography). However, a simple mathematical prediction of coronary reperfusion after acute myocardial infarction by means of cTn-I dynamics determination is not possible due to relatively low cTn-I differences in individual analyses (CK-MB mass analysis shows more significant differences). Thus, in order to determine coronary revascularization, we recommend to use common analyses of dynamics of cTn-T or CK-MB mass.     

Early assessment of viable myocardium after acute myocardial infarction by low-dose echo-dobutamine

BACKGROUND: The aim of the study was to evaluate the usefulness of low-dose dobutamine echocardiographic testing performed within 48 hours from anterior AMI in order to identify the extent of viable myocardium and predict its functional outcome. The early echo-dobutamine test was also compared with a predischarge test in order to evaluate the effects of different timing on the accuracy of the test. METHODS: Nineteen consecutive patients, aged 54 +/- 11 years, with a first anterior AMI entered the study. All patients underwent a low-dose dobutamine echocardiographic test within 48 hours from hospital admission and at predischarge. In all the patients, a rest follow-up echocardiogram was performed three months after hospital discharge. Eleven patients underwent a revascularization procedure (7 underwent PTCA and 4 CABG). RESULTS: Of the 159 dyssynergic segments, 26% improved spontaneously at predischarge and 51% improved at the three-month follow-up. Of the 145 predischarge dyssynergic segments, 38% improved at three months. Considering the results on a segmental basis, early low-dose dobutamine echocardiography showed a sensitivity of 52%, a specificity of 87%, a positive predictive value of 81%, a negative predictive value of 64% and a diagnostic accuracy of 69% for wall-motion improvement at three months. The predischarge test showed very similar values. A slight enhancement of the sensitivity of both tests was observed considering the akinetic segments only. Finally, considering the amount of segmental reversible dysfunction inside the infarct area in the single patients, early low-dose dobutamine echocardiography showed a sensitivity of 86% and a specificity of 80%. CONCLUSIONS: Our results indicate that: 1) recovery of regional wall motion after AMI is slow and progressive, with substantial improvement ensuing within the first days after infarction; 2) considering results on a segmental basis, low-dose dobutamine echocardiography performed within 48 hours of AMI shows a high specificity but a low sensitivity for late recovery of regional function, although it gave information similar to what was obtained performing the test at predischarge; 3) the efficiency of test can be improved by considering the amount of reversible segmental dysfunction inside the infarct area in the single patients.