Right- and left-subclavian vein port-a-cath systems: comparison of complications.

BACKGROUND: Central venous access systems are frequently used for delivery of medications; however, few studies have compared surgical and postoperative complications of right versus left access via the subclavian vein (SCV). The aim of this study was to compare the surgical and postoperative complications associated with Port-A-Cath system insertion via the right and left SCV. METHODS: The medical records of patients who received Port-A-Cath insertion via the SCV for parenteral chemotherapy between August 2004 and July 2008 were reviewed. The incidence of surgical and postoperative complications was compared between patients who received right- versus left-SCV Port-A-Cath insertion. RESULTS: A total of 1,848 patients were included in the study. Right-SCV catheterization was attempted in 1,029 (55.7%) patients and was successful in 866 (84.2%). Left-SCV catheterization was attempted in 819 (44.3%) patients and was successful in 651 (79.5%). The mean length of postoperative follow-up was 417.3 ± 401.3 and 396.7 ± 379.9 days for the right- and left-SCV groups, respectively. The incidence of SCV puncture failure was significantly lower in the right-SCV group (12.3%) compared with the left-SCV group (16.8%, p = 0.006). The incidence of catheter knotting at the ipsilateral brachiocephalic vein was also significantly lower in the right-SCV group (0.0%) compared with the left-SCV group (0.5%, p = 0.038), as was the incidence of catheter occlusion (1.0% for right SCV vs. 3.5% for left SCV, p = 0.001). CONCLUSION: These findings suggest that the right-SCV approach is superior to the left-SCV approach for Port-A-Cath insertion.

Surgical treatment of 26 patients with necrotizing pneumonia.

BACKGROUND: This study aimed to review the outcome of patients treated with surgical resection for necrotizing lung infection with various co-morbidities and complications. METHODS: The records of 26 patients treated with pulmonary resection for necrotizing pneumonia between July 2004 and January 2010 were retrospectively reviewed. Surgical procedures included large wedge resection (n = 1), lobectomy (n = 19) and bilobectomy (n = 6). RESULTS: The study cohort consisted of 21 men and 5 women aged 35-85 years (mean 64.7 ± 15.0 years). Twenty-three (88.5%) patients had underlying risk factors. At surgical consultation, 17 patients presented with progressive respiratory distress; 6 required ventilatory support; 12 had empyema, and in 5 patients the conditions were complicated by bronchopleural fistula. Four patients had septic shock requiring vasopressor support. Three patients developed hemoptysis. Two patients had bilateral diffuse pneumonia. Klebsiella pneumoniaeand Streptococcusviridans were the most common pathogens. The right lower (n = 13) and right middle lobes (n = 10) were the most frequently affected. Four deaths (15.4%) occurred: 3 due to perioperative progressing pulmonary infection/inflammation and 1 due to hepatorenal failure. Postoperative empyema occurred in 3 patients. One patient became ventilator dependent. CONCLUSION: Pulmonaryresection for necrotizing pneumonia is a feasible treatment option in patients with progressive pulmonary sepsis.

Resistance exercise did not alter intramuscular adipose tissue but reduced retinol-binding protein-4 concentration in individuals with type 2 diabetes mellitus.

Lipid accumulation in muscle is associated with diminished insulin sensitivity. It was hypothesized that resistance exercise decreases muscular adipose tissue and reduces the level of retinol-binding protein-4 (RBP4), which is linked to adipose tissue and insulin sensitivity in diabetics. Forty-four women with type 2 diabetes were randomly assigned to three groups for a period of 12 weeks: control (asked to maintain a sedentary lifestyle); resistance exercise (elastic band exercise at moderate intensity five times per week); and aerobic exercise (walking for 60 min at moderate intensity five times per week). Subcutaneous (SCAT), subfascial (SFAT) and intramuscular (IMAT) adipose tissues at mid-thigh level were assessed using computed tomography, and RBP4 level and insulin sensitivity (fractional disappearance rate of insulin, k(ITT)) were assessed before and after intervention. Changes in SCAT, SFAT, IMAT, RBP4 and k(ITT) were similar among the three groups. Within-group analysis revealed that body mass index and waist circumference decreased significantly in both exercise groups, but RBP4 decreased significantly only with resistance exercise. Resistance exercise did not alter muscular adipose tissue or improve insulin sensitivity.

Bilateral cerebral hemispheric infarction associated with sildenafil citrate (Viagra) use.

Sildenafil citrate (Viagra) is one of the frequently prescribed drugs for men with erectile dysfunction. We describe a 52-year-old man with bilateral middle cerebral artery (MCA) territory infarction after sildenafil use. He ingested 100 mg of sildenafil and about 1 h later, he complained of chest discomfort, palpitation and dizziness followed by mental obtundation, global aphasia and left hemiparesis. Brain magnetic resonance imaging documented acute bilateral hemispheric infarction, and cerebral angiography showed occluded bilateral MCA. Despite significant bilateral MCA stenosis and cerebral infarction, systemic hypotension persisted for a day. We presume that cerebral infarction was caused by cardioembolism with sildenafil use.

Role of limbic peptidergic circuits in regulation of arterial pressure, relevant to development of essential hypertension.

It is generally accepted that the essential hypertension (EH) is caused by interactions among congenital gene, multiple pathogenetic pressor factors, and disorder of physiologic depressor factors. The central nervous system may play a key role in the development of EH. The underlying mechanisms, however, are not well understood. Studies show that peptidergic transmitters in the limbic forebrain are involved in long-term regulation of arterial pressure and in the pathogenesis of EH. In the limbic forebrain there are peptidergic pressor and depressor circuits. The former includes corticotropin releasing factor-, substance P-, and angiotensin II-circuits; and the latter includes beta-endorphin- and atrial natriuretic peptide-circuits. These circuits extensively interconnect and interact with each other. The altered functions of them may be the pathogenesis of EH. In this review, we focus on the roles of limbic peptidergic circuits in regulation of arterial pressure, relevant to the neurogenetic mechanisms in developing EH.

Shear-dependent aggregation characteristics of red blood cells in a pressure-driven microfluidic channel.

Though the aggregation of red blood cells (RBCs) is a major determinant of blood viscosity, there have not been any available techniques to measure the effect of RBC aggregation on blood viscosity over a range of shear rates. The microfluidic shearing technique with vibration has been applied to an aggregometer for measuring the dynamic aggregation characteristic of RBCs. In measuring backscattered light intensity I(t) and pressure p(t) over time, both aggregation and the stress-shear rate information can be determined simultaneously. The feasibility and accuracy of the new aggregation measurement technique has been demonstrated to correlate with blood viscosity for normal and heated blood. We found that RBC aggregability showed shear-dependent behavior, which can be correlated directly with shear-thinning blood viscosity. The present measurements of the dynamic aggregation characteristic over shear rate enable the interpretation of the shear-rate dependent blood viscosity, which is greatly affected by RBC aggregation.

Electrocoagulation combined with the use of an intermittently aerating bioreactor to enhance phosphorus removal.

Biological Oxygen Demand (BOD), nitrogen, and phosphorus were treated with the use of an intermittently aerating bioreactor combined with electrocoagulation. Experiments consisting of batch reactor tests were conducted to identify the most efficient electrode material and the best condition for electrolysis so that the current density would not impede the biological treatment. The operating conditions needed when using an intermittently aerating bioreactor combined with electrocoagulation to enhance phosphorus removal were also identified. Iron was found to be more efficient than aluminum as an electrode material in terms of electricity requirement. When electrocoagulation was conducted and an intermittently aerating bioreactor was used, the electrolysis of the iron electrode in the aerobic stage was observed to be more favorable compared to continuous electrolysis. Sludge rise occurred at the current density of 5.7 mA cm(-2), and lysis of cell at 11.2 mA cm(-2). The applicable current density was found to be less than 4 mA cm(-2). Based on the results of this study, it can be concluded that the use of an intermittently aerating bioreactor combined with electrocoagulation enhances phosphorus removal in sewage treatment plants.

Brain atriopeptin mediates AV3V depressor response.

In urethane-anesthetized rats, sodium L-glutamate (Glu) microinjection into the anteroventral third ventricle region (AV3V) induced a depressor response, but the heart rate remained unchanged, whereas Glu injection into its surrounding areas or normal saline injection into the AV3V had no effect on the arterial pressure and heart rate. Bilateral preinjection of procaine or atriopeptin III antiserum into the nucleus paraventricularis (NPV) and methyl atropine (IV) markedly attenuated the AV3V depressor response, but the hypotensive response was not significantly affected by phentolamine or propranolol (IV), indicating that atriopeptin in the NPV mediates the AV3V depressor response, and excitation of the cardiac vagus is also involved in this response.

Beta-endorphin- and GABA-mediated depressor effect of specific electroacupuncture surpasses pressor response of emotional circuit.

It has been proved that input of specific electroacupuncture (EA) can activate beta-endorphin(beta-EP)ergic and noradrenergic neurons projecting to the rostral ventrolateral medulla (RVL), the latter acting upon the RVL-GABAergic interneurons, thereby produce depressor effect. The present study further shows that: (1) The EA depressor effect is strong enough to surpass the pressor response of the AC (nucleus amygdaloideus centralis)-emotional circuit, (2) both beta-endorphin (beta-EP) and GABA in the RVL mediate the EA antagonistic effect, (3) the EA effect does not take place in the AC and paraventricular nucleus (two key nuclei besides the RVL, which also have beta-EPergic input) in the emotional circuit.

Role of corticotropin-releasing factor and substance P in pressor responses of nuclei controlling emotion and stress.

The wide distribution of corticotropin-releasing factor (CRF) and substance P (SP)-immunoreactive cell bodies, nerve terminals and corresponding receptors in pressor nuclei controlling emotion and stress implies that CRF and SP may play important roles in pressor responses of these nuclei; hence CRF or SP was microinjected into these nuclei respectively in Wistar male rats anesthetized with urethane to test this possibility. Microinjection of CRF into nucleus amygdaloideus centralis, nucleus paraventricularis, nucleus ventromedialis, lateral hypothalamus-perifornical region, periaqueductal gray matter, nucleus parabrachialis, locus coeruleus or rostral ventrolateral medulla respectively could evoke pressor responses (but CRF injection into nucleus dorsomedialis could not elicit significant pressor responses). Injection of substance P into all the above nuclei could also elicit hypertensive responses of different magnitudes, whereas normal saline injection into these nuclei had no effect. These results indicate that both CRF and SP in the above mentioned nuclei may play important roles in hypertension induced by prolonged emotional stress.

Mechanisms underlying pressor response of subfornical organ to angiotensin II.

In urethane-anesthetized rats, microinjection of angiotensin II (AII) into either the subfornical organ (SFO), nucleus paraventricularis (NPV), or rostral ventrolateral medulla (RVL), respectively, all induced pressor responses, but the heart rate remained unchanged. Preinjection of [Sar1, Thr8]-angiotensin II (ST-AII, an AII antagonist) into bilateral NPV blocked the SFO-pressor response to AII. Bilateral RVL pretreated with ST-All markedly attenuated the pressor response of the SFO or NPV to AII. Hexamethonium or methyl atropine (IV) also reduced the SFO-pressor response. The results show that All can activate the SFO, NPV, and RVL successively, thereby inducing the pressor response; both excitation of sympathetic nerves and inhibition of the cardiac vagus are involved in this response.

Properties of favored patterns in spontaneous spike trains and responses of favored patterns to electroacupuncture in evoked trains.

By using 'the modified detection method', our previous study has shown that all spontaneous spike trains recorded from several areas of brain and spinal cord have favored patterns (FPs). The present study further shows that: (1) all newly detected spike trains from substantia nigra zona compacta, nucleus periventricularis hypothalami and nucleus hypothalamicus posterior also have FPs, and some spike trains from neurons in the same nucleus have a common favored pattern (CF, i.e. they share the same FP), indicating that FP and CF in spike trains are common phenomena; (2) all serial correlation coefficients of FP repetitions (in serial order) in different spike trains detected are less than 0.3 (close to 0), revealing that the repetition of FPs is a renewal process; (3) in different periods of the spike trains evoked by electroacupuncture (EA), the number of different FPs and the number of repetitions of the same representative FP either increase or decrease along with the change of firing rate. The tendencies of these changes are very similar, but after EA the repetitions of different FPs in the same spike trains change differently, showing that different (hidden) responses exist at the same time. The above results suggest that the FPs in spike trains may represent various neural codes, and 'the modified detection method of FP' can pick up more information from spike trains than the firing rate analysis, hence it is a very useful tool for the study of neural coding.

Favored patterns in spontaneous spike trains.

By using the modified detection method, favored patterns can be detected in a total of 44 spontaneous spike trains. Among these the 'periodical burst' discharge of one sympathetic preganglionic neuron and the 'fast-slow' alternative discharge of some hypothalamic neurons have visible characteristics, hence we use them to test the reliability of our method by comparing the detected patterns with the non-sequential interval histograms and oscillograms of the spike trains. The comparisons show that our method is reliable. The spike trains of nucleus raphe magnus (NRM) and the locus coeruleus (LC) have no visible characteristics; from these the following results have been observed: (1) all spike trains have one or more favored patterns; (2) some spike trains from neurons in the same nucleus have common fragments of favored patterns; (3) the favored patterns in spike trains recorded from different nuclei are different from each other; (4) some favored patterns in spike trains of the NRM neurons remain unchanged from beginning to end in 35-min records and their repetitions are relatively stable; and (5) microinjection of normal saline or normal serum into the LC has no significant influence on the occurrence of favored patterns in 35-min records of spike trains of the LC neurons. The above results indicate that the favored patterns in spike trains are objective and regular phenomena with relative stability. It seems likely that favored pattern may be used (as an index of the neuronal activity) in combination with the microinjection technique, etc., for various studies including studies on neural coding.

Corticotropin releasing factor and substance P mediate the nucleus amygdaloideus centralis-nucleus ventromedialis-nucleus dorsomedialis pressor system.

Prolonged emotional stress is an important factor in the development of neurogenic hypertension, but its mechanism is still unclear. The purpose of the present study is to analyze the possible neural basis of hypertension induced by prolonged emotional stress. In the brain many nuclei are involved in emotional reaction, stress or defense response; among them the nucleus amygdaloideus centralis (AC) is the most important one which widely connects with other nuclei controlling emotion and stress, such as nucleus ventromedialis (NVM), nucleus dorsomedialis (NDM), nucleus paraventricularis (NPV) etc. These nuclei contain corticotropin releasing factor (CRF)- and substance P (SP)-immunoreactive cell bodies, nerve terminals and corresponding receptors. Our previous and present studies showed that microinjection of CRF or SP into these nuclei induced pressor responses. These data imply that excitation of the AC can activate many nuclei controlling emotion and stress via CRF and SP, and excessive activities of these nuclei may be the neural basis of hypertension induced by prolonged emotional stress. The present study revealed that (1) the AC pressor response to glutamate (Glu) could be reduced by preinjection of CRF antagonist (alpha-Helical CRF[9-41] or SP antagonist ([D-Pro(2), D-Phe(7), D-Trp(9)]-substance P) into bilateral NVM, (2) the NVM pressor response to Glu were decreased by pretreatment of the NDM with CRF- or SP-antagonist, (3) the AC-, NVM- or NDM-pressor responses were all attenuated by preinjection of CRF- or SP-antagonist into bilateral NPV or rostral ventrolateral medulla (RVL). The results indicate that excitation of the AC can indirectly activate the NPV and RVL to evoke pressor response via the NVM-NDM, CRF and SP are transmitters in each connection of this pathway; this is one component of the mechanism underlying the AC pressor response. Taken together with the findings of our previous studies, it provides neurophysiological basis for the above-mentioned implications.

[Central neural mechanism underlying pressor response to excitation of locus coeruleus in rats].

Experiments were done on urethane anesthetized, tubocurarine immobilized and artificially ventilated rats and the following results were observed: (1) Injection of sodium L-glutamate (Glu) into locus coeruleus (LC) could evoke a pressor response, but heart rate was not significantly affected; while depressor and bradycardia effects were observed when injecting into closely adjacent areas. (2) The LC-pressor response decreased after a brain transection caudal to nucleus paraventricularis was made but remained unchanged if the transection was rostral to the nucleus; The LC-pressor response could also be attenuated by preinjection of phentolamine propranolol or atropine respectively into the rostral ventrolateral medulla (RVL). The above results suggest that LC-pressor response is not only mediated by RVL, but also by nucleus paraventricularis.

[Pressor response induced by glutamate injection into caudal ventrolateral part of periaqueductal gray matter and its efferent pathway in brain-stem].

In urethane-anesthetized, tubocurarine-immobilized artificially ventilated rats, the following results were observed: (1) Sodium glutamate (Glu) microinjection into the caudal ventrolateral part of the periaqueductal gray matter (PAG) produced a marked rise in blood pressure. (2) This effect was attenuated by phentolamine or propranolol but not by atropine, injected bilaterally into the rostral ventrolateral medulla (RVL), indicating that this pressor response is mediated by RVL and alpha- and beta-receptors. (3) Propranolol-injection into RVL also attenuated the pressor response induced by electrical stimulation of the nucleus parabrachialis ventralis (NPV), while the pressor response initiated by injecting Glu into the same area (NPV) was not affected. Taken together with the previous findings that phentolamine blocks the pressor response produced by NPV-electrostimulation, but not of Glu-injection into NPV, the above results suggest that neurons in the caudal ventrolateral part of PAG may either send axons passing through the nucleus parabrachialis (NPB) and directly acting upon beta-receptors in RVL, or relay in NPB and act indirectly on alpha-receptors in RVL to produce the pressor response.

Tinggong(SI 19), a novel acupoint for 2Hz electroacupuncture-induced depressor response.

In urethane-anesthetized, tubocurarine-immobilized and artificially ventilated rats, the specific electroacupuncture (EA, 2 Hz, 3 V) being delivered to bilateral "Tinggong (SI 19)-Quchi (LI 11)" induced a depressor response, while 10 Hz-EA, and 2 Hz-EA to either non-acupoints, "Hegu (LI 4)-Quchi" or "Taichong (Liv 3)-Quchi" did not. Pretreatment of either phentolamine, Propranolol or methyl atropine (i.v.) could markedly reduce the depressor response, indicating that the sympathetic vasoconstrictor nerve, the cardia sympathetic nerve and cardiac vagal nerve all are involved in the hypotensive response.

Beta-endorphinergic neurons in nucleus arcuatus and nucleus tractus solitarii mediated depressor-bradycardia effect of "Tinggong" 2Hz-electroacupuncture.

The central neural mechanisms underlying the depressor-bradycardia effect of the "Tinggong" 2Hz-electroacupuncture (EA-DpB) were analyzed: (1) Brain transection caudal to nucleus arcuatus (AR) or procaine preinjection into bilateral AR could block the EA-DpB; (2) preinjection of naloxone into bilateral nucleus paraventricularis could even reverse the EA-DpB, but beta-endorphin antiserum had no significant effect on the EA-DpB; (3) after procaine injection into the nucleus commissuraris (the caudal part of NTS), the EA-DpB was also blocked; (4) preinjection of naloxone or beta-endorphin antiserum into bilateral rostral ventrolateral medulla (RVL) attenuated or reversed the EA-DpB response, taken together with our previous findings that the RVL mediates the depressor response to the excitation of the beta-endorphinergic neurons in AR or NTS, the above results suggest that the EA-DpB is mediated by the beta-endorphinergic projections from the AR and NTS to RVL. Finally the mechanism underlying the reverse of the EA-DpB by naloxone injection into nucleus paraventricularis was discussed.