Biomedical subjects

X M Yang

Publications and source records attributed to X M Yang.

At least 19 recordsLinked to original sources

PubMed2026

[Intestinal microbiota alterations after digestive tract reconstruction surgery and their impacts on host physiology].

The gut microbiota, acknowledged as the human body's 'second genome', plays a pivotal role in maintaining health. Digestive tract reconstruction surgery profoundly alters the anatomical structure and physiological environment of the gastrointestinal tract, thereby inducing significant shifts in the intestinal microbiota. These microbial changes subsequently influence host physiological functions through metabolic, immune, neuroendocrine, and other pathways. For instance, Roux-en-Y gastric bypass surgery enriches short-chain fatty acid(SCFA)-producing Bacteroides, improving systemic insulin sensitivity. Conversely, pancreaticoduodenectomy leads to a marked enrichment of potential pathobionts such as Klebsiella and Clostridium, which may elevate the risk of infections and tumor recurrence. This review comprehensively summarizes the characteristic changes in the gut microbiota following various digestive tract reconstruction procedures and discusses their multifaceted impacts on host physiology, aiming to provide insights for future experimental research and clinical practice.

Humans↗

PubMed1995

Human mammary artery endothelial sparing with fibrous jaw clamping.

BACKGROUND: Temporary clamping of the internal mammary artery pedicle is required for visualization during coronary artery bypass grafting. A nylon fibril jaw surface has been developed for these clamps that exerts pressure only at discrete sites on the pedicle surface. The effect of this new jaw surface on endothelial cell function and integrity after compression is investigated in this study. METHODS: Internal mammary artery specimens from 10 patients each were divided into three separate rings, and two of these rings were clamped for 30 minutes with either a smooth or fibrous jaw clamp. Isometric tensions were measured in organ chambers after contraction by relaxing the rings with the endothelium-dependent agent acetylcholine followed by the endothelium-independent agent sodium nitroprusside. The intimal surfaces of similar rings were silver stained to assess the percentage of intact endothelium. RESULTS: Endothelium-dependent relaxation was spared after fibrous jaw clamping (75% versus 89%) but significantly impaired after smooth jaw clamping (25% versus 89%; p < 0.001). Endothelium-independent relaxation was unaffected by either intervention. The percentage of remaining intact endothelium upon silver staining was significantly less after smooth than after fibrous jaw clamping (24% versus 48%; p < 0.01). CONCLUSIONS: Foam silicone with nylon fibrils on the jaw surface of internal mammary artery clamps preserves endothelial cell function and integrity. The remaining undamaged cells also may facilitate the subsequent regeneration of a confluent endothelial cell layer.

Acetylcholine↗

PubMed1995

Role of bradykinin in protection of ischemic preconditioning in rabbit hearts.

Bradykinin receptor activation has been proposed to be involved in ischemic preconditioning. In the present study, we further investigated the role of this agent in preconditioning in both isolated and in situ rabbit hearts. All hearts were subjected to 30 minutes of regional ischemia followed by reperfusion for 2 hours (in vitro hearts) and 3 hours (in situ hearts). Infarct size was measured by tetrazolium staining and expressed as a percentage of the size of the risk zone. Preconditioning in situ hearts with 5 minutes of ischemia and 10 minutes of reperfusion significantly reduced infarct size to 10.2 +/- 2.2% of the risk region (P < .0005 versus control infarct size of 36.7 +/- 2.6%). Pretreatment with HOE 140 (26 micrograms/kg), a bradykinin B2 receptor blocker, did not alter infarct size in nonpreconditioned hearts (40.6 +/- 5.3% infarction) but abolished protection from ischemic preconditioning (34.1 +/- 1.6% infarction). However, when HOE 140 was administered during the initial reflow period following 5 minutes of ischemia, protection was no longer abolished (15.6 +/- 3.9% infarction versus 13.3 +/- 3.8% without HOE 140, P = NS). Bradykinin infusion in isolated hearts mimicked preconditioning, and protection was not affected by pretreatment with the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester or the prostaglandin synthesis inhibitor indomethacin but could be completely abolished by the protein kinase C (PKC) inhibitors polymyxin B and staurosporine as well as by HOE 140. HOE 140 could not block the protection of ischemic preconditioning in isolated hearts. That failure was apparently due to the absence of blood-borne kininogens rather than autonomic nerves. When the preconditioning stimulus in the in situ model was amplified with four cycles of 5-minute ischemia/10-minute reperfusion, HOE 140 pretreatment could no longer block protection (infarct size was 10.7 +/- 3.5% versus 6.4 +/- 2.0% without HOE 140, P = NS). We propose that bradykinin receptors protect by coupling to PKC as do adenosine receptors, and blockade of either receptor will diminish the total stimulus of PKC below threshold and prevent protection. A more intense preconditioning ischemic stimulus can overcome bradykinin receptor blockade, however, by simply enhancing the amount of adenosine and possibly other agonists released.

Animals↗

PubMed1995

Expression of the hepatocyte growth factor/scatter factor receptor tyrosine kinase is localized to epithelia in the adult mouse.

The met proto-oncogene receptor tyrosine kinase has been identified as a receptor for hepatocyte growth factor (HGF)/scatter factor (SF). HGF/SF is a multifunctional cytokine that stimulates mitogenesis, dissociation, and motility of a broad spectrum of epithelial and endothelial cells in culture, promotes the progression of carcinoma cells to a more invasive phenotype, and acts as a morphogenic factor for tubular epithelia. HGF/SF is predominantly expressed by mesenchymal cells, whereas the met/HGF/SFR is predominantly expressed by epithelial and carcinoma cells in culture. We have shown by Northern analyses that the met/HGF/SFR is expressed in many adult mouse tissues. To elucidate the normal physiologic role for the met/HGF/SFR and the possible pathologic consequences of deregulation of this pathway, we have examined the expression of the met/HGF/SFR in adult mouse tissue by in situ hybridization. We show that the met/HGF/SFR is generally expressed in epithelia, including hepatocytes, epithelial cells that line the proximal and distal convoluted tubules of the kidney, epithelia of stomach, esophagus, uterus, lung and skin, as well as in granulosa cells of developing and mature oocytes. By reverse transcriptase PCR amplification, we show that the HGF/SF gene is expressed at low levels in many of these tissues. Our data support a possible role for the met/HGF/SFR in epithelial cell growth and tissue organization.

Animals↗

PubMed1995

Acadesine extends the window of protection afforded by ischaemic preconditioning in conscious rabbits.

OBJECTIVE: Ischaemic preconditioning protects myocardium from infarction if the reperfusion interval between the brief and prolonged ischaemic intervals is less than 1 h. In anaesthetised rabbits acadesine (5-amino-4-imidazolecarboxamide riboside, AICAR), an adenosine enhancer which increases tissue adenosine during ischaemia, prolongs the window of protection to 2 h. The aim of this study was to try to determine the maximum extension of this window of protection, using chronically instrumented, unsedated rabbits. METHODS: Rabbits were instrumented with a balloon occluder around a major branch of the left coronary artery for reversible coronary occlusion. Five to seven days after surgery all animals underwent a 30 min coronary occlusion. Animals were randomised to one of seven groups: (1) No additional treatment (control); (2) Ischaemic preconditioning with 5 min regional ischaemia followed by 10 min reperfusion before the 30 min coronary occlusion; (3) and (4) Ischaemic preconditioning followed by 2 or 4 h of reperfusion before the 30 min occlusion, respectively; (5) Treatment with acadesine (2.5 mg.kg-1.min-1 intravenously for 5 min and then 0.5 mg.kg-1.min-1 beginning 45 min before and continuing until 30 min after release of the 30 min occlusion) without ischaemic preconditioning; (6) and (7) Treatment with the higher dose of acadesine for 5 min beginning 35 min before the 5 min ischaemic period, and then the lower dose continuing until 30 min after release of the 30 min coronary occlusion in rabbits with 4 or 6 h reperfusion intervals, respectively. RESULTS: Rabbits with ischaemic preconditioning with 10 min reperfusion preceding the 30 min coronary occlusion (group 2) had only 5.6(SEM 1.1)% infarction of the ischaemic zone. Ischaemic preconditioning followed by 2 h reperfusion (group 3) offered continued protection [18.2(2.2)% infarction] as compared to control animals [37.7(2.6)% infarction]. However, protection waned if ischaemic preconditioning was followed by 4 h reperfusion (group 4) [36.7(3.0)% infarction]. Additionally, treatment with acadesine alone did not modify infarct size (group 7) [39.5(4.0)%], but acadesine largely restored the protection of ischaemic preconditioning despite a 4 h reperfusion interval (group 5) [20.4(3.0)% infarction, P < 0.01 v control]. However, when reperfusion was extended to 6 h (group 6) acadesine could no longer restore protection [36.2(0.9)% infarction]. CONCLUSIONS: The protection afforded by a 5 min ischaemic preconditioning period lasts from 2 to 4 h in the awake, unsedated rabbit, and acadesine can extend the duration of this window of protection to at least 4 h but not to 6 h.

Adenosine↗

PubMed1995

Defecography.

Defecography, a dynamic imaging modality, plays an important role in the diagnosis of functional and morphologic abnormalities of the anorectal region. We have here summarized the principle and techniques as well as observations of defecography, with special emphasis on morphologic measurements, clinical relevance, and limitations. The application of MR imaging in examination of anorectal function has also been addressed.

Barium Sulfate↗

PubMed1994

Involvement of hepatocyte growth factor in kidney development.

Using PCR, hepatocyte growth factor (HGF) and c-met (HGF receptor) expression were analyzed in the developing mouse kidney. Both HGF and c-met were expressed from Gestational Day 11.5 onward, the time at which branching morphogenesis of ureteric bud occurs. Coculturing the embryonic kidney with MDCK cells seeded in Type I collagen induced branching morphogenesis of the MDCK cells. When a monospecific antiserum against HGF was included in the culture medium, the branching morphogenesis induced by the embryonic kidney was markedly inhibited (73%). This anti-HGF serum also inhibited metanephric growth when incubated with 11.5- to 12.5-day embryonic kidneys in an organ culture assay. No inhibition was observed by nonimmune serum. Perturbation of ureteric duct development as well as extraductal metanephric development was observed in embryonic kidneys incubated with the anti-HGF serum. Together, our data indicates an important role for HGF in kidney development.

Animals↗

PubMed1994

Enhanced recovery of ischemic myocardium by combining percutaneous bypass with intraaortic balloon pump support.

Although percutaneous bypass (PB) can support the failing myocardium, regional ischemic damage may still occur beyond a coronary occlusion. This study sought to determine whether the addition of intraaortic balloon pump (IABP) support to PB would result in more optimal salvage of ischemic myocardium. In 30 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 3 hours of reperfusion with the snares released. During the period of coronary artery occlusion, 10 pigs were placed on PB, 10 pigs received PB plus IABP support, and 10 pigs received no support (the unmodified group). The hearts treated with the combination of PB and IABP support exhibited the highest wall motion scores (3.3 +/- 0.20 for the PB plus IABP group [p < 0.05 from the unmodified group and from the PB group]; versus 1.40 +/- 0.30 for the PB group versus 1.37 +/- 0.33 for the unmodified group), the least tissue acidosis (change in pH, -0.30 +/- 0.2 for the PB plus IABP group [p < 0.05 from the PB group] versus -0.60 +/- 0.10 for the PB group versus -0.41 +/- 0.13 for the unmodified group), and the least area of necrosis (25% +/- 5% for the PB plus IABP group [p < 0.05 from the unmodified group and from the PB group]; versus 43% +/- 2% for the PB group [p < 0.05 from the unmodified group] versus 73% +/- 3% for the unmodified group).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1994

A new animal model of controlled coronary artery occlusion in conscious rabbits.

OBJECTIVE: The aim was to develop a method for installing a pneumatic occluder on the coronary artery of a rabbit, and to see whether repetitive coronary occlusions could induce collateral development as in dogs. METHODS: A superficial branch of the left coronary artery was encircled with a balloon occluder, and a catheter was inserted into the left atrial appendage of New Zealand White rabbits, with a survival rate of 89.5%. Baseline collateral flow was measured 5-7 d after surgery with radioactive microspheres while the artery was occluded. According to a predetermined schedule animals were assigned to control and experimental groups. In the latter the balloon was inflated for 2 min once every 15 min for 8 h per d, 5 d per week. Collateral flow measurements were repeated after 100 and 300 occlusions. In control animals repeat flow measurements were made approximately 4 and 14 d after the first determination. RESULTS: Inflation of the balloon occluder reliably resulted in marked S-T segment elevation which quickly resolved after balloon deflation. These changes were nearly identical after two weeks of observation. Average baseline collateral flows in both groups were less than 5% of normal myocardial flow. There was no appreciable change during the two week period of observation in either control rabbits or those receiving at least 300 2 min coronary occlusions. CONCLUSIONS: The rabbit tolerates implantation of a pneumatic coronary occluder without noticeable problem and can successfully serve as a small animal model of repetitive or chronic myocardial ischaemia. The surgical preparation is not difficult, and ischaemia can be reproducibly created and relieved for at least three weeks following surgery. Coronary collaterals are sparse in the rabbit, and repetitive occlusions can be instituted without the complication of collateral development.

Animals↗

PubMed1994

Acadesine extends the window of protection afforded by ischaemic preconditioning.

OBJECTIVE: The aim was to test whether acadesine (5-amino-4-imidazolecarboxamide riboside, AICAR), an adenosine regulating agent which increases tissue adenosine during ischaemia, could prolong the window of protection from ischaemic preconditioning. METHODS: A branch of the left coronary artery of a rabbit heart was occluded for 30 min and reperfused for 180 min to induce infarction. Infarct size was determined with triphenyl tetrazolium staining. Prior to the 30 min ischaemia, rabbits were subjected to one of the following seven protocols: (1) No treatment (controls). (2) Preconditioning with 5 min of regional ischaemia followed by 2 h of reperfusion. (3) Treatment with acadesine (2.5 mg.kg-1.min-1 intravenously for 5 min starting 155 min prior to 30 min ischaemia followed by 210 min infusion of 0.5 mg.kg-1.min-1. (4) Treatment with acadesine (same schedule as in group 3) plus preconditioning as in group 2. (5) Treatment with acadesine for a shorter period (acadesine 2.5 mg.kg-1.min-1 for 5 min starting 30 min prior to preconditioning followed by 0.5 mg.kg-1.min-1 for only 60 min) plus preconditioning as in group 2. (6) Treatment with preconditioning followed by adenosine receptor blockade with 8-(p-sulphophenyl)theophylline (SPT) 10 mg.kg-1 intravenously immediately after and again 15 min after preconditioning. (7) Treatment with short infusion of acadesine plus preconditioning plus SPT. RESULTS: Preconditioning followed by 2 h of reperfusion offered little protection against infarction [28.6(SEM 2.7)% of the ischaemic zone infarcted] as compared to control [38.7(3.1)% infarction]. Treatment with acadesine alone did not modify the infarct size [37.8(3.5)%], but both of the acadesine plus preconditioning groups showed a significant limitation of infarct size with 13.9(3.1)% infarction in group 4 and 12.7(2.2)% infarction in group 5 (both p < 0.01 v control). Although SPT alone did not modify the infarct size [26.8(3.3)%], SPT blocked the protective effect of acadesine [25.3(2.9)%, p < 0.05 v group 5]. CONCLUSION: Acadesine can delay the natural decay of preconditioning. This delay appeared to be mediated by adenosine and may have therapeutic potential.

Adenosine↗

PubMed1994

Rat and rabbit heart infarction: effects of anesthesia, perfusate, risk zone, and method of infarct sizing.

Rabbits and rats are becoming popular models for in vitro as well as in situ studies of myocardial infarction. In the present analysis we evaluated the results of several of our completed investigations and tested whether blood-free perfusate, anesthesia, or risk zone size affects infarction in these species. In addition, the influence of the method used for determining infarct size (histology or histochemistry) was examined in rabbits. All hearts experienced 30 min of regional ischemia followed by either 2-3 h of reperfusion in animals in which infarct size was assessed by staining with triphenyltetrazolium chloride or 72 h in those in which histological methods were used to measure infarct size. Eighteen rabbit and seven rat hearts perfused with Krebs buffer, seventeen open-chest rabbits, eight rats anesthetized with pentobarbital, and ten conscious rabbits were studied. Risk zone size measured with fluorescent particles was plotted against infarct size. Infarct size was linearly correlated with risk zone size and did not differ among models for each species. In rat hearts the regression line passed through the origin so that zero infarction occurred with zero risk zone size. However, in the rabbit heart there was no apparent infarction for risk zone sizes < 0.3 cm3. Although the relationship between risk zone and infarction was found to be remarkably independent of the model chosen, the nonzero intercept for the rabbit heart can be an important, previously unrecognized source of experimental variability when infarct size is expressed as a percentage of the risk zone.

Anesthesia↗

PubMed1994

Conscious rabbits become tolerant to multiple episodes of ischemic preconditioning.

Although ischemic preconditioning protects myocardium from infarction in isolated hearts and in anesthetized open-chest animals, its effects have not been examined in unanesthetized animals. Furthermore, it is unknown whether animals become tolerant to multiple episodes of ischemic preconditioning. Rabbits were chronically instrumented with a balloon occluder around a major branch of the left coronary artery for reversible coronary occlusion, a left atrial catheter for radioactive microsphere injections, ECG electrodes for monitoring of myocardial ischemia, and, in some cases, a carotid artery catheter for pressure measurements and timed withdrawal of reference arterial blood samples. Eight control rabbits underwent a 30-minute coronary occlusion and then 180 minutes of reperfusion. Five of the eight rabbits developed ventricular tachycardia or fibrillation during ischemia, and infarct size averaged 37.7 +/- 2.6% of the risk area. Eight rabbits experienced a 5-minute coronary occlusion and 10 minutes of reperfusion before the 30-minute occlusion. In these preconditioned animals, potentially fatal arrhythmias during ischemia were significantly reduced (one of eight, P < .05), and infarct size was much smaller (5.6 +/- 1.1%, P < .0001). The difference could not be explained by hemodynamics or collateral blood flow, which were nearly identical in the two groups. But when the 30-minute coronary occlusion was preceded by 40 to 65 five-minute occlusions during a 3- to 4-day period in seven animals, protection was markedly attenuated. Potentially lethal arrhythmias were very common, and infarct size averaged 26.5 +/- 2.9%, substantially larger than in rabbits with only one preconditioning occlusion (P < .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Accuracy of digital videodensitometry in quantitating contrast medium concentration.

To evaluate the accuracy of digital videodensitometric technique in directly quantitating concentration of contrast medium, iohexol 300 mg I/ml was injected into a 2-mm-diameter plastic tube, in which clean water was circulated at a 190 ml/min flow, for digital subtraction angiography. Altogether 27 injections were performed with 3, 4 and 5 ml volumes at 3-, 4- and 5-ml/s flows of the contrast medium. A time-density curve was achieved by selecting a "vessel" region of interest (ROI) and a background ROI. Then, a frame corresponding to the maximum opacification of the contrast medium could be calculated. Finally, the average density and the time to peak density of the contrast medium were obtained. The average density was statistically higher (p < 0.01) with 5 ml/s flow than with 4- and 3-ml/s flows. Times to peak density reduced as injection flows or volumes increased. The results support the conclusion that digital videodensitometric technique is an accurate method for quantitation of contrast medium concentration during angiography. The angiographic opacification may be improved by injecting the iodine contrast medium with higher flows or larger volumes.

Absorptiometry, Photon↗

PubMed1993

NAD-dependent methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase is the mammalian homolog of the mitochondrial enzyme encoded by the yeast MIS1 gene.

The recombinant human bifunctional NAD-dependent methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase is unique in its absolute requirement for Mg2+ and inorganic phosphate. Both ions affect the affinity of the enzyme for NAD and have no effect on the binding of methylenetetrahydrofolate. The NAD cofactor can be replaced by NADP with a much higher KM and lower VMAX. Kinetic investigation using NADP supports the role of Mg2+ in dinucleotide binding and illustrates that the 2'-phosphate can substitute for phosphate in this process. The human NAD-dependent bifunctional enzyme has a 44% amino acid sequence identity with the dehydrogenase-cyclohydrolase domain of the yeast mitochondrial NADP-dependent trifunctional enzyme encoded by the MIS1 gene, compared to 37% identity with the corresponding domain of the cytosolic trifunctional enzyme. The sequence comparison and the kinetic properties suggest that the NAD bifunctional enzyme is the mammalian homolog of the yeast mitochondrial trifunctional enzyme, which has evolved a unique use of inorganic phosphate to change its dinucleotide specificity from NADP to NAD. Its role is proposed to be in providing formyltetrahydrofolate for the synthesis of formylmethionyl transfer RNA required for the initiation of protein synthesis in mitochondria.

Aminohydrolases↗

PubMed1993

The protection of ischaemic preconditioning can be reinstated in the rabbit heart after the initial protection has waned.

OBJECTIVE: Preconditioning the heart with 5 min of ischaemia followed by reperfusion renders the myocardium resistant to infarction from subsequent ischaemia. This protection lasts for about 1 h. The aim of this study was to test whether the protection could be reinstated with a second episode of preconditioning after protection from an initial episode had worn off. METHODS: To induce infarction animals experienced 30 min of coronary artery occlusion and then 3 h reperfusion. Ischaemic preconditioning was accomplished with 5 min of coronary branch occlusion. In one group of rabbits the subsequent reperfusion period was prolonged to 2 h to permit protection to wear off before the 30 min coronary occlusion was initiated. In another group a second 5 min coronary occlusion was performed at the end of the 2 h reperfusion. After 10 min of reperfusion the 30 min ischaemic period began. Control animals experienced only the 30 min ischaemia and 3 h reperfusion. Infarct volume was measured with tetrazolium and expressed as a percentage of the ischaemic zone volume. RESULTS: Average infarct size in seven control rabbits [36.0 (SEM 2.0)% of the ischaemic zone] was not significantly different from that in eight rabbits with the prolonged coronary occlusion occurring 2 h after the preconditioning stimulus [28.6 (2.9)% infarction]. In contrast infarcts were significantly smaller in the re-preconditioned group of seven rabbits [8.3 (4.2)%] and comparable to those previously seen with a single preconditioning stimulus followed 10 min later by the 30 min occlusion [6.1 (1.8)%]. CONCLUSIONS: The rabbit heart can be protected with a second preconditioning stimulus after protection from an initial period of preconditioning has subsided.

Animals↗

PubMed1993

[Suppurative mediastinitis as a complication of deep neck infection (report of 15 cases)].

Fifteen cases of suppurative mediastinitis secondary to perforation of pharynx or esophagus are reported. The cervical fascial spaces are the main route of spread of infection from the neck to the mediastinum. The infection is caused by both aerobic and anaerobic bacteria. Major treatments for suppurative mediastinitis are early surgical drainage and proper use of antibiotics; Irrigation of the mediastinum with povidone-iodine is a safe and effective treatment. Of these 15 patients, 11 survived and 4 died. One case complicated by common carotid artery rupture was cured by surgical repair.

Adolescent↗

PubMed1993

Detrimental effects of interrupting warm blood cardioplegia during coronary revascularization.

Warm blood cardioplegia has emerged as a substitute for cold blood cardioplegia as a method of myocardial protection. However, the continuous infusion of blood in this technique may obscure the operative field and necessitate interruption of warm blood cardioplegia. This experimental study was therefore undertaken to determine whether interrupting warm blood cardioplegia during coronary revascularization would increase myocardial damage. In 30 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals underwent cardiopulmonary bypass and 45 minutes of cardioplegic arrest. During the period of cardioplegic arrest, 10 pigs received intermittent antegrade/retrograde infusion of cold blood cardioplegic solution (4 degrees C) 10 pigs received continuous retrograde infusion of warm blood cardioplegic solution (37 degrees C) at 100 ml/min, and 10 pigs received retrograde infusion of warm blood cardioplegic solution that was interrupted for three 7-minute periods. After aortic unclamping, the coronary snares were released and all hearts were reperfused for 180 minutes. Interrupting retrograde warm blood cardioplegia resulted in more tissue acidosis during cardioplegic arrest (6.20 +/- 0.16 interrupted retrograde warm blood cardioplegia and 6.45 +/- 0.12 continuous retrograde warm blood cardioplegia, both p < 0.05 compared with 6.98 +/- 0.17 intermittent antegrade and retrograde cold blood cardioplegia), decreased echocardiographic wall-motion scores (4 [normal] to -1 [dyskinesis]; 2.06 +/- 0.30 interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 3.30 +/- 0.40 intermittent antegrade and retrograde cold blood cardioplegia, 2.80 +/- 0.40 continuous retrograde warm blood cardioplegia), and increased tissue necrosis as measured by the area of necrosis/area at risk (38% +/- 5% interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 21% +/- 2% intermittent antegrade and retrograde cold blood cardioplegia; 25% +/- 2% continuous retrograde warm blood cardioplegia). We concluded that interrupting warm blood cardioplegia during coronary revascularization diminishes the effectiveness of warm blood cardioplegia and results in increased ischemic damage.

Animals↗

PubMed1992

Anxiogenic effects of acute and chronic cocaine administration: neurochemical and behavioral studies.

The effects of cocaine on defensive withdrawal behavior in rats and elevated plus-maze behavior in mice were investigated. Cocaine (20 mg/kg IP) injected daily for 7 or 14 days induced defensive withdrawal; that is, the latency to emerge from a small chamber in an open field and the mean time in the chamber were both significantly increased. Acute cocaine administration also induced defensive withdrawal, and this effect was prevented by prior treatment with chlordiazepoxide (5 mg/kg IP). Both acute and chronic cocaine treatments significantly increased plasma concentrations of corticosterone and reduced the ratios of 3,4-dihydroxyphenylacetic acid to dopamine and 5-hydroxyindoleacetic acid to serotonin in several brain regions. Further evidence for an acute anxiogenic effect of cocaine was obtained from mice studied in the elevated plus-maze. Acute cocaine administration decreased both the number of entries into and the time spent in the open arms of the maze. These results taken together strongly support an anxiogenic action of acute and chronic cocaine administration.

Animals↗