PubMed Health⌕ Search

Biomedical subjects

A Dana

Publications and source records attributed to A Dana.

At least 19 recordsLinked to original sources
PubMed2006

The use of multiple "buddies" during transradial angioplasty in a complex calcified coronary tree.

We report our experience in transradial coronary angioplasty on a tortuous, calcified coronary tree in a patient who had been turned down for surgical revascularization. In view of the complexity of the coronary anatomy, successful completion of the procedure required plaque modification with the use of rotational atherectomy in the left anterior descending coronary artery, and the use of an inflated buddy balloon in the circumflex artery. The latter represents a novel, simple, and inexpensive technique, which may allow successful advancing of coronary stents in calcified and tortuous coronary arteries.

Aged↗
PubMed2004

[Urinary tract imaging: conventional radiology and ultrasound].

Conventional radiology includes intravenous urography for evaluation of the entire urinary tract and direct opacifications by retrograde cystography, supra-pubic cystography, and retrograde urethro-cystography for evaluation of the lower urinary tract. Intravenous urography remains the gold standard for evaluation of the upper excretory tract. The accuracy of ultrasound examination has increased with the availability of multiple frequency probes, harmonic imaging and color Doppler imaging. Because it is non-invasive, ultrasound now is the first line imaging technique for evaluation of the renal parenchyma, renal vessels and bladder.

Cystoscopy↗
PubMed2001

Delayed or second window preconditioning induced by adenosine A1 receptor activation is independent of early generation of nitric oxide or late induction of inducible nitric oxide synthase.

Transient adenosine A1 receptor (A1R) activation induces a second window or delayed preconditioning against myocardial infarction 24-72 h later. Early generation of nitric oxide and delayed induction of nitric oxide synthase have been implicated in mediating delayed cardioprotection after ischemic preconditioning in rabbits. Recent evidence indicates that some of the regulatory roles of adenosine in cardiac tissue may be mediated by A1R-induced generation of nitric oxide. This study examined the role of nitric oxide in the mediation of A1R-induced delayed preconditioning against infarction. Pharmacologic preconditioning of rabbits with the selective A1R agonist 2-chloro-N6-cyclopentyladenosine 100 microg/kg (CCPA) significantly reduced myocardial infarct size compared with control animals, after 30 min regional ischemia and 2 h reperfusion in vivo 24 h later (27.3+/-4.7 vs. 46.0+/-3.7%, respectively; p = 0.001). Nonselective inhibition of nitric oxide synthase with N(G)-nitro-L-arginine methyl ester (10 mg/kg) before administration of CCPA did not affect this infarct limitation at 24 h. Selective inhibition of inducible nitric oxide synthase before the prolonged ischemic insult on day 2, with two structurally independent inducible nitric oxide synthase inhibitors, L-N(6)-(1-iminoethyl)-lysine (10 mg/kg) or aminoguanidine (300 mg/kg), did not abrogate the reduction in infarction observed by pharmacologic preconditioning with CCPA 24 h earlier. These results suggest that the second window or delayed protection against myocardial infarction observed 24 h after pharmacologic preconditioning with an adenosine A1 agonist occurs independently of either early generation of nitric oxide or subacute induction of inducible nitric oxide synthase.

Adenosine↗
PubMed2001

Turicella otitidis mastoiditis in a healthy child.

Turicella otitidis, a coryneform bacterium, has been associated with acute otitis media. A 5-year-old girl developed acute mastoiditis. Turicella was isolated from the right and left middle ear fluid.

Actinomycetales↗
PubMed2000

The preconditioning phenomenon: A tool for the scientist or a clinical reality?

The possibility that an innate mechanism of myocardial protection might be inducible in the human heart has generated considerable excitement and enthusiastic research. The potential to enhance myocardial resistance to ischemic injury in patients suffering the consequences of coronary artery disease has led to studies with more direct clinical relevance. However, in common with many other areas of clinical interest based on advances in basic scientific understanding, early enthusiasm may be disproportionate to ultimate therapeutic significance. There can be little doubt that our understanding of the mechanisms underlying the pathogenesis of ischemia-reperfusion injury has been enhanced significantly by the plethora of research stimulated by interest in endogenous myocardial protection. Direct extrapolation of observations in the laboratory to the cardiology clinic or operating theater is tempting but should be avoided. The results of recent clinical experiments that suggest that preconditioning can protect against ischemia, although encouraging, should be interpreted cautiously, with particular attention to the limitations of the end points available. A reasoned evaluation of recent research should prevent unrealistic expectations and allow improved design of future trials so that this potent adaptive phenomenon can be exploited to its maximum potential.

Angina, Unstable↗
PubMed2000

Adenosine A(1) receptor activation induces delayed preconditioning in rats mediated by manganese superoxide dismutase.

BACKGROUND: We have previously described a second window of protection against infarction in rabbits 24 to 72 hours after adenosine A(1) receptor (A(1)R) activation. In this study, we examined the potential role of the mitochondrial antioxidant manganese superoxide dismutase (Mn-SOD) as a potential end effector in mediating this protection. METHODS AND RESULTS: Rats were treated with an intravenous bolus of the A(1)R agonist 2-chloro-N(6)-cyclopentyladenosine (CCPA, 75 microg/kg) or saline vehicle. They were also given a 5 mg/kg IV infusion of a 22-mer phosphorothioate oligodeoxynucleotide (ODN) with sequence antisense to the initiation site of rat Mn-SOD mRNA. Sense ODN and scrambled ODN were used as controls. Twenty-four hours later, hearts were isolated and perfused with buffer at constant pressure and subjected to 35 minutes of regional ischemia and 2 hours of reperfusion. Treatment with CCPA compared with saline vehicle (control) significantly reduced infarct size, expressed as percentage of myocardium at risk (22.3+/-3.3% versus 42.1+/-3.8%, respectively; P=0.001). This protection was completely abolished by prior treatment with antisense ODN, which had no effect on its own. Neither sense ODN nor scrambled ODN had an effect on the CCPA-induced delayed cardioprotection. In separate animals, 24 hours after the same treatment, hearts were assayed for Mn-SOD content and activity. CCPA treatment induced a significant increase in myocardial Mn-SOD content and activity compared with the control condition; this increase was abolished by pretreatment with antisense ODN. CONCLUSIONS: This is the first study to show that transient A(1)R activation induces delayed cardioprotection in the rat. These results strongly suggest an important role for mitochondrial Mn-SOD as a potential end effector of this protection.

Adenosine↗
PubMed2000

Adenosine A(1) receptor induced delayed preconditioning in rabbits: induction of p38 mitogen-activated protein kinase activation and Hsp27 phosphorylation via a tyrosine kinase- and protein kinase C-dependent mechanism.

Transient adenosine A(1) receptor (A(1)R) activation in rabbits induces delayed preconditioning against myocardial infarction 24 to 72 hours later. The cellular mechanisms downstream of A(1)R mediating this delayed cardioprotection have not been elucidated. This study examined the role of protein kinase C (PKC) and tyrosine kinases (TKs) in the signaling cascade mediating A(1)R-induced late preconditioning in rabbits. The small heat shock protein Hsp27 has been shown to confer cytoskeletal protection when in the phosphorylated state. We therefore also evaluated the potential role of the p38 mitogen-activated protein kinase (p38 MAPK) and Hsp27 as distal mediators of A(1)R-induced delayed preconditioning. Pharmacological preconditioning of rabbits with the selective A(1) agonist 2-chloro-N(6)-cyclopentyladenosine (CCPA; 100 microgram/kg) significantly reduced myocardial infarct size compared with control animals, after 30-minute regional ischemia/2-hour reperfusion in vivo 24 hours later (23.7+/-3.1 versus 43.0+/-4.1%; P<0.05). This delayed protection was abrogated by prior inhibition of either PKC with chelerythrine chloride (5 mg/kg) or of TKs with lavendustin A (1.3 mg/kg), suggesting that both PKC and TK are crucial for the development of delayed preconditioning after A(1) receptor activation in the rabbit. Myocardial tissue extracts obtained 24 hours after CCPA treatment were analyzed for p38 MAPK catalytic activity using an in vitro kinase assay. This showed an almost 7-fold increase in p38 MAPK activity in myocardial samples pretreated with CCPA compared with control hearts. Two-dimensional gel electrophoresis revealed an increase in the phosphorylated isoforms of Hsp27 in hearts pretreated with CCPA compared with control hearts. Prior inhibition of either PKC or TK prevented the CCPA-induced increase in p38 MAPK activity and phosphorylation of Hsp27. This study identifies new components of the signaling mechanism of A(1)R-induced delayed preconditioning. Our results suggest an important role for both PKC and TK as mediators of late preconditioning against infarction after A(1)R activation and, although correlative, point to the p38 MAPK/Hsp27 pathway as a potential distal effector of this protection.

Animals↗
PubMed1999

[Uroradiology].

Explore the source record for details and available documents.

Adrenal Gland Diseases↗
PubMed1998

Prolonging the delayed phase of myocardial protection: repetitive adenosine A1 receptor activation maintains rabbit myocardium in a preconditioned state.

OBJECTIVES: This study was designed to examine whether the myocardium can be maintained in a protected state by extending the delayed phase of cardioprotection with chronic, intermittent adenosine A1 receptor activation. BACKGROUND: Several recent studies have explored the temporal characteristics of the protective effects of ischemic preconditioning. Two distinct phases of myocardial protection have been described: the short-lived immediate phase, or "classic" preconditioning, and the delayed phase, or "second window of protection" (SWOP). Previous studies have examined the potential for extending the duration of classic preconditioning by repeated application of the preconditioning stimulus. Pretreatment with either multiple episodes of ischemia or continuous infusion of a selective adenosine A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine (CCPA), resulted in attenuation of the protective effects of preconditioning, implying downregulation of the receptors involved in triggering classic preconditioning. METHODS: Male New Zealand White rabbits were treated with repeated intravenous boluses of CCPA, 100 microg/kg body weight, or 0.9% saline at 48-h intervals. Forty-eight hours after the fifth dose (day 10), the animals were anesthetized and subjected to 30 min of coronary occlusion, followed by 120 min of reperfusion. Infarct size was determined as a percentage of myocardial risk volume using tetrazolium staining. To further explore whether the rabbits had developed tolerance to the effects of adenosine A1 receptor activation, a subgroup of animals were treated with a further bolus of CCPA, 100 microg/kg, at the end of the reperfusion period, and the hemodynamic response was monitored for 10 min before excision of the heart. RESULTS: Pretreatment with intermittent doses of CCPA resulted in a 42% reduction in the infarct to risk ratio compared with vehicle pretreatment (26.6+/-3.7% vs. 45.9+/-5.5%, p < 0.01). Furthermore, CCPA treatment at the end of reperfusion resulted in identical hypotension and bradycardia in both groups. CONCLUSIONS: We conclude that rabbits can be maintained in a protected state against myocardial infarction by repeated activation of adenosine A1 receptors, with no evidence of tachyphylaxis to the infarct-limiting or hemodynamic effects of CCPA. This finding suggests that adenosine A1 receptor activation may hold promise as a new approach to long-term cardioprotection.

Adenosine↗
PubMed1998

Angina: who needs it? Cardioprotection in the preconditioning era.

Over the past two decades, it has been demonstrated in various animal species that the myocardium possesses innate adaptive mechanisms that may render it more resistant to ischemic injury. Ischemic preconditioning, defined as the protection conferred to ischemic myocardium by prior episodes of brief sublethal ischemia, is one of the most potent of such adaptive phenomena. Extensive research over the past decade has alluded to the cellular mechanisms underlying this powerful means of reducing myocardial ischemia-reperfusion injury. Moreover, the possibility that such adaptive mechanisms might be inducible in the human heart has generated considerable excitement and enthusiastic research, which has significantly enhanced our understanding of the pathogenesis of ischemia-reperfusion injury. An insight into the mechanisms underlying the cardioprotective properties of ischemic preconditioning has, on the one hand, directed research aimed at identification of novel therapeutic agents for the treatment of ischemic heart disease, and on the other, questioned the use of potentially deleterious agents that may abolish the cardioprotective actions of ischemic preconditioning in patients with angina. Current studies are under way to evaluate the potential protection afforded by these "preconditioning" agents in patients with acute coronary syndromes, and some early reports provide some basis for optimism that a beneficial and clinically detectable improvement in myocardial protection may be possible. This article reviews our current knowledge of the cellular mechanisms responsible for mediation of ischemic preconditioning, the evidence for the existence of this phenomenon in humans, and its potential therapeutic applications.

Angina Pectoris↗
PubMed1998

Ischaemic preconditioning: a clinical perspective.

Ischaemic preconditioning is an endogenous mechanism of myocardial protection which may allow us to slow the progress of myocardial necrosis, increasing the time available for effective reperfusion. Recent evidence suggests that the human myocardium can be preconditioned. This article reviews the current literature and suggests clinical situations where this potent treatment might be relevant.

Humans↗