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Arterial Responses (arterial + response)
Selected AbstractsLong-term clopidogrel administration following severe coronary injury reduces proliferation and inflammation via inhibition of nuclear factor-kappaB and activator protein 1 activation in pigsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2009K. Pels ABSTRACT Background, The optimal duration of clopidogrel treatment following percutaneous coronary intervention (PCI) and the patient population that would benefit most are still unknown. In a porcine coronary injury model, we tested two different durations of clopidogrel treatment on severely or moderately injured arteries and examined the arterial response to injury. To understand the molecular mechanism, we also investigated the effects on transcription factors nuclear factor-kappaB (NF-,B) and activator protein 1 (AP-1). Materials and methods, In 24 cross-bred pigs, one coronary artery was only moderately injured by percutaneous transluminal coronary angioplasty (PTCA) and one coronary artery was severely injured by PTCA and subsequent beta-irradiation (Brachy group). Animals received 325 mg aspirin daily for 3 months and 75 mg clopidogrel daily for either 28 days [short-term (ST) clopidogrel group] or 3 months [long-term (LT) clopidogrel group]. Results, After 3 months, the number of proliferating cells per cross-section differed significantly between ST and LT in both injury groups (PTCAST 90·2 ± 10·3 vs. PTCALT 19·2 ± 4·7, P < 0·05; BrachyST 35·8 ± 8·4 vs. BrachyLT 7·5 ± 2·0, P < 0·05). Similar results were seen for inflammatory cells (CD3+ cells): PTCAST 23·5 ± 3·55 vs. PTCALT 4·67 ± 0·92, P < 0·05; BrachyST 83·17 ± 11·17 vs. BrachyLT 20 ± 4·82, P < 0·05). Long-term administration also reduced the activity of NF-,B and AP-1 by 62,64% and 42,58%, respectively. However, the effects of different durations of clopidogrel administration on artery dimensions were not statistically significant. Conclusions, Regarding inflammation and transcription factor activity at the PCI site, long-term clopidogrel administration is superior to short-term administration, especially in severely injured arteries. Transferring our results to the human situation, patients with more severely diseased arteries may benefit from a prolonged clopidogrel medication after PCI. [source] Microstructural alterations of the retinal arterial blood column along the vessel axis in healthy volunteers with ageACTA OPHTHALMOLOGICA, Issue 2009IM LANZL Purpose We demonstrated previously that roughness of the retinal arterial blood column measured along the vessel axis increases in anamnestically healthy volunteers with increasing age. We termed it longitudinal retinal arterial profile (LAP). Whether LAP is altered with age in medically supervised healthy persons is investigated. Methods 82 medically healthy volunteers were examined by Dynamic Vessel Analyzer (IMEDOS, Jena, Germany) using stimulation with flickering light. 3 age groups were formed: young (N=27, 30,5±4,3 years), middle age (N=28, 42,3±3,3 years) and seniors (N=27, 64,0±5,0 years). Included in the analysis were volunteers without medical vascular risk factors defined as: blood pressure < 140/90 mmHg, HDL > 35 mg/dl, LDL < 190 mg/dl and glucose levels < 110 mg/dl. Retinal arterial diameters were measured along 1 mm vessel segments to obtain LAP. Differences were analyzed using Fourier transformation. Results In all age groups LAP do not change during all stages of the arterial response. Arterial diameters in the senior group were reduced in comparison to the young group at all stages of the vessel reaction (p<0,05). There are differences in LAP between the age groups. Compared to young persons, seniors showed significantly diminished waves with a period of 417 µm at all stages of the arterial reaction, whereas young volunteers showed less pronounced waves with a period of 208 µm (p<0,05). Conclusion Our results represent the healthy aging process in retinal vasculature. Age related microstructural changes in longitudinal profiles of retinal arteries in medically healthy persons might be an indication for alterations in the vascular endothelium and smooth musculature. [source] Effects of C-peptide on forearm blood flow and brachial artery dilatation in patients with type 1 diabetes mellitusACTA PHYSIOLOGICA, Issue 3 2001E. Fernqvist-Forbes Recent studies suggest that C-peptide increases blood flow in both exercising and resting forearm in patients with type 1 diabetes. Now we have studied the effect of C-peptide administration on endothelial-mediated and non-endothelial-mediated arterial responses as well as central haemodynamics in 10 patients with type 1 diabetes in a placebo-controlled double-blind study. Euglycaemia was maintained with an i.v. insulin infusion before and during the study. A high-resolution ultrasound technique and Doppler echocardiography were used to assess haemodynamic functions. Brachial artery blood flow and brachial artery diameter were measured in the basal state, 1 and 10 min after reactive hyperaemia and 4 min after sublingual glyceryl trinitrate administration (GTN; endothelial-independent vasodilatation), both before and after the end of 60-min C-peptide (6 pmol kg,1 min,1) or saline infusion periods. Echocardiographic measurements were also performed before and at the end of the infusion periods. Seven healthy age-matched males served as controls for vascular studies. The patients showed a blunted brachial dilatation after reactive hyperaemia in comparison with the healthy controls (2.1 ± 0.5% vs. 9.3 ± 0.3%, P < 0.001), indicating a disturbed endothelial function. C-peptide infusion compared with saline resulted in increased basal blood flow (33 ± 6%, P < 0.001) and brachial arterial dilatation (4 ± 1%, P < 0.05). Left ventricular ejection fraction seemed to be improved (5 ± 2%, P < 0.05) at the end of C-peptide infusion compared with placebo. The vascular response to reactive hyperaemia and GTN was not affected by C-peptide infusion. Our results demonstrate that physiological concentrations of C-peptide increase resting forearm blood flow, brachial artery diameter and left ventricular systolic function in patients with type 1 diabetes. [source] Morphine, opioids, and the feline pulmonary vascular bedACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2008A. D. KAYE Background: Opioid-induced vasodepressor responses have been reported in a variety of species and laboratory models. The aim of this study was to ascertain the relative potencies of different clinically relevant opioids compared with traditional vasodepressor agents in the feline pulmonary vascular bed. A second aim was to study the effects of morphine and to identify the receptors involved in the mediation or the modulation of these effects. Methods: This was a prospective vehicle-controlled study involving an intact chest preparation of adult mongrel cats. The effects of various opioids, morphine, fentanyl, remifentanil, sufentanil, and meperidine were compared with other vasodepressor agents. Additionally, the effects of l - N5 -(1-iminoethyl) ornithine hydrochloride (l -NIO) (nitric oxide synthase inhibitor), nimesulide [selective cyclooxygenase (COX)-2 inhibitor], glibenclamide (ATP-sensitive K+ channel blocker), naloxone (non-selective opioid receptor antagonist), and diphenhydramine (histamine H1 -receptor antagonist) were investigated on pulmonary arterial responses to morphine and other selected agonists in the feline pulmonary vascular bed. The systemic pressure and lobar arterial perfusion pressure were continuously monitored, electronically averaged, and recorded. Results: In the cat pulmonary vascular bed of the isolated left lower lobe, morphine, remifentanil, fentanyl, sufentanil, and meperidine induced a dose-dependent moderate vasodepressor response and it appeared that sufentanil was the most potent on a nanomolar basis. The effects of morphine were not significantly altered after administration of l -NIO, nimesulide, and glibenclamide. However, the vascular responses to morphine were significantly attenuated following administration of naloxone and diphenhydramine. Conclusion: The results of the present study suggest that sufentanil appears to have slightly more potency and morphine the least of the five opioid agonists studied on a nanomolar basis. Morphine-induced vasodilatory responses appeared to be mediated or modulated by both opioid receptor and histamine-receptor-sensitive pathways. [source] Ephedrine in the cat lung vasculatureACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2003A. M. Fields Background:, Ephedrine is one of the most commonly used non-catecholamine sympathomimetic agents. It is used in operating rooms and critical care settings worldwide. While it has many side effects, its ability to rapidly raise blood pressure makes it an ideal agent to maintain homeostasis as well as in emergency situations. While its effects are known to be mediated by an ,-mediated mechanism, the exact , subtype is unknown. In addition, no studies using ephedrine have been performed in the pulmonary vascular bed of the cat. Methods:, The effects of phentolamine, a non-selective ,-receptor blocker, and prazosin, an ,1 -selective antagonist, were investigated on pulmonary arterial responses to ephedrine, phenylepherine, norepinephrine, and U-46619. Lobar arterial perfusion pressure was continuously monitored, electronically averaged, and recorded with constant flow in the isolated left lower lobe vascular bed of the cat. Results:, Phentolamine and prazosin significantly reduced vasoconstrictor pulmonary perfusion pressure increases induced by ephedrine. Conclusion:, Ephedrine has significant vasopressor activity in the pulmonary vascular bed of the cat meditated predominantly by ,1 adrenergic receptor activation. [source] | ||||||||||