| 1. |
- Lindstedt Ingemansson, Sandra, et al.
(author)
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Myocardial topical negative pressure increases blood flow in hypothermic, ischemic myocardium.
- 2008
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In: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1651-2006 .- 1401-7431. ; 42, s. 345-353
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Journal article (peer-reviewed)abstract
- Objectives. Hypothermia protects the myocardium from oxidative injury during ischemic stress and reperfusion. We have previously shown that topical negative pressure (TNP) of -50 mmHg significantly increases microvascular blood flow in the underlying myocardium in normal, ischemic, and reperfused porcine myocardium. The present study was designed to elucidate the effect of TNP between -50 mmHg and -150 mmHg on microvascular blood flow in ischemic myocardium during hypothermia. Design. The microvascular blood flow in the myocardium was recorded, in seven pigs, using laser Doppler velocimetry. Analyses were performed in the epicardium and in the myocardium, after 40 minutes of occlusion of the LAD followed by cooling to 31 degrees C. Results. A TNP of -50 mmHg applied to the epicardium, from 23.3+/-3.8 PU to 104.2+/-31.3 PU (*p <0.05), and in the myocardium, from 35.0+/-7.2 PU to 74.2+/-21.8 PU (*p <0.05). Conclusions. Only a TNP level of -50 mmHg significantly increased the microvascular blood flow in both the epicardium and in the myocardium during hypothermia.
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| 2. |
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| 3. |
- Borgquist, Ola, et al.
(author)
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Tissue Ingrowth Into Foam but Not Into Gauze During Negative Pressure Wound Therapy
- 2009
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In: Wounds. - 1044-7946. ; 21:11, s. 302-309
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Journal article (peer-reviewed)abstract
- Background. Foam and gauze are two types of wound fillers used for negative pressure wound therapy (NPWT). Differences in the wound healing effects of foam and gauze have been observed clinically. The aim of the present study was to examine the effects of NPWT on the wound bed using foam and gauze. Methods. A porcine peripheral wound model was treated with NPWT at 0, -75 mmHg, or -125 mmHg for 72 hours. The effects of foam and gauze on the wound bed were compared, and the force required to remove the dressings was measured. Sections of biopsies from the wound bed with an overlying dressing were stained with hematoxylin-eosin and Giemsa and were examined histologically. Results. The force ratio needed to remove the wound filler from the wound bed after treatment with negative pressure was greater for foam than for gauze. NPWT caused the wound bed tissue to grow into the foam, while there was I no such ingrowth into gauze. Furthermore, beneath the foam there was more leukocyte infiltration, tissue disorganization, disruption of contact among cells, and differences in size among cells. The results were similar regardless of the level of negative pressure. Conclusion. More force was required to remove foam compared to gauze following NPWT, which may have been due to greater ingrowth into foam. These findings may explain the patient discomfort and wound bed disruption upon removal of foam. The observed differences in wound bed tissue morphology under foam and gauze are in accordance with the clinically observed differences in quality of granulation tissue formation.
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| 4. |
- Dimitrijevic, Ivan, et al.
(author)
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Increased angiotensin II type 1 receptor expression in temporal arteries from patients with giant cell arteritis.
- 2009
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In: Ophthalmology. - : Elsevier BV. - 1549-4713 .- 0161-6420. ; 116:5, s. 990-996
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Journal article (peer-reviewed)abstract
- PURPOSE: Currently, giant cell arteritis (GCA) is primarily treated with corticosteroids or immunomodulating agents, but there is interest in identifying other noncorticosteroid alternatives. Similarities exist in the injury pathways between GCA and atherosclerosis. Angiotensin II is a vasoactive peptide involved in vessel inflammation during atherosclerosis, and angiotensin II receptor inhibitors are effective in preventing atherosclerosis. The present study was performed to elucidate the role of angiotensin type 1 (AT(1)) and type 2 (AT(2)) receptors in GCA. DESIGN: Experimental retrospective immunohistochemical study of temporal arteries using archival formalin-fixed, paraffin-embedded tissue. PARTICIPANTS: Ten patients with GCA and 10 control patients, who were clinically suspected of having GCA but were diagnosed as not having GCA, were included. METHODS: Immunohistochemistry, using anti-AT(1) and anti-AT(2) antibodies, was performed on formalin-fixed and paraffin-embedded temporal arteries. MAIN OUTCOME MEASURES: AT(1) and AT(2) receptor immunostaining intensity was quantified. RESULTS: Hematoxylin-eosin-stained sections of temporal arteries from patients with GCA showed intimal hyperplasia, internal elastic lamina degeneration, and band-shaped infiltrates of inflammatory cells, including lymphocytes, histocytes, and multinucleated giant cells. AT(1) receptor staining was primarily observed in the medial layer of the temporal arteries and was higher in the patients with GCA than in the control patients. This was a result of increased AT(1) receptor immunostaining of both vascular smooth muscle cells and infiltrating inflammatory cells. Only faint immunostaining was seen for AT(2) receptors, primarily in the endothelial cells, and to a lesser extent on the smooth muscle cells. Immunostaining with antibodies for the AT(2) receptor was similar in the patients with GCA and in controls. CONCLUSIONS: These results suggest that AT(1) receptors play a role in the development of GCA. Inhibition of the angiotensin system may thus provide a noncorticosteroid alternative for the treatment of GCA. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.
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| 5. |
- Dimitrijevic, Ivan, et al.
(author)
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Increased expression of vascular endothelin type B and angiotensin type 1 receptors in patients with ischemic heart disease
- 2009
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In: BMC Cardiovascular Disorders. - : Springer Science and Business Media LLC. - 1471-2261. ; 9
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Journal article (peer-reviewed)abstract
- Background: Endothelin-1 and angiotensin II are strong vasoconstrictors. Patients with ischemic heart disease have elevated plasma levels of endothelin-1 and angiotensin II and show increased vascular tone. The aim of the present study was to examine the endothelin and angiotensin II receptor expression in subcutaneous arteries from patients with different degrees of ischemic heart disease. Methods: Subcutaneous arteries were obtained, by biopsy from the abdomen, from patients undergoing coronary artery bypass graft (CABG) surgery because of ischemic heart disease (n = 15), patients with angina pectoris without established myocardial infarction (n = 15) and matched cardiovascular healthy controls (n = 15). Endothelin type A ( ETA) and type B (ETB), and angiotensin type 1 (AT(1)) and type 2 (AT(2)) receptors expression and function were examined using immunohistochemistry, Western blot and in vitro pharmacology. Results: ETA and, to a lesser extent, ETB receptor staining was observed in the healthy vascular smooth muscle cells. The level of ETB receptor expression was higher in patients undergoing CABG surgery (250% +/- 23%; P < 0.05) and in the patients with angina pectoris (199% +/- 6%; P < 0.05), than in the healthy controls (100% +/- 28%). The data was confirmed by Western blotting. Arteries from CABG patients showed increased vasoconstriction upon administration of the selective ETB receptor agonist sarafotoxin S6c, compared to healthy controls (P < 0.05). No such difference was found for the ETA receptors. AT(1) and, to a lesser extent, AT(2) receptor immunostaining was seen in the vascular smooth muscle cells. The level of AT(1) receptor expression was higher in both the angina pectoris (128% +/- 25%; P < 0.05) and in the CABG patients (203% +/- 41%; P < 0.05), as compared to the healthy controls (100% +/- 25%). The increased AT(1) receptor expression was confirmed by Western blotting. Myograph experiment did however not show any change in vasoconstriction to angiotensin II in CABG patients compared to healthy controls (P = n.s). Conclusion: The results demonstrate, for the first time, upregulation of ETB and AT(1) receptors in vascular smooth muscle cells in ischemic heart disease. These receptors may play a role in the pathophysiology of ischemic heart disease and could provide important targets for pharmaceutical interventions.
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| 6. |
- Edvinsson, Lars, et al.
(author)
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Triptan-induced contractile (5-HT1B receptor) responses in human cerebral and coronary arteries: relationship to clinical effect
- 2005
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In: Clinical Science. - 1470-8736. ; 109:3, s. 335-342
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Journal article (peer-reviewed)abstract
- Triptans are agonists at 5-HT1B and 5-HT1D (where 5-HT is 5-hydroxytryptamine; serotonin) receptors and cause vasoconstriction of isolated blood vessels. The aim of the present study was to determine vasoconstrictor potency (EC50) of triptans in human coronary and cerebral arteries and to examine whether there was any relationship with the maximal plasma concentrations (Cmax; nM) of the drugs achieved following oral administration of clinically relevant doses to man using values reported in the literature. We also examined the expression of 5-HT1B receptors in atherosclerotic and normal coronary arteries. The vasocontractile responses to sumatriptan, rizatriptan or eletriptan were characterized by in vitro pharmacology. The ratio of Cmax/EC50 was calculated. 5-HT1B and 5-HT1D receptors were visualized by immunohistochemical techniques in coronary arteries. Sumatriptan, rizatriptan and eletriptan were powerful vasoconstrictors in cerebral artery. The rank order of agonist potency was eletriptan = rizatriptan = sumatriptan. In the coronary artery, the triptans were weaker vasoconstrictors. The rank order of potency was similar. In cerebral artery the ratio of Cmax/EC50 was not significantly different from unity, indicating a relationship between these two parameters. In general for the coronary artery, the ratios were significantly less than unity, indicating no direct relationship. Immunohistochemistry showed expression of 5-HT1B receptors in the medial layer, but did not reveal any obvious difference in 5-HT1B receptor expression between normal and atherosclerotic coronary arteries. The results support the notion that triptans are selective vasoconstrictors of cerebral arteries over coronary arteries and that there is a relationship between vasoconstrictor potency in cerebral arteries and clinically relevant plasma levels.
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| 7. |
- Gesslein, Bodil, et al.
(author)
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Protein kinase C in porcine retinal arteries and neuroretina following retinal ischemia-reperfusion.
- 2009
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In: Molecular Vision. - 1090-0535. ; 15:Apr 13, s. 737-746
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Journal article (peer-reviewed)abstract
- PURPOSE: Identification of the intracellular signal-transduction pathways activated in retinal ischemia may be important in revealing novel pharmacological targets. To date, most studies have focused on identifying neuroprotective agents. The retinal blood vessels are key organs in circulatory failure, and this study was therefore designed to examine the retinal vasculature separately from the neuroretina. METHODS: Retinal ischemia was induced by elevating the intraocular pressure in porcine eyes, followed by 5, 12, or 20 h of reperfusion. Protein kinase C (PKC)alpha, PKCbeta1, and PKCbeta2 mRNA levels, and protein expression were determined using real-time PCR, western blot, and immunofluorescence staining techniques. RESULTS: The retinal arteries could easily be dissected free and studied separately from the neuroretina in this porcine model. The PKCalpha, PKCbeta1, and PKCbeta2 mRNA levels tended to be lower in ischemia-reperfused than in sham-operated eyes in both the retinal arteries and the neuroretina. This was most prominent after 5 h, and less pronounced after 12 h and 20 h of reperfusion. Likewise, the protein levels of PKCalpha, PKCbeta1, and PKCbeta2 were slightly lower following ischemia-reperfusion when compared to sham-operated eyes. PKCalpha, PKCbeta1, and PKCbeta2 immunostaining were observed in bipolar cells of the neuroretina and in endothelial cells, and to a low extent in the smooth muscle layer, of the retinal arteries. CONCLUSIONS: Retinal ischemia followed by reperfusion results in lower levels of PKC in both the neuroretina and retinal arteries. New targets for pharmacological treatment may be found by studying the retinal vasculature so as to identify the intracellular signal-transduction pathways involved in the development of injury following retinal circulatory failure.
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| 8. |
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| 9. |
- Johansson, Kristina, et al.
(author)
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Tailored vitrectomy and laser photocoagulation without scleral buckling for all primary rhegmatogenous retinal detachments.
- 2006
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In: British Journal of Ophthalmology. - : BMJ. - 1468-2079 .- 0007-1161. ; 90:10, s. 1286-1291
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Journal article (peer-reviewed)abstract
- Aim: To investigate the anatomical and functional results and the complications in eyes operated on using vitrectomy without scleral buckling for all forms of rhegmatogenous retinal detachment ( RRD). Methods: All cases of primary RRD at the University Hospital of Lund, Lund, Sweden, treated by one surgeon during a period of 3 years were retrospectively reviewed. In 131 ( 98%) of 134 consecutive cases, a final follow-up record of 3 - 14 months was obtained, and these eyes were included in the study. The surgical protocol was tailored for each case and consisted of vitrectomy, laser photocoagulation and tamponade. Preoperative and intraoperative variables were analyses for risk for redetachment and postoperative proliferative vitreoretinopathy ( PVR). Results: Complete reattachment was achieved in 87% of cases ( 114/131) after one operation and in 95% cases after >= 1 operation. A primary detachment of > 1 quadrant was the only significant risk factor for redetachment ( p < 0.05). The most common cause of redetachment was progressive PVR. Significant risk and factors for PVR postoperatively were a poor preoperative visual acuity and a high number of laser effects during surgery ( p < 0.05). The visual acuity for the total number of eyes, macula-off eyes, and pseudophakic as well as phakic eyes, improved significantly. The visual acuity for macula-on eyes did not change significantly. Six patients developed ocular hypertension and another 6 an epiretinal membrane. Three patients reported a visual field defect. Increased lens opacification was seen in 64 of the 94 ( 68%) phakic eyes. Conclusions: The tailored vitrectomy protocol is well suited to all types of RRD. Increased lens opacification in phakic eyes is common, but visual acuity is considerably improved in phakic as well as pseudophakic eyes. PVR development postoperatively is related to the extent of laser treatment, indicating that the protocol may be even further optimised in the future.
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| 10. |
- Lindstedt Ingemansson, Sandra, et al.
(author)
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A compare between myocardial topical negative pressure levels of-25 mmHg and-50 mmHg in a porcine model
- 2008
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In: BMC Cardiovascular Disorders. - : Springer Science and Business Media LLC. - 1471-2261. ; 8:14
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Journal article (peer-reviewed)abstract
- Background: Topical negative pressure (TNP), widely used in wound therapy, is known to stimulate wound edge blood flow, granulation tissue formation, angiogenesis, and revascularization. We have previously shown that application of a TNP of -50 mmHg to the myocardium significantly increases microvascular blood flow in the underlying tissue. We have also shown that a myocardial TNP levels between -75 mmHg and -150 mmHg do not induce microvascular blood flow changes in the underlying myocardium. The present study was designed to elucidate the difference between -25 mmHg and -50 mmHg TNP on microvascular flow in normal and ischemic myocardium. Methods: Six pigs underwent median sternotomy. The microvascular blood flow in the myocardium was recorded before and after the application of TNP using laser Doppler flowmetry. Analyses were performed before left anterior descending artery (LAD) occlusion (normal myocardium), and after 20 minutes of LAD occlusion (ischemic myocardium). Results: A TNP of -25 mmHg significantly increased microvascular blood flow in both normal (from 263.3 +/- 62.8 PU before, to 380.0 +/- 80.6 PU after TNP application, *p = 0.03) and ischemic myocardium (from 58.8 +/- 17.7 PU before, to 85.8 +/- 20.9 PU after TNP application, *p = 0.04). A TNP of -50 mmHg also significantly increased microvascular blood flow in both normal (from 174.2 +/- 20.8 PU before, to 240.0 +/- 34.4 PU after TNP application, *p = 0.02) and ischemic myocardium (from 44.5 +/- 14.0 PU before, to 106.2 +/- 26.6 PU after TNP application, **p = 0.01). Conclusion: Topical negative pressure of -25 mmHg and -50 mmHg both induced a significant increase in microvascular blood flow in normal and in ischemic myocardium. The increase in microvascular blood flow was larger when using -25 mmHg on normal myocardium, and was larger when using -50 mmHg on ischemic myocardium; however these differences were not statistically significant.
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