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Hypertension

Hypertension is a leading cause for cardiovascular and renal disease. We use different models to analyse the anti-hypertensive respond of blood pressure medications and to analyse the impact on end-organ damage.

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In vivo Models

• DOCA salt

This model of hypertension is induced by implanting a pellet containing DOCA salt.

• Angiotensin II infusion

This model of hypertension is induced by implanting an osmotic mini pump that delivers angiotensin II for 2 - 8 weeks s.c. Consequently, the blood pressure rises and cardiac and renal damage can be observed.

• Renal artery stenosis

In this hypertensive model, a silver clip is placed around the left renal artery, what leads to an activation of the renin-angiotensin system and a subsequent rise in blood pressure.

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Available Readouts

1. Blood pressure​

2. Renal function

   • Urine volume

   • Clinical chemistry for serum creatinine, BUN

   • Albuminuria

   • Glomerular Filtration Rate (GFR)

3. Organ size and weight

4. Organ morphology

   • Histology (H&E, Masson Trichrome, Periodic Acid Schiff (PAS) staining)

5. Immunohistochemistry and RT-PCR for specific markers of interests

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Techniques

• Clinical chemistry

• Metabolic cages

• Blood pressure analysis

• Assessment of Glomerular Filtration Rate (GFR)

• Flow cytometry including Bead-based flow cytometry

• Histology (H&E, Masson Trichrome, Periodic Acid Schiff (PAS) staining)

• Immunohistochemistry

• ELISA

• Molecular biology (Real-Time PCR, Western blot)

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Need further Readouts? We routinely develop new models to fit our cutomer needs.

 

Speak with us for tailor-made solutions!

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Myocardial Infarction, LAD Occlusion​

Cardiovascular disease is one of the leading causes of death worldwide. A major contributor to mortality is myocardial infarction. Acute myocardial infarction is an irreversible injury of the myocardial tissue with subsequent necrosis due to severe and prolonged reduction in coronary perfusion.

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In vivo Models

• Permanent LAD Occlusion

Myocardial infarction is induced by permanent ligation of the left anterior descending coronary artery. Infarct size is usually 30 - 40% of the left ventricle.

• Transiente LAD Occlusion

LAD is temporarily occluded to induce ischaemia-reperfusion injury (IRI).

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Available Readouts

1. Survival​

2. Echocardiography

3. Infarct size

4. Area at risk size

5. ​Inflammation

   • Cytokine / chemokine profile

6. Fibrosis

   • Immunohistochemistry for fibronectin, a-SMA, collagen IV

   • Expression of profibrotic mediators

7. Morphology

   • Histology (H&E, Masson Trichrome, Periodic Acid Schiff (PAS) staining)

8. Troponin I ELISA​

9. Immunohistochemistry and RT-PCR for specific markers of interests

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Techniques

• Clinical chemistry

• Echokardiography

• Flow cytometry including Bead-based flow cytometry

• Histology (H&E, Masson Trichrome, Periodic Acid Schiff (PAS) staining)

• Immunohistochemistry

• ELISA

• Molecular biology (Real-Time PCR, Western blot)

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Need further Readouts? We routinely develop new models to fit our cutomer needs.

 

Speak with us for tailor-made solutions!

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Stroke

Stroke is a common cause of death in western countries and the leading medical cause of acquired adult disability. Approximately 70% of strokes result from thromboembolic occlusion of the middle cerebral artery (MCA) and its branches. The vascular occlusion results in less oxygen and energy, which leeds to the formation of reactive oxygen species, release of glutamate, accumulation of intracellular calcium, and induction of inflammatory processes. This ischemic cascade results in irreversible tissue injury.

 

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In vivo Models​

Middle cerebral artery occlusion

The middle cerebral artery and its branches are the cerebral vessels that are most often affected in human ischemic stroke. Thus, this is one of the models that most closely simulate human ischemic stroke. Occlusion can be done by intraluminal suture or craniectomy, respectively.

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Available Readouts

1. Survival​

2. Infarct size

3. Behavioral analysis

   • corner test

   • adhesive removal test (sticky tape test)

   • others (on request)

4. ​Inflammation

   • Cytokine / chemokine profile

5. Morphology

   • Histology (H&E, Masson Trichrome, Periodic Acid Schiff (PAS) staining)

6. Immunohistochemistry, RT-PCR and Western blotting for specific markers of interests

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Techniques

• Clinical chemistry

• Flow cytometry including Bead-based flow cytometry

• Histology (H&E, Masson Trichrome, Periodic Acid Schiff (PAS) staining)

• Immunohistochemistry

• ELISA

• Molecular biology (Real-Time PCR, Western blot)

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Need further Readouts? We routinely develop new models to fit our cutomer needs.

 

Speak with us for tailor-made solutions!

 

 

 

 

Cornea Neovascularization Assay

In this assay the neovascularization of the physiologically avascular cornea is used to identify pro- or anti-angiogenic properties of different substances.

 

In vivo Model

Corneal pockets are created with a modified von Graefe cataract knife. Into each pocket, a sucrose aluminium sulphate pellet containing e.g. VEGF is implanted ~1.0mm from the corneal limbus artery. The corneas are routinely examined by slit-lamp biomicroscopy. Vessel length and circumference of the limbus are measured to quantify angiogenic effects. On the day of sacrifice, animals are perfused with fluorescent dyes to stain the developed vessels. In combination with prior bone-marrow transplantation, this model can also be used to investigate the effect of different compounds on endothelial progenitor cells (EPCs).

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