Loss of endothelium-mediated vascular relaxation as a response to various clamping pressures.
The contraction/relaxation responses of thoracic aortal rings clamped with two clamping pressures to potassium chloride (KC1), noradrenaline and carbachol were studied using a scanning electron microscope (SEM) to ascertain endothelial lacerations. Clamp A had the tip pressure PA = 0.60 N/mm2 and clamp B PB = 5.16 N/mm2. In 15 Wistar albino rats, weighing 328 +/- 19 g (mean +/- SD), the thoracic aorta was occluded for 15 min and then three vascular rings (2 mm wide) were excised. The proximal unclamped ring served as a control. The aorta diameter was calculated from the circumference of distal rings 1.61 +/- 0.01 mm (n = 15, dmin = 1.51 mm, dmax = 1.70 mm). The rings were challenged with cumulative additions of KC1 (10-80 mmol/l) to measure the contraction. Then cumulative relaxation on the administration of carbachol (0.01-100 mumol/l) as a response to noradrenaline precontraction (0.1 mumol/l) was determined. A significant loss (P < 0.05) of vascular relaxation in all clamped rings (clamped with PA and PB clamping pressures) was seen. No significant differences (P > 0.05) were observed for contraction between clamped and control rings clamped with clamp A, however the rings clamped with clamp B showed significantly reduction of contraction (P < 0.05). No significant differences were seen from control rings between groups A and B (P > 0.05), as well as from clamped rings between groups A and B (P > 0.05) for both the contraction and relaxation parts of the experiments. With SEM, great endothelial lacerations with complete disruption of the endothelial layer in the rings clamped with the clamp B were seen, but no disruption in rings clamped with clamp A. Therefore endothelial vascular layers are much more susceptible to pressure injuries than was previously believed. The clamped vessel wall injuries, particularly in endothelial layers, depend on the momentary peak clamping pressure (MPCP) as well as on the lower stationary clamping pressure (SCP).
Gersak
B
B
Department of Cardiovascular Surgery, Medical Center Ljubljana, Slovenia.
Trobec
R
R
Krisch
I
I
Psenicnik
M
M
D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D002217:Carbachol / Q000008:administration & dosage / Q000494:pharmacology*; D003250:Constriction; D004108:Dilatation, Pathologic / Q000503:physiopathology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000293:injuries*; D008854:Microscopy, Electron; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000008:administration & dosage / Q000494:pharmacology*; D010277:Parasympathomimetics / Q000008:administration & dosage / Q000494:pharmacology*; D011189:Potassium Chloride / Q000008:administration & dosage / Q000494:pharmacology*; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D013895:Thoracic Arteries / Q000187:drug effects* / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects*
D000316:Adrenergic alpha-Agonists; D010277:Parasympathomimetics; D011189:Potassium Chloride; D002217:Carbachol; D009638:Norepinephrine