Effect of postischemic hypoperfusion on vasodilatory mechanisms in cats

1994 ◽  
Vol 267 (5) ◽  
pp. H2012-H2018 ◽  
Author(s):  
N. Clavier ◽  
J. R. Kirsch ◽  
P. D. Hurn ◽  
R. J. Traystman
Keyword(s):  
Vascular Reactivity ◽  
Signal Transduction Pathway ◽  
Global Cerebral Ischemia ◽  
Transduction Pathway ◽  
Muscarinic Agonists ◽  
No Donor ◽  
A 23187 ◽  
Muscarinic Stimulation ◽  
Arterial Dilation ◽  
Pial Vessel

We addressed the mechanism for reduced pial vascular reactivity to muscarinic stimulation by evaluating pial vessel responses to receptor-dependent [10(-5) M acetylcholine (ACh)] and independent (10(-5) M A-23187) agonists and the endothelium-independent nitric oxide (NO) donor [10(-5) M nitroprusside (NP)]. Cerebral blood flow (CBF, microspheres) and pial arteriolar diameters (intravital microscopy) were measured in halothane-anesthetized cats. Cats (n = 13) were treated with 12 min of near-complete global cerebral ischemia, whereas control animals (n = 9) were identically instrumented but were not submitted to ischemia. Postischemic hypoperfusion was evident in most animals at 60 min of reperfusion, accompanied by attenuated pial arterial dilation to topical ACh (baseline dilation 23 +/- 4% vs. postischemia 11 +/- 3%) and A-23187 (16 +/- 4 vs. 0 +/- 3% dilation). Dilation to NP was unaffected. CBF response to intravenous administration of the muscarinic receptor agonist oxotremorine was also decreased throughout the forebrain (162 +/- 12 vs. 116 +/- 6% increase in flow) in these cats. These data suggest that endothelium-dependent vasodilation with topical muscarinic agonists is impaired during hypoperfusion, but vascular smooth muscle responsivity to NO remains intact. We conclude that the defect in the signal transduction pathway is not limited to the receptor and may involve an abnormality with NO synthesis or its destruction within endothelium.

Enhanced pulmonary arterial dilation to arginine vasopressin in chronically hypoxic rats

1994 ◽  
Vol 267 (6) ◽  
pp. H2413-H2419 ◽  
Author(s):  
M. R. Eichinger ◽  
B. R. Walker
Keyword(s):  
Sodium Nitroprusside ◽  
Arginine Vasopressin ◽  
Chronic Hypoxia ◽  
Pressor Response ◽  
Hypoxic Exposure ◽  
Sprague Dawley ◽  
No Donor ◽  
A 23187 ◽  
Pulmonary Arterial ◽  
Arterial Dilation

Chronic hypoxic exposure elicits pulmonary vascular remodeling and may alter normal pulmonary endothelial function. We examined the vasodilatory response to the receptor-mediated endothelium-dependent dilator arginine vasopressin (AVP), the non-receptor-mediated endothelium-dependent dilator A-23187, and the nitric oxide (NO) donor sodium nitroprusside in lungs isolated from control or chronically hypoxic rats. Lungs were isolated from male Sprague-Dawley rats and perfused with a physiological saline solution containing 4% albumin. Arterial and venous pressures were monitored and microvascular pressure was estimated by double occlusion, allowing assessment of segmental resistances. After equilibration, lungs were constricted with the thromboxane mimetic U-46619. Upon development of a stable pressor response, lungs were dilated with one of the above agents. A series of doses of AVP was administered to separate groups of lungs from control or chronically hypoxic rats. Lungs from chronically hypoxic rats exhibited an augmented dilatory response to AVP compared with control lungs, and this effect was due to enhanced dilation of precapillary segments. The total and segmental vasodilatory responses to A-23187 and sodium nitroprusside were not different between the two groups of lungs, suggesting that chronic hypoxia did not upregulate the enzyme NO synthase or enhance the vascular smooth muscle responsiveness to NO. Thus our data suggest that the augmented total and pulmonary arterial dilation to AVP after chronic hypoxia is most likely due to altered receptor-mediated processes of the hormone.

Sign in / Sign up

Export Citation Format

Share Document