Effect of Vasoactive Intestinal Peptide and Naloxone Combination on Urinary N-Acetyl-&beta;-<i>D</i>-Glucosaminidase Level and Kidney Histology of Rats Exposed to Severe Hemorrhage

Abstract

Renal hypoperfusion which occurs in hemorrhagic shock creates an environment in which cellular injury and organ dysfunction can occur during the episode of shock as well as re-oxygenation and reperfusion. At the same time, mast cell degranulation which is observed during hemorrhage may have an additinal deleterious effect on the kidney. Twenty-two (Mus norvegicus albinos) rats (200–250 g) of either sex were used. The animals were divided into three groups. Group 1, the control group, was exposed to a 40% hemorrhage. Group 2 was exposed to 40% hemorrhage and then shed blood reperfused. Group 3 was exposed to 40% hemorrhage, and in addition to shed blood reperfusion 25 ng kg^–1 vasoactive intestinal peptide (VIP) + 5 mg kg^–1 naloxone (NLX) were given. At the end of the experiment the kidneys were evaluated either histologically or by measurement of the urinary N-acetyl-β-D-glucosaminidase (NAG) activity. Shed blood reperfusion caused continuation of ischemic tissue damage and elevation of urinay NAG activity. Addition of VIP and NLX to the blood reperfusion caused a decrease in urinary NAG excretion, and the histology of renal tissue was almost normal.

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

“…In our previous reports, it was stated that VIP administration in experimental hemorrhagic shock models inhibits mast cell degranulation, increases the survival rate, and protects the renal tissue from reperfusion injury. 19,20,24 In our subsequent studies, it was also shown that VIP protects the renal, retinal, and skeletal muscle tissue from ischemia reperfusion injury by acting as an antioxidant. 25‐27 In addition to experimental hemorrhagic shock model, VIP also inhibits mast cell degranulation and proliferation and decreases histamine level in testicular tissue of rats exposed to cold‐restraint stress.…”

Naloxone Inhibits A6 Cell Na⁺/H⁺ Exchange by Activating Protein Kinase C via the Mobilization of Intracellular Calcium

“…In the kidney, naloxone at high concentrations has been shown to reduce damage during ischemia [3], hemorrhagic shock [4, 5]and chronic renal failure [6]. Also in specific conditions naloxone, at high doses, has been implicated in alteration of renal salt and water excretion [7, 8, 9].…”

Endogenous opiates: 1993

“…In the spinal cord, chronic morphine produced increased binding sites for the 6 agonist [D-Ala2]deltorphin-I but not for the ~ ligand FK33,824, so that the 6 receptors may be of special relevance with regard to the development of tolerance in the spinal cord (189). Although chronic morphine produced no change in dynorphin (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) immunoreactivity in the brain, removal of the morphine rats reduced dynorphin(l-17) in the nucleus accumbens, suggesting a possible suppressive role of the dynorphinergic neurons in the limbic system during dependence (560), although its nature was unclear.…”

“…When Met-enkephalin was injected into the medial hyperstriatum, it produced amnesia, but when administered to the lobus parolfactorius, it had no effect on chicks trained on a peck-avoidance task (91). In the same situation, microinjection of DAMGO into the medial hyperstriatum also failed to alter retention (301), but injection ofdynorphin (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) into that area did impair memory, (92), suggesting that in this structure of the brain, the effect was receptor specific. In these studies, the opiates were given before training, which could have affected the results, as found in a comparison of pre-and posttraining injections of TAPA.…”

“…During hypotension induced by acute hemorrhage, the opiate system might play a role, because concentrations of preproenkephalin in the CNS changed during it (140). Dynorphin (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) administered ICV during hemorrhage exacerbated the decrease in blood pressure and slowed recovery of cardiovascular functions ( 141 ), but dynorphin(l-13) attenuated recovery only of stroke volume, not affecting heart rate or cardiac output (141). When given before hemorrhage into the nucleus ambiguus, dynorphin(l-17) and -(2-17) produced a transient further suppression of blood pressure, but U50,488 did not alter it at all (445).…”