These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Arteriolar reactivity of endotoxin-tolerant rats after hemorrhage and reinfusion.
    Author: Baker CH, Sutton ET, Price JM.
    Journal: Shock; 1995 Dec; 4(6):455-60. PubMed ID: 8608404.
    Abstract:
    Adrenergic and endothelium-dependent arteriolar reactivity are greatly reduced in hemorrhagic shock. However, development of tolerance to endotoxin may prevent the decrease. The reactivity of cremaster muscle arterioles was tested in pentobarbital-anesthetized endotoxin-tolerant (ENDT-T) and nontolerant control rats. Tolerance was developed by sublethal intraperitoneal injections of Escherichia coli endotoxin for 4 days (n = 9). Controls received saline (n = 9). Mean arterial pressure (MAP), arteriolar diameter-response curves to topical norepinephrine (NE) (10-9M to 10-3M) and responses to 10-3M acetylcholine (ACh) were obtained as follows 1) at control, 2) following hemorrhage to 40 mmHg. 3) after uptake of 25% of bled volume with the remainder infused, and 4) at 240 min post-hemorrhage. The A1, A2, and A3 arterioles were constricted following hemorrhage in the ENDT-T group and in the saline group. After reinfusion and in late shock, vessel diameters remained constricted. MAP increased to control levels (106 +/- 5 and 101 +/- 4 mmHg, respectively) following re-infusion in both groups but in late shock it decreased until death in the nontolerant group and decreased only minimally (96 +/- 4 mmHg) in the ENDT-T group. The nontolerant group NE ED50 increased from pre-hemorrhage to late shock (p < .05). The ENDT-T group ED50 was unchanged. The bleeding volumes of the two groups were not different. The survival time of the nontolerant group was 234 +/- 36 min, whereas the ENDT-T group all survived and were sacrificed at 427 +/- 30 min. The response to endothelium-dependent ACH vasodilation in late shock was significantly reduced in the saline group but was unchanged in the ENDT-T group. Alpha 1 receptor activity was maintained in both groups. Alpha 2 receptor activity was attenuated pre-hemorrhage and at 240 min post-hemorrhage in ENDT-T rats. In late shock, alpha 2 receptor activity was attenuated in nontolerant rats. The development of endotoxin tolerance prevents the loss of arteriolar responsiveness to NE and ACh. ENDT-T rats have attenuated alpha 2 receptor activity but not alpha 1 receptor activity.
    [Abstract] [Full Text] [Related] [New Search]