Alcohol ingestion before burn injury decreases splanchnic blood flow and oxygen delivery

2005 ◽  
Vol 288 (2) ◽  
pp. H716-H721 ◽  
Author(s):  
Mashkoor A. Choudhry ◽  
Zheng F. Ba ◽  
Shadab N. Rana ◽  
Kirby I. Bland ◽  
Irshad H. Chaudry

Recent studies from our laboratory have shown that alcohol and burn injury impair intestinal barrier and immune functions. Although multiple factors can contribute to impaired intestinal barrier function, such an alteration could result from a decrease in intestinal blood flow (BF) and oxygen delivery (Do2). Therefore, in this study, we tested the hypothesis that alcohol ingestion before burn injury reduces splanchnic blood flow and oxygen delivery. Rats (250 g) were gavaged with alcohol to achieve a blood ethanol level in the range of 100 mg/dl before burn or sham injury (25% total body surface area). Day 1 after injury, animals were anesthetized with methoxyflurane. Blood pressure, cardiac output (CO), ±dP/d t, organ BF (in ml·min−1·100 g−1), and Do2 (in mg·ml−1·100 g−1) were determined. CO and organ BF were determined using a radioactive microsphere technique. Our results indicate that blood pressure, CO, and +dP/d t were decreased in rats receiving a combined insult of alcohol and burn injury compared with rats receiving either burn injury or alcohol alone. This is accompanied by a decrease in BF and Do2 to the liver and intestine. No significant change in BF to the coronary arteries (heart), brain, lung, skin, and muscles was observed after alcohol and burn injury. In conclusion, the results presented here suggest that alcohol ingestion before burn injury reduces splanchnic BF and Do2. Such decreases in BF and Do2 may cause hypoxic insult to the intestine and liver. Although a hypoxic insult to the liver would result in a release of proinflammatory mediators, a similar insult to the intestine will likely perturb both intestinal immune cell and barrier functions, as observed in our previous study.

Shock ◽  
2004 ◽  
Vol 21 ◽  
pp. 3-4
Author(s):  
M. A. Choudhry ◽  
Z. F. Ba ◽  
S. Rana ◽  
I. H. Chaudry

2021 ◽  
Vol 8 (2) ◽  
pp. 84-87
Author(s):  
Evania Setiawan ◽  
Aditya Wardhana ◽  
Wina Sinaga ◽  
Ayu Diandra Sari ◽  
Metta Satyani ◽  
...  

Backgrounds: Diarrhea frequently occurs in severely burned patients attributable to impaired intestinal integrity and dysbiosis. Soluble fiber may improve intestinal barrier function, avoid bacterial translocation, then subsequently prevent and treat diarrhea. Soluble fiber is rapidly fermented by commensal bacteria and produces short-chain fatty acids (SCFA). Case Reports: A 51-year-old male with severe burn injury involving 53,5% total body surface area (TBSA) and diarrhea were given soluble fiber as part of his diet. Results: Administration of 6–10 g/d soluble fiber clinically improves stool consistency, assessed by Bristol Stool Scale, in the severely burned patient. The patient was discharged after 19 days of hospitalization with improvement in clinical condition. Summary: SCFA maintains intestinal integrity, supports the growth of commensal bacteria, and inhibits pathogens. There is no specific recommendation regarding fiber intake in burned patients


1957 ◽  
Vol 189 (3) ◽  
pp. 576-579 ◽  
Author(s):  
E. Allbaugh Farrand ◽  
R. Larsen ◽  
Steven M. Horvath

The changes in splanchnic blood flow and related metabolic functions which occurred as the result of the infusion of 0.1 µg/kg/min. of l-epinephrine and l-norepinephrine for 10 minutes were measured in anesthetized dogs. l-Epinephrine elicited a marked increase in estimated splanchnic blood flow and no change in mean arterial pressure. While a significantly increased mean arterial blood pressure was observed following the administration of l-norepinephrine, no change in estimated splanchnic blood flow occurred. Arterial oxygen content was increased significantly with both drugs. Utilization of oxygen by the splanchnic bed was not changed during the infusion of either drug but was increased during the postepinephrine infusion period.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Stephanie Franzén ◽  
Robert Frithiof

Abstract Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated. We hypothesised that anaesthesia-induced hypotension causes renal vasoconstriction and decreased oxygen delivery via angiotensin II-mediated renal vasoconstriction. Pigs were anaesthetised, surgically prepared and randomised to vehicle/losartan treatment (0.15 mg*kg−1). A deliberate reduction in arterial blood pressure was caused by infusion of propofol (30 mg*kg−1) for 10 min. Renal function and haemodynamics were recorded 60 min before and after hypotension. Propofol induced hypotension in all animals (p < 0.001). Renal blood flow (RBF) and renal oxygen delivery (RDO2) decreased significantly regardless of treatment but more so in vehicle-treated compared to losartan-treated (p = 0.001, p = 0.02, respectively). During recovery RBF and RDO2 improved to a greater extent in the losartan-treated compared to vehicle-treated (+ 28 ml*min−1, 95%CI 8–50 ml*min−1, p = 0.01 and + 3.1 ml*min−1, 95%CI 0.3–5.8 ml*min−1, p = 0.03, respectively). Sixty minutes after hypotension RBF and RDO2 remained depressed in vehicle-treated, as renal vascular resistance was still increased (p < 0.001). In losartan-treated animals RBF and RDO2 had normalised. Pre-treatment with losartan improved recovery of renal blood flow and renal oxygen delivery after propofol-induced hypotension, suggesting pronounced angiotensin II-mediated renal vasoconstriction during blood pressure reductions caused by anaesthesia.


1980 ◽  
Vol 238 (5) ◽  
pp. F363-F371 ◽  
Author(s):  
C. McCaffrey ◽  
M. Levy

Furosemide 20 mg/kg was given intravenously to 12 anesthetized dogs with clamped renal pedicles. Thoracic duct lymph flow (TDLF) increased promptly by 38% (P less than 0.05), an increment that lasted 80 min. Because in 6 of 12 dogs there was a transient increase in splanchnic blood flow, in separate groups splanchnic blood flow was either markedly constricted or markedly increased by intravenous isoproterenol. Thoracic duct lymph flow increased by 95 and 90%, respectively, following furosemid despite no further change in splanchnic blood flow. Furosemide had no effect on blood pressure, lymph protein, or plasma sodium. In four chronic caval dogs, TDLF was increased by 400%, yet furosemide produced a further increment in lymph flow of 30% (P less than 0.05). Infusion of a 25% albumin solution to contract the interstitial fluid did not abolish the furosemide effect, but a 10% mannitol solution did. Furosemide increased TDLF even after the infusion of papaverine reduced blood pressure to 60 mmHg. We conclude that furosemide increases TDLF by acting directly on splanchnic capillaries to allow increased filtration of fluid in the absence of increased splanchnic blood flow or capillary hydrostatic pressure.


1998 ◽  
Vol 84 (2) ◽  
pp. 695-702 ◽  
Author(s):  
Jureta W. Horton ◽  
Jean White ◽  
David Maass ◽  
Billy Sanders

Horton, Jureta W., Jean White, David Maass, and Billy Sanders. Arginine in burn injury improves cardiac performance and prevents bacterial translocation. J. Appl. Physiol. 84(2): 695–702, 1998.—This study examined the effects of arginine supplement of fluid resuscitation from burn injury on cardiac contractile performance and bacterial translocation after a third-degree burn comprising 43% of the total body surface area in adult rats. Before burn injury, rats were instrumented to measure blood pressure; after burn (or sham injury), paired groups of sham-burned and burned rats were given vehicle (saline), l-arginine,d-arginine, or N-methyl-l-arginine (300 mg/kg in 0.3 ml of saline 30 min, 6 h, and 23 h postburn) plus fluid resuscitation; sham-burned rats received drug only. Twenty-four hours after burn trauma, hemodynamics were measured; the animals were then killed and randomly assigned to Langendorff heart studies or to studies examining translocation of gut bacteria. Burn rats treated with vehicle,d-arginine, or N-methyl-l-arginine had well-defined cardiocirculatory responses that included hypotension, tachycardia, respiratory compensation for metabolic acidosis, hypocalcemia, cardiac contractile depression, and significant bacterial translocation. Compared with values measured in vehicle-treated burn rats, l-arginine given after burn improved blood pressure, prevented tachycardia, reduced serum lactate levels, improved cardiac performance, and significantly reduced bacterial translocation, confirming thatl-arginine administration after burn injury provided significant cardiac and gastrointestinal protection. Circulating neutrophil counts fell after burn trauma and serum glucagon levels rose, but these changes were not altered by pharmacological intervention. Our finding of significantly higher coronary perfusate guanosine 3′,5′-cyclic monophosphate concentration inl-arginine-treated burn rats suggests that the beneficial effects ofl-arginine were mediated by nitric oxide production.


2017 ◽  
Vol 24 (4) ◽  
pp. e12345 ◽  
Author(s):  
Christian Vollmer ◽  
Andreas P. M. Weber ◽  
Martin Wallenfang ◽  
Till Hoffmann ◽  
Tabea Mettler-Altmann ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Ya-Jun Wang ◽  
Jie Su ◽  
Jing-Jing Yu ◽  
Mei-Qiu Yan ◽  
Meng-Lin Shi ◽  
...  

As the number of patients with metabolic hypertension (MH) is increasing, there is an essential require for global measures to prevent and treat MH. Flavonoids such as buddleoside (BUD) from Chrysanthemum indicum L. are the main pharmacological components of cardiovascular activities. Previous studies have suggested that the buddleoside-rich Chrysanthemum indicum L. extract (BUDE) can reduce blood pressure in spontaneously hypertensive rats (SHR). However, its effect on MH and how it works remains to be researched. In this study, it was observed that BUDE could lower blood pressure, improve dyslipidemia, and decrease the level of plasma LPS in MH rats. Moreover, BUDE improved intestinal flora and increased the expression of occludin and claudin-1 in the colon, and improved the pathological injury of the colon. Western bolt and qRT-PCR experiments showed that BUDE could down-regulate TLR4 and MyD88 protein and mRNA expression and inhibit phosphorylation of IKKβ, IκBα and NF-κB p65 in vessels of MH rats. These results showed that BUDE could regulate intestinal flora, improve intestinal barrier function, reduce the production and penetration of LPS, thereby inhibiting the vascular TLR4/MyD88 pathway, improving vascular endothelial function, and ultimately lowering blood pressure in MH rats. This study provides a new mechanism of BUDE against MH by inhibiting the enteric-origin LPS/TLR4 pathway.


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