Hypertonic/hyperoncotic resuscitation after intestinal superior mesenteric artery occlusion: early effects on circulation and intestinal reperfusion.
The objective of the study was to determine the early effects of hypertonic/hyperoncotic starch resuscitation after 2 h occlusion of the superior mesenteric artery (SMA) in comparison to animals reperfused without treatment and isotonic resuscitation. SMA was clamped (18 pigs, 19-23 kg) for 2 h followed by a 2-h reperfusion period, which was initiated with isotonic (ISO) (35 mL/kg 0.9% NaCl and 5 mL/kg 10% hydroxyethyl starch within 30 min) or hypertonic/hyperoncotic resuscitation (HHES) (7.5% NaCl/10% hydroxyethyl starch within 5 min). Cardiac output (CO), mean arterial blood pressure (MAP), serum lactate, antimesenteric serosal Laser-Doppler values (LD), and intramural pHi (tonometry) were measured. Without resuscitation at the onset of reperfusion MAP (70 +/- 3 mmHg) decreased to 40 +/- 3 mmHg and CO to 31% of baseline values after 30 min. Serum lactate increased to 5.1 +/- 1.6 mmol/L without improvement. The decrease of CO was attenuated only during the initial 30 min of reperfusion in the ISO group, but significantly better counteracted by hypertonic/hyperoncotic resuscitation. Without treatment, LD flow of the ileum (baseline 23-27 LD units) recovered but intramural pH (pHi) remained significantly decreased (7.26 +/- 0.05). With isotonic resuscitation LD values (21.8 +/- 2.1 LD units) and intramural pHi (7.09 +/- 0.14) decreased even more (P < 0.05) whereas the HHES group showed a significant hyperemic reaction and a normalization of the intramural pHi and serum lactate within 30 min. Hypertonic/hyperoncotic resuscitation significantly improves MAP and CO during reperfusion shock and induces an immediate hyperemic reperfusion reaction of the intestinal microcirculation. Adequate isotonic fluid replacement in order to restore the postischemic plasma volume loss may cause a pronounced deterioration of intestinal perfusion.
Jonas
J
J
Department of Surgery, Städtisches Klinikum, Karlsruhe, Germany.
Heimann
A
A
Strecker
U
U
Kempski
O
O
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications* / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D003250:Constriction; D005440:Fluid Therapy / Q000009:adverse effects; D006439:Hemodynamics / Q000187:drug effects*; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology / Q000627:therapeutic use*; D006940:Hyperemia / Q000209:etiology; D006982:Hypertonic Solutions / Q000494:pharmacology / Q000627:therapeutic use*; D007082:Ileum / Q000098:blood supply*; D007410:Intestinal Diseases / Q000209:etiology / Q000517:prevention & control*; D007511:Ischemia / Q000150:complications*; D019344:Lactic Acid / Q000097:blood; D008638:Mesenteric Arteries / Q000473:pathology*; D008833:Microcirculation / Q000187:drug effects; D009994:Osmolar Concentration; D015427:Reperfusion Injury / Q000517:prevention & control*; D012151:Resuscitation / Q000379:methods*; D012462:Saline Solution, Hypertonic / Q000494:pharmacology / Q000627:therapeutic use; D012965:Sodium Chloride / Q000494:pharmacology / Q000627:therapeutic use / Q000633:toxicity; D013552:Swine
D006895:Hydroxyethyl Starch Derivatives; D006982:Hypertonic Solutions; D012462:Saline Solution, Hypertonic; D019344:Lactic Acid; D012965:Sodium Chloride