SummaryAlthough histamine release is recognised as a common event during anaesthesia and surgery, few clinicians judge the resultant cardiorespiratory disturbances serious enough to warrant prophylaxis with antihistamines. We have assessed the incidence and importance of histamine release in a randomised 2 × 2 factorial study. 240

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Ischemic preconditioning is a protective endogenous mechanism to reduce ischemia/reperfusion injury and is defined as a brief period of ischemia the authors term "preclamping." This is followed by tissue reperfusion and is believed to increase the ischemic tolerance. The objective of this study was to determine whether acute remote ischemic preconditioning, which has been reported to be successful for other organs, such as the heart, kidney, intestine, and liver, will also result in an enhancement of survival in flaps, and whether remote ischemic preconditioning is as effective as preclamping. Forty male Wistar rats were divided into four experimental groups. An extended epigastric adipocutaneous flap (6 x 10 cm) was raised, based on the left superficial epigastric artery and vein. In the control group, a 3-hour flap ischemia was induced. In the preclamping group, a brief ischemia of 10 minutes was induced by clamping the flap pedicle, followed by 30 minutes of reperfusion. Ischemia of the right hind limb was induced in the femoral ischemia group by clamping the femoral artery and vein for 10 minutes after flap elevation. The limb was then reperfused for 30 minutes. Thereafter, flap ischemia was induced as in the control group. A similar protocol was used in the tourniquet group. A tourniquet was used to induce hind-limb ischemia. The experiment was then performed as in the femoral ischemia group. Mean flap necrosis area was assessed for all groups on the fifth postoperative day using planimetry software. Average flap necrosis area was 68.2 +/- 18.1 percent in the control group, 11 +/- 8.38 percent in the preclamping group, 12.5 +/- 5.83 percent in the femoral ischemia group, and 24 +/- 11.75 percent in the tourniquet group. All preconditioned animals demonstrated a significantly lower area of flap necrosis than the control group (p< 0.001, one-way analysis of variance, post hoc Tukey's test). The data show that ischemic preconditioning and enhancement of flap survival can be achieved not only by preclamping of the flap pedicle but also by induction of an ischemia/reperfusion event in a body area distant from the flap before harvest. These findings indicate that remote ischemic preconditioning is a systemic phenomenon, leading to an enhancement of flap survival. The exact mechanism is not yet completely understood. The data suggest that remote ischemic preconditioning could be performed simultaneously with flap harvest in the clinical setting, resulting in an improved flap survival without prolongation of the operation. This may decrease the rate of partial flap loss or fat necrosis, especially in high-risk groups such as smokers, those with irradiated tissues, and obese patients.

The purpose of this study was to determine whether nitric oxide (NO) plays a role in the mechanism of acute "classic" as well as acute remote ischemic preconditioning (IP). Thirty-two male Wistar rats were divided into five experimental groups. The rat cremaster flap in vivo microscopy model was used for assessment of ischemia/reperfusion injury. In the control group (CG, n = 8), a 2-hr flap ischemia was induced after preparation of the cremaster muscle. The animals of group NO (n = 6) received 500 nmol/kg of the NO-donor spermine/nitric oxide complex (Sper/NO) intravenously 30 min prior to ischemia. The group LN + P (L-NAME + preclamping, n = 6) received 10 mg/kg Nomega-nitro-L-arginine methyl ester (L-NAME) intravenously before preclamping of the flap pedicle (10-min cycle length, 30-min reperfusion). L-NAME (10 mg/kg) was administered in group LN + T (L-NAME + tourniquet, n = 6) before ischemia of the right hindlimb was induced, using a tourniquet for 10 min after flap elevation. The limb was then reperfused for 30 min. Thereafter, flap ischemia was induced in each group as in group CG. In vivo microscopy was performed after 1 hr of flap reperfusion in each animal. Group NO demonstrated a significantly higher red blood cell velocity (RBV) in the first-order arterioles and capillaries, a higher capillary flow, and a decreased number of leukocytes adhering to the endothelium (stickers) of the postcapillary venules by comparison to all other groups (P < 0.05). The average capillary RBV and capillary flow were still higher in the CG than in the groups receiving L-NAME (P < 0.05). The data show that NO plays an important role in the mechanism of both acute "classic" as well as acute remote IP, since the administration of a NO-donor previous to ischemia simulates the effect of IP, whereas the nonspecific blocking of NO synthesis by L-NAME abolishes the protective effect of flap preconditioning.