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Acute testicular torsion is a surgical emergency which requires immediate intervention. Although damage to the gonad has been well documented, it remains unknown whether the majority of injury occurs during the period of torsion (ischemia) or following detorsion (reperfusion). The aims of this study were to determine: (1) whether damage following testicular torsion-detorsion has a reperfusion component similar to that described in other tissues, and (2) whether iron-catalyzed oxygen radical formation or altered calcium homeostasis plays a role in this injury. To study this, anesthetized prepubertal rats underwent 720 degrees intravaginal testicular torsion and were divided into groups of torsion only (ischemia) and torsion with reperfusion (ischemia/reperfusion). Reperfusion groups were treated prior to detorsion with either deferoxamine (iron chelator), diltiazem (calcium channel blocker), or saline vehicle. The results indicated that detorsion produces a qualitatively distinct reperfusion injury from that of non-reperfused testicles; however, such damage was not ameliorated by deferoxamine or diltiazem. Thus, testicular torsion-detorsion appears to have a significant reperfusion component that appears to not be mediated by iron-catalyzed oxygen radical formation or calcium injury.

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Although cellular dysfunction occurs very early in sepsis, it remains controversial whether this is solely due to a decrease in tissue perfusion. Recent studies have indicated that while active hepatocellular function was depressed, hepatic surface microvascular blood flow (MBF) increased in early sepsis but decreased in late sepsis as produced by cecal ligation and puncture (CLP). However, it is not known whether microvascular hyperperfusion in early sepsis and microvascular hypoperfusion in late sepsis are common events in other organs under such conditions. To study this, rats were subjected to sepsis by CLP, after which these and the corresponding shams received 3 ml/100 g body wt normal saline. Microvascular perfusion and MBF in various tissues were assessed by colloidal carbon infusion and laser-Doppler flowmetry, respectively, at 5 h (i.e., early sepsis) or 20 h (late sepsis) after CLP or sham operation. Carbon-perfused areas were quantitated by an Optomax image analyzer. The results indicate that the carbon-perfused areas and MBF in the liver, renal cortex, spleen, and small intestinal serosa (only MBF) increased significantly 5 h after CLP. In late sepsis, however, the carbon-perfused areas and MBF were found to be significantly decreased. A highly linear relationship was observed between the changes of carbon-perfused areas and MBF during sepsis in the tested organs. Thus the microvascular responses in the fluid-resuscitated sepsis model are characterized by hyperperfusion in the early stage and hypoperfusion in the late stage of sepsis in the tested tissues. The cellular dysfunctions observed during the early stage of sepsis are, therefore, not due to any reduction in tissue perfusion.