Microvascular blood flow is altered after repair of testicular torsion in the rat.

PURPOSE: Previous studies have shown that experimental testicular torsion with a duration of 1 hr. or longer causes irreversible damage to the rat testis, but that testicular blood flow values are normal 24 hrs. after repair of torsion. More acute evaluation of return blood flow after repair of torsion has not been performed and was the topic of this study. MATERIALS AND METHODS: Laser-Doppler flowmetry was used to evaluate testicular microvascular blood flow before application of 1, 2, or 4 hr., 720 degrees torsion, during torsion, and at several time points after repair of torsion. Experiments were performed in both adult and prepubertal rats. RESULTS: Testicular torsion essentially eliminated blood flow in both adult and prepubertal testes. Considering all the flow data within each group after torsion repair, increasing time of torsion was associated with significantly less return blood flow in both adult and prepubertal animals. Interestingly, only the four hour torsion data was associated with reduced return flow in prepubertal animals while both two and four hour torsion were associated with poor return flow in adult animals. Vasomotion, or pulsatile microvascular flow, often seen before torsion in both adult and prepubertal animals, was never seen after torsion repair. CONCLUSIONS: Increasing times of torsion are associated with lower microvascular blood flow values during the hour following the relief of torsion. Vasomotion is eliminated by torsion during the period studied. Whether vasomotion returns is unknown, but altering this flow pattern might be involved in the mechanism of injury caused by acute torsion.

Rescue of testicular function after acute experimental torsion.

PURPOSE: Spermatic cord torsion results in impairment of testicular function. The mechanism of this injury is unclear; however, intracellular Ca++ influx and reactive oxygen species have been implicated in the testicular damage following torsion and reperfusion. In the present study a model of testicular torsion in the rat was used to determine whether testicular function following torsion can be rescued by the administration of antioxidants and Ca++ channel blockers. MATERIALS AND METHODS: Seventy-two animals were divided into 9 groups. Animals underwent 1 hr. or 2 hrs., 720 degrees experimental torsion. Animals received combinations of superoxide dismutase (SOD), catalase, allopurinol, and verapamil. Drugs were administered intravenously during the last 15 minutes of experimental torsion and the first hour of reperfusion. Bilateral testicular function was determined 60 days after experimental torsion by measuring testis weights, daily sperm production (DSP), and testicular venous testosterone concentrations. Ipsilateral values were compared to both control and contralateral values. RESULTS: SOD + catalase and SOD + catalase+verapamil treatments caused significant rescue of tests function following 1 hr. experimental torsion. Mean +/- s.e. testis weights and DSP in control animals were 1.75 +/- 0.6 g. and 18.4 +/- 0.3 x 10(6) sperm/g./d. The same value for testes experiencing 1 hr. experimental torsion were 0.72 +/- 0.6 g. and 2.3 +/- 0.5 x 10(6) sperm/g./d. The values from testes receiving 1 hr. experimental torsion followed by SOD + catalase were 1.45 +/- 0.17 g. and 9.9 +/- 1.8 x 10(6) sperm/g./d. Neither allopurinol nor verapamil added benefit. No significant rescue was seen in testes undergoing 2 hrs. experimental torsion. CONCLUSIONS: Treatment with oxygen radical scavengers provides significant rescue of testicular function after acute experimental torsion.

The effect of pancreatic polypeptide on glucose disposal after surgical alterations of the pancreas.

Surgical alterations of the pancreas result in anatomic changes that can affect postoperative glucose metabolism. Pancreas transplantation results in reduction of beta-cell mass, systemic release of insulin, and denervation. The authors hypothesized that such alterations affect peripheral glucose disposal to induce an "insensitivity" to endogenously (systemically) released insulin. Additionally, they hypothesized that surgically induced deficiency of the postprandial hormone, pancreatic polypeptide, might contribute to altered glucose disposal. The authors studied two surgical models in dogs known to be devoid of pancreatic polypeptide--70% proximal pancreatectomy (PPx) and PPx plus distal pancreas autotransplantation (PAT/B). Oral glucose challenge and euglycemic hyperinsulinemic clamp studies were performed before and after a 16-day "pulsed" infusion of pancreatic polypeptide. Both surgical procedures resulted in elevations in the integrated glucose response after oral glucose, which was not affected by pancreatic polypeptide infusion. Euglycemic clamp studies showed decreased hepatic glucose output (Ra) and overall glucose disposal (Rd) in the fasted state for both surgical groups. The transplant animals demonstrated significant decreases in Rd during the hyperinsulinemic challenge (3.2 +/- 0.01 versus 5.7 +/- 0.01 mg/kg/minute at 60 to 120 minutes for PAT/B versus control). After 16 days of pancreatic polypeptide infusion, however, basal Ra, as well as basal and 60- to 120-minute Rd values, were returned to control values in the transplant group. The authors conclude that pancreas transplantation results in altered glucose disposal, possibly due to an altered effectiveness of systemically released insulin. They conclude that pancreatic polypeptide is an important modulator of peripheral insulin action. Therefore, the role of pancreatic polypeptide must be taken into account when evaluating postoperative glucose metabolism in canine models of pancreas transplantation.