Internal Pudendal Artery Angioplasty to Rescue Penile Gangrene.

Internal pudendal artery (IPA) is a branch of internal iliac artery that mainly supplies the perineal organs and external genitalia. Any obstruction in the artery seen in diabetics, hypertensives, or chronic kidney disease-induced calciphylaxis leads to decreased blood flow and may cause gangrene. IPA angioplasty is a known therapeutic procedure for erectile dysfunction and has shown promising results. However, similar procedure to relieve arterial blockade may be used to stop spread of penile gangrene and save the anatomical and physiological functions of the penis. We report a novel case of IPA angioplasty in patient of penile gangrene to circumvent total penectomy.

Renal ischemia induces an increase in nitric oxide levels from tissue stores

Tissue nitric oxide (NO) levels increase dramatically during ischemia, an effect that has been shown to be partially independent from NO synthases. Because NO is stored in tissues as S-nitrosothiols and because these compounds could release NO during ischemia, we evaluated the effects of buthionine sulfoximine (BSO; an intracellular glutathione depletor), light stimulation (which releases NO, decomposing S-nitrosothiols), and N-acetyl-l-cysteine (a sulfhydryl group donor that repletes S-nitrosothiols stores) on the changes in outer medullary NO concentration produced during 45 min of renal artery occlusion in anesthetized rats. Renal ischemia increased renal tissue NO concentration (+223%), and this effect was maintained along 45 min of renal arterial blockade. After reperfusion, NO concentration fell below preischemic values and remained stable for the remainder of the experiment. Pretreatment with 10 mg/kg nitro-l-arginine methyl ester (l-NAME) decreased significantly basal NO concentration before ischemia, but it did not modify the rise in NO levels observed during ischemia. In rats pretreated with 4 mmol/kg BSO and l-NAME, ischemia was followed by a transient increase in renal NO concentration that fell to preischemic values 20 min before reperfusion. A similar response was observed when the kidney was illuminated 40 min before the ischemia. The coadministration of 10 mg/kg iv N-acetyl-l-cysteine with BSO + l-NAME restored the increase in NO levels observed during renal ischemia and prevented the depletion of renal thiol groups. These results demonstrate that the increase in renal NO concentration observed during ischemia originates from thiol-dependent tissue stores.

Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise

Buckwalter, John B., Patrick J. Mueller, and Philip S. Clifford. Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise. J. Appl. Physiol. 83(5): 1575–1580, 1997.—Studies utilizing systemic administration of α-adrenergic antagonists have failed to demonstrate sympathetic vasoconstriction in working muscles during dynamic exercise. The purpose of this study was to examine the existence of active sympathetic vasoconstriction in working skeletal muscles by using selective intra-arterial blockade. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and with a catheter in one femoral artery. All dogs ran on a motorized treadmill at three intensities on separate days. After 2 min, the selective α1-adrenergic antagonist prazosin (0.1 mg) was infused as a bolus into the femoral artery catheter. At mild, moderate, and heavy workloads, there were immediate increases in iliac conductance of 76 ± 7, 54 ± 11, and 22 ± 6% (mean ± SE), respectively. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected. These results demonstrate that there is sympathetic vasoconstriction in active skeletal muscles even at high exercise intensities.