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This pilot study was designed to test the feasibility of using purified clostridial collagenase in the clinical management of Peyronie's disease. The basic properties of this agent are discussed. We studied its effect on Peyronie's plaque tissue by a quantitative in vitro assay utilising the liberation of free alpha-amino groups as an index of enzymatic collagenolysis. Tissue from three patients with Peyronie's disease was used. Tunica albuginea from a second group of three normal patients was studied in the same manner, and no selectivity for the collagen of Peyronie's plaques was identified. Utilising human pericardium as a uniform collagenous substrate, a simple dose-effect relationship was established, and the distribution characteristics of injected collagenase observed. Its effects on blood vessels and nerves in vivo was determined as well as the effects of collagenase on the histology of normal and diseased human tissue in vitro. A tentative dose for use in Peyronie's disease was established, which is discussed in light of existing toxicological data. The study was designed to test the feasibility of purified collagenase in the clinical management of Peyronie's disease. Data included detail plaque digestion and dose-effect relationships in vitro, as well as the histological effects on plaques, blood vessels, and nerves in vivo and in vitro. It is concluded that collagenase may warrant further clinical testing in the treatment of Peyronie's disease.

The effects of ethanol intoxication on brain injury and cerebral blood flow (CBF) were investigated in a porcine fluid-percussion model of traumatic brain injury (TBI). Immature swine, under halothane anesthesia (1%), had a TBI delivered with a fluid-percussion device. The experimental group (n = 10) received ethanol (3.5 gm/kg) via gastric tube followed in 1 h by TBI. Two groups of control animals received normal saline and TBI (n = 10) or ethanol and no TBI (n = 5). Mean arterial blood pressure (MAP), intracranial pressure (ICP), arterial blood gases, and serum lactate were monitored for 3 h after the injury. CBF was measured with radiolabelled 15-micron diameter microspheres. Neuropathologic changes were evaluated and graded after formalin perfusion and brain removal at 3 h postinjury. The ethanol level 60 min post-head injury was 198 +/- 70 (SD) mg/dL in the ethanol+TBI group. At 90 min postinjury and thereafter, ethanol+TBI animals compared with TBI only animals had significantly lower MAP (63 +/- 26 mmHg vs 91 +/- 15 mmHg) and lower cerebral perfusion pressure (50 +/- 25 mmHg vs 78 +/- 15), and at 180 min postinjury, lower CBF (87 +/- 37% vs 62 +/- 79% of preinjury levels). Ethanol+TBI animals had higher blood lactates (28 +/- 11 mg/dL vs 13 +/- 6 mg/dL) than TBI only animals. Ethanol+TBI animals also had significantly longer postinjury apneas (11 +/- 8 min vs 0.6 +/- 0.4 min), with three of ten ethanol-treated animals never recovering spontaneous respiration. Ethanol intoxication produced hemodynamic and respiratory changes, which may have a deleterious effect on outcome and mortality after brain injury.

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