Three-phase radionuclide scintigraphy of the hand

Three-phase radionuclide scintigraphy of the hand was performed on 116 patients. Normal and abnormal patterns for radionuclide angiography, immediate post-injection blood-pool images, and delayed scans (3-4 hr.) were established. Of 80 patients with normal circulation, 61 (76%) had equal radial and ulnar artery flow bilaterally, while in 19 (24%) either the radial or ulnar artery was dominant. Abnormal studies were grouped into three categories: suspected vascular lesions (Group I), pain of uncertain etiology (Group II), and patients evaluated before and after reconstructive surgery (Group III). The diagnosis was correct in 89% of the patients in Group I (34/38), 89% of those in Group II (57/64), and all of those in Group III (14/14). Three-phase scintigraphy of the hand yields significant information about perfusion and bone metabolism.     

Restoration of thrombolytic potential in plasminogen-deficient mice by bolus administration of plasminogen

Homozygous plasminogen-deficient (Plg-/-) mice had a significantly reduced thrombolytic capacity toward intravenously injected 125I-fibrin labeled plasma clots prepared from Plg-/- murine plasma (9% +/- 3% lysis after 8 hours; (mean +/- SEM, n = 6), as compared with 82% +/- 8% in wild-type mice; P < .0001). Bolus injection of 1 mg purified murine plasminogen in 10- to 17-week-old Plg-/- mice increased the plasminogen antigen and activity levels at 8 hours to normal levels (130 +/- 5 micrograms/mL). Plasminogen administration was associated with significant restoration of thrombolytic potential (64% +/- 7% spontaneous clot lysis; P < .0001 versus lysis without plasminogen injection). Bolus injection of 1 mg plasminogen in homozygous tissue- type plasminogen activator-deficient (t-PA-/-) mice doubled the plasminogen antigen and activity levels after 8 hours and increased 125I-fibrin clot lysis at 8 hours from 13% +/- 3% to 34% +/- 5% (P = .008). Fibrinogen, t-PA antigen and alpha 2-antiplasmin activity levels after 8 hours were not significantly different in the groups with or without plasminogen injection. Injection of plasminogen induced a variable increase (on average 7- to 10-fold) of PAI-1, but no correlation with the extent of spontaneous clot lysis was observed. Histopathologic examination at the end of the experiments revealed that fibrin deposition in the liver of Plg-/- mice was slightly reduced 8 hours after bolus plasminogen injection (P = .007) and markedly reduced after 24 hours (P < .0001). Plasminogen antigen levels in liver extracts were comparable with those found in wild-type mice at 8 hours (130 +/- 20 versus 110 +/- 15 ng/mg protein) and decreased to 25 +/- 3.2 ng/mg protein at 24 hours. Thus, restoration of normal plasminogen levels in Plg-/- mice normalized the thrombolytic potential toward experimentally induced pulmonary emboli, and resulted in removal of endogenous fibrin deposits within 24 hours.     

Fatal hemoptysis in acute bacterial endocarditis

Massive hemoptysis is a rare complication of bacterial endocarditis. When seen, it is most often due to septic pulmonary emboli with infarction or rupture of a mycotic aneurysm of the pulmonary artery; these conditions are usually associated with endocarditis of the tricuspid valve. We report a case of fatal hemorrhage into the lung from a mycotic aneurysm of the subclavian artery, which eroded into the left upper lobe; this condition arose as a sequela of staphylococcal endocarditis involving the mitral valve.     

α-Methylnoradrenaline-induced contractions in rat aorta are mediated via α1D-adrenoceptors

Summary— The subtype(s) of α-adrenoceptor-mediating contractions to α-methynoradrenaline in the rat aorta has been investigated by using α-adrenoceptor-selective competitive antagonists and the α₁-adrenoceptor selective agonist, phenylephrine, for comparison. α-Methylnoradrenaline and phenylephrine elicited concentration-dependent contractions in the endothelium-denuded and endothelium-intact aortic rings with similar potencies and maximal effects. α-Methylnoradrenaline- and phenylephrine-induced contractions in endothelium-denuded aortic rings were competitively antagonized by prazosin (pA₂ = 9.38 and 9.13; respectively) and rauwolscine (pA₂ = 7.19 and 6.60, respectively). This confirms that there is an α₁- and a non α₂-adrenoceptor response to α-methylnoradrenaline in the rat aorta. The subtype selective α_1D-adrenoceptor antagonist, BMY 7378, was found to antagonize contractions to α-methylnoradrenaline and phenylephrine competitively in endothelium-denuded and endothelium-intact aortic rings. The pA₂ values of BMY 7378 against α-methylnoradrenaline (8.39 and 8.41; endothelium-intact and endothelium-denuded, respectively) and phenylephrine (8.64 and 8.76; endothelium-intact and endothelium-denuded, respectively), are consistent with its published functional potency and clonal α_1d-adrenoceptor binding affinity. In addition, contractions to α-methylnoradrenaline and phenylephrine in endothelium-denuded aortic rings, were potently inhibited by WB 4101 with pA₂ values of 9.75 and 9.25, respectively. The high pA₂ values for WB 4101 indicate that the α_1B-adrenoceptor subtype does not seem to participate in α-methylnoradrenaline (and phenylephrine) induced contractions in this artery. These results suggest that the α_1D-subtype plays a determining role in rat aorta contractions induced by α-methylnoradrenaline.