Objectives: The objective of this study was to compare the accuracy of contrast-enhanced CT (CECT) and contrast-enhanced MRI (CEMRI) in the detection of perineural spread (PNS) of adenoid cystic carcinoma (ACC) in the oral and maxillofacial regions. Methods: This study consisted of 13 ACCs from 13 patients, all of which were histopathologically diagnosed. Both CECT and CEMRI were performed in all patients before the treatment. The images of each patient were retrospectively evaluated for the detection of PNS. The definitions of PNS included abnormal density/signal intensity, contrast enhancement or widening of the pterygopalatine fossa, palatine foramen, incisive canal, mandibular foramen and mandibular canal, and enlargement or excessive contrast enhancement of a nerve. Results: 11 out of 13 cases were proven to exhibit PNS histopathologically. 8 of the 11 cases for which PNS was histopathologically proven exhibited PNS on MR images. Six of the eight cases for which PNS was exhibited on MR images also exhibited PNS on CT images. The sensitivity, specificity and accuracy for the detection of PNS were 55%, 100% and 62% on CT images and 73%, 100% and 77% on MR images, respectively. Although the accuracy of PNS on MR images was slightly superior to that on CT images, there were no statistically significant differences between the detection of PNS on CT images and on MR images. Conclusions: CT and MR images are equally useful for the detection of PNS of ACC in the oral and maxillofacial regions.

We investigated effects of three kinds of putative protein kinase C (PKC) inhibitors, calphostin C, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and stauro-sporine, on aortic muscle contractions induced by KCl, phenylephrine, 12-O-tetradecanoylphorbol-13-acetate (TPA), and phorbol 12, 13-dibutyrate (PDBu). Calphostin C noncompetitively inhibited TPA-induced contractions in a concentration-dependent manner. At 10(-6) M, calphostin C completely abolished responses to TPA and also effectively inhibited PDBu-induced contractions. Such a concentration of calphostin C had no effect on KCl-induced contractions but decreased the maximal tension of phenylephrine-induced response curve by 35.3 +/- 6.6% H-7 (10(-5) M had little effect on TPA-induced contraction but significantly inhibited contractile responses to phenylephrine and KCl. Staurosporine (10(-8) M, 3 x 10(-8) M) inhibited contractile responses to KCl, phenylephrine, and TPA. We suggest that staurosporine and H-7, which are known to act on the catalytic domain of PKC carrying high degree of sequence homology with other protein kinases, are relatively nonselective for PKC. On the other hand, calphostin C acting on the regulatory domain of PKC, which is distinct from other protein kinases, may serve as a relatively more selective PKC inhibitor.

1 Calphostin C at 10-6M was shown to be selective and highly effective in inhibiting contractile responses of rat aortae to 12-o-tetradecanoylphorbol-13-acetate, while it had no effect on contractile responses to elevated KCL. 2 In the rat aorta, endothelin-l (ET-1) developed a sustained tonic contraction dose-dependently in both normal Ca2"-containing Krebs and Ca2 +-free Krebs containing 1 mM EGTA. Calphostin C (10-6M ), a selective protein kinase C inhibitor, antagonized the maximal tensions for cumulative addition of 10-8 M ET-1 by 13.2% in Ca2"-containing medium and 25.8% in Ca2+-free Krebs containing 1 mM EGTA.3 In both Ca2"-containing medium and Ca2'-free Krebs containing 1 mM EGTA, precontraction with 10-8 M ET-1 had no effects on the contractile response to subsequently added 10-6 M 12-otetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C. 4 In Ca2+-free Krebs containing 1 mM EGTA, precontraction with 10-6 M TPA potentiated the contractile response to subsequently added 10-8 M ET-1, whereas this potentiation was abolished by pretreatment with 10-6 M calphostin C. The mechanism of the TPA-induced potentiating effect remains to be determined. 5 These results suggest that the participation of protein kinase C in the 10-8 M ET-l-induced contraction may be 13.2% and 25.8% in the presence and absence of extracellular Ca2+, respectively, and that mechanisms other than protein kinase C may be predominantly responsible for ET-1-induced tonic contraction.

We compared the systemic and regional hemodynamic effects of nifedipine and lisinopril in 26 elderly hypertensive patients with the use of the pulsed Doppler ultrasound technique. Nifedipine is a dihydropyridine calcium antagonist, and lisinopril is an angiotensin-converting enzyme inhibitor. The study had a single-blind crossover design: nifedipine and lisinopril were given for 8 weeks each after washout periods of 4 weeks. Both nifedipine and lisinopril significantly reduced mean arterial pressure to the same extent (P < .01); cardiac output remained unchanged in both nifedipine- and lisinopril-treated groups. Lisinopril increased renal flow significantly (P < .01), but nifedipine did not. Common carotid, vertebral, celiac, and superior mesenteric arterial and diaphragmatic and terminal aortic flows did not show a significant change with either nifedipine or lisinopril. The specific action of lisinopril on the thoracic aorta was a marked improvement of aortic compliance compared with nifedipine, which might be partly responsible for an increase in renal flow. Lisinopril may provide more desirable regional hemodynamic effects and additional benefits for elderly hypertensive patients.

An electromagnetic flow probe was chronically implanted around the common carotid, superior mesenteric, or renal artery or the terminal aorta in deoxycorticostrerone acetate (DOCA) hypertensive rats (prepared with DOCA and saline after uninephrectomy) and uninephrectomized control rats. A catheter for pressure measurement was inserted into the terminal aorta through a femoral artery. At rest the carotid and hindquarter (measured at the terminal aorta) blood flows in DOCA hypertensive rats were similar to the respective, corresponding values in normal rats with intact bilateral kidneys. The group mean of superior mesenteric flow was about 70% and that of renal flow about 40% larger than in normal rats. Cardiac output was estimated to be greater in DOCA hypertensive rats than in normal rats. In uninephrectomized control rats, superior mesenteric flow was larger than in normal rats to such an extent that an increase in cardiac output was assumed as in DOCA hypertensive rats, but renal flow was normal (about twice the unilateral renal flow in normal rats). Estimation of regional sympathetic vasoconstrictor tone from the decrease in peripheral resistance with hexamethonium and vasopressin antagonist revealed a substantial tone also in the superior mesenteric and hindquarter areas, where the tone was estimated to be almost absent in normal rats and uninephrectomized rats. It is suggested that hypertension in DOCA hypertensive rats is sustained by an increase in cardiac output and an elevation of vasoconstrictor tone in resistance vessels. Since increase in cardiac output appears to be similarly present in uninephrectomized control rats, the elevation of sympathetic tone due to administration of DOCA and salt seems to be indispensable for DOCA hypertension.