Do parotid duct abnormalities occur in patients with chronic alcoholic pancreatitis?

OBJECTIVE: Several studies have suggested that ethanol affects the pancreas and parotid gland. We performed a prospective study to determine whether ductal lesions of ethanol-induced chronic pancreatitis occur in the parotid. METHODS: Parotid sialograms were performed in 11 alcoholic patients who had endoscopic retrograde pancreatograms. Sialograms and pancreatograms were examined in all subjects for ductal abnormalities. RESULTS: Seven of nine patients (77.8%) with ductal lesions of the pancreas had coexistent ductal abnormalities of the parotid gland (Kendall's tau = 0.578, p = 0.035). CONCLUSIONS: Chronic ethanol intake induces ductal alterations in the parotid gland similar to those seen in the pancreas. These results suggest a common histopathological effect of alcohol in the ductal system of the parotid gland and pancreas and raise the possibility that the parotid sialogram could be useful as an adjunct in the diagnosis of ethanol-induced chronic pancreatitis.

Posttraumatic pseudoaneurysm of the posterior meningeal artery associated with intraventricular hemorrhage.

A 22-year-old man sustained a severe head injury and had a torn posterior meningeal artery that caused massive intraventricular hemorrhage. Traumatic pseudoaneurysm of the posterior meningeal artery should be considered in cases where intraventricular hemorrhage occurs in the presence of occipital bone fracture and contiguous epidural hematoma; vertebral angiography is of value in this regard.

Effect of aspirin on vascular tone and reactivity to vasoactive amines in the dog lung.

The effect of increasing blood levels of aspirin on pulmonary hemodynamics and pressor response to vasoactive amines was examined in the isolated canine lung lobe, blood perfused at constant flow. At steady state lobar vascular resistance (LVR), lobes were challenged with either 250 micrograms serotonin (5-HT; n = 4), 5.0 mumol acetylcholine (ACh; n = 4) or 50 micrograms norepinephrine (NE; n = 4) before and after blood aspirin concentration [ASA] was incrementally increased from 17 to 3140 microM. LVR was partitioned into arterial (Ra) and venous (Rv) segments by venous outflow occlusions 20 min after each ASA addition and at the peak of the pressor response to each amine. ASA treatment was associated with a dose-related 105% increase in LVR (P < 0.01) accounted for by a 154% increase in Ra (P < 0.01) and a 70% increase in Rv (P < 0.01) at 3150 microM ASA (n = 12). In spite of increased vascular tone, higher [ASA] also potentiated increases in both pulmonary arterial pressure and LVR to both 5-HT and NE whereas only Ra increased with ACh challenge. Thus, the increase in pulmonary vascular tone and reactivity to vasoactive amines is positively correlated with blood aspirin levels in the dog.