Effects of beta-blockade on neurohumoral responses and neurochemical markers in pacing-induced heart failure.

We investigated neurohumoral profiles and transmitter and neuroenzyme markers of cardiac autonomic innervation in control (unpaced) dogs and three groups of dogs with pacing-induced heart failure (paced, paced + beta-adrenergic blockade, and paced + cardiac denervation). Left ventricular ejection fraction decreased significantly and to a comparable extent in all paced groups. Pacing increased plasma norepinephrine (NE); increases in NE were not attenuated but instead tended to be exaggerated by treatment with propranolol or cardiac denervation. Atrial hypertrophy occurred in all paced groups compared with the control group. However, atrial and right ventricular hypertrophy were not as pronounced in the paced plus cardiac denervation group as in the paced and paced plus propranolol groups. Pacing also depleted neuropeptide Y and NE from all heart chambers; propranolol treatment did not modify these local tissue changes. Pacing caused selective depletion of neuroenzymes predominantly in the left ventricle; again, propranolol did little to modify these changes. In this study of paced animals with experimentally maintained cardiac dysfunction, failure to modify noradrenergic responses with intrapericardial cardiac denervation suggests that noncardiac sources contribute predominantly to high plasma NE. Failure to modify neurohumoral, neuropeptide, and neuroenzyme responses with beta-antagonist suggests this treatment has little practical direct influence on sympathetic vasomotor activity or neuronal function in heart failure.

Allograft vein patency in a canine model. Additive effects of cryopreservation and cyclosporine.

Autogenous saphenous vein is the preferred conduit for many cardiovascular operations. Attempts to use allograft veins for arterial reconstruction have had poor results. To define circumstances under which allograft veins might prove to be acceptable vascular conduits, dogs underwent femoral artery bypass using reversed saphenous veins. Veins were transplanted fresh or after cryopreservation. Group I dogs received a fresh autograft to replace one femoral artery (group I F) and a cryopreserved (CP) autograft (group I C) to replace the other. Group II dogs received fresh allograft veins, and group III received CP allograft veins, neither group receiving additional treatment. Group IV received fresh allograft veins and Group V received CP allograft veins; both groups received cyclosporine 15 mg/kg. Animals were maintained until grafts occluded or until six months elapsed. Patency was observed in all group I F grafts throughout the observation period. Six-month patency rates in the other groups were: group I C, 9/10 (P = NS vs. group I F); group II, 0/10 (P less than 0.01), group III, 0/10 (P less than 0.01), group IV, 1/10 (P less than 0.01), group V, 7/11 (P = NS). In a separate series of observations 10 cryopreserved allograft veins were implanted in 10 dogs that received CsA for 30 days. CsA was then discontinued. All of these grafts occluded within 30 days of discontinuing the CsA. Long-term patency of saphenous vein allografts was achieved only with the combination of cryopreservation and immunosuppression with continued CsA.

Effect of SMS201-995 (a long-acting somatostatin analog) on bile-induced acute hemorrhagic pancreatitis in the dog.

Recent reports claim a beneficial role for SMS201-995 (SMS) in pancreatitis. To study the effects of SMS in a canine pancreatitis model, four groups of eight dogs each were subjected to laparotomy; and after cannulation of the dorsal pancreatic duct, a mixture of bile and trypsin was infused to induce pancreatitis. Group I constituted the control group and received no SMS. Group II received SMS intravenously at 5 micrograms/hr beginning 1 hour before the induction of pancreatitis. Group III and Group IV received SMS at the same dose starting at 2 hours and 6 hours, respectively, after the induction of pancreatitis. Infusions were maintained until 24 hours after the induction of pancreatitis. Leukocyte counts, serum lipase and amylase levels were obtained preoperatively and at 24 hours. All dogs were killed at 24 hours and autopsies performed. At autopsy, severity of pancreatitis was graded, based on survival, the presence or absence of pancreatic edema, hemorrhage, and necrosis, as well as the presence and severity of bloody ascites. Only on a dog (Group III) died before the 24-hour period. When SMS was used before the induction of pancreatitis, the pancreatitis seen was less severe (Group I vs Group II, P = .022). No effects were found when using SMS after the induction of pancreatitis (Group III or Group IV vs Group I). The serum lipase, amylase, and leukocyte counts changed significantly in all the dogs (P less than .001) with the onset of pancreatitis, but this difference was not significant between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatic resections: an eight year experience at a community hospital.

Between April 1979 and March 1987 24 patients underwent 26 hepatic resections. Colorectal liver metastases constituted the largest group (n = 18), followed by hepatocellular carcinoma (n = 2), Echinococcal liver cyst (n = 1), cholangiocarcinoma (n = 1), and leiomyosarcoma (n = 1). The mean age was 41.8 +/- 14.6 years (range: 23-69 years). Fifteen women and nine men comprised the group. The operative morbidity was 21 per cent, the 30-day operative mortality was 8 per cent (two deaths). Both operative deaths occurred in patients with colorectal liver metastases. The 18 patients with colorectal liver metastases included ten women and eight men. The mean age was 59.1 +/- 6.5 years (range: 46-69 years). There were seven synchronous and 11 metachronous liver metastases. Carcinoembryonic antigen (CEA) was found elevated in 14 of the original primary colonic carcinomas, and in all but one patient with metachronous liver metastases. The mean time from colorectal carcinoma resection to occurrence of metachronous metastases was 17.1 +/- 5.8 months. To date, 10 patients have had recurrences of liver metastases after hepatic resection for colorectal liver metastases. The mean time of recurrence was 12.6 +/- 11.9 months. The size of the metastases was 3.8 +/- 3.2 cm (range: 0.2-17 cm). The mean number of lesions present was 1.5 +/- 1.0. The 1 year and 2 year actuarial survival rates were 87.5 and 43.8 per cent respectively. The longest survivor is alive 54 months after his hepatic resection for colorectal liver metastases and remains to this date disease free.(ABSTRACT TRUNCATED AT 250 WORDS)