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N D Karanjia

Publications and source records attributed to N D Karanjia.

At least 19 recordsLinked to original sources
PubMed1995

Pancreatic vascular regulation in chronic pancreatitis in cats.

In experimental obstructive chronic pancreatitis the normal hyperaemic response to secretory stimulation is lost, suggesting abnormal vascular regulation. Vascular regulatory mechanisms were investigated by observing the effect of increments in portal pressure on pancreatic blood flow in normal cats and cats with chronic pancreatitis. Normal cats maintained pancreatic blood flow until portal pressure was > 15 mm Hg, after which it decreased. Total vascular resistance decreased until the portal pressure was 15 mm Hg and increased thereafter. These observations suggested that metabolic regulatory mechanisms prevailed while portal pressure was in the physiological range but myogenic mechanisms became dominant during portal hypertension. In chronic pancreatitis the basal pancreatic blood flow was reduced and was inversely proportional to portal pressure. Total vascular resistance increased as portal pressure increased. In chronic pancreatitis myogenic regulatory responses prevailed at all levels of portal pressure. In conclusion, intrinsic regulation of pancreatic blood flow was abnormal in cats with chronic pancreatitis. The loss of the predominance of metabolic regulation over the normal range of portal pressure may partly explain the reduction of pancreatic blood flow in response to secretory stimulation.

Animals↗
PubMed1994

Compartment syndrome in experimental chronic obstructive pancreatitis: effect of decompressing the main pancreatic duct.

Chronic pancreatitis is characterized by persistent and severe pain, which can be relieved by decompression of the main pancreatic duct (MPD). Both ductal and interstitial pressures have been shown to be increased in chronic pancreatitis in patients. A study was carried out of pancreatic interstitial pressure and pancreatic blood flow in normal cats and those in which chronic obstructive pancreatitis had been induced 5 weeks earlier to determine the effect of decompression of the MPD. In the normal pancreas, median(interquartile range (i.q.r.)) basal interstitial pressure was 0.05(1.2) mmHg and median(i.q.r.) basal pancreatic blood flow 58.3(24.3) ml per min per 100 g. Secretory stimulation did not change the interstitial pressure significantly, but was associated with a 40 per cent increase in median(i.q.r.) blood flow to 81.8(45.8) ml per min per 100 g. In contrast, in chronic obstructive pancreatitis, the median(i.q.r.) basal interstitial pressure was 2.0(1.5) mmHg, which was significantly higher than in the normal gland, and median(i.q.r.) pancreatic blood flow was 38.3(9.8) ml per min per 100 g, significantly lower than in the normal pancreas. Furthermore, secretory stimulation was associated with a significant increase in median(i.q.r.) interstitial pressure to 3.3(1.6) mmHg and a simultaneous decrease in median(i.q.r.) blood flow to 31.5(13.7) ml per min per 100 g. After decompression of the MPD in cats with chronic obstructive pancreatitis, the median(i.q.r.) basal interstitial pressure was 2.0(1.4) mmHg and on secretory stimulation 1.8(1.5) mmHg. Decompression thus prevented the increase in interstitial pressure seen in the animals with obstruction. In contrast, ductal decompression improved the median(i.q.r.) basal pancreatic blood flow to 45.9(38.4) ml per min per 100 g and, furthermore, this increased significantly on secretory stimulation to a median(i.q.r.) of 81.4(47.8) ml per min per 100 g. Decompression thus restored the normal pattern of secretory hyperaemia. Within the confines of this model, these observations demonstrate that chronic obstructive pancreatitis exhibits a compartment syndrome that is relieved by duct drainage.

Animals↗
PubMed1994

Antimicrobial treatment of pancreatic infection in cats.

An investigation examined the efficacy of antibiotics in a novel feline model of pancreatic infection in acute pancreatitis. Acute pancreatitis was induced in cats using an established technique. In control animals (no pancreatitis) and cats with pancreatitis, Escherichia coli (10(4) in 0.1 ml) was placed in the pancreatic duct. Reoperation was performed after 24 h in six controls and six cats with pancreatitis. E. coli was cultured from the pancreas in five control animals and five cats with pancreatitis. Reoperation was performed after 1 week in ten controls, in 11 cats with pancreatitis and in nine with pancreatitis that were treated with cefotaxime (50 mg/kg intramuscularly three times daily) started 12 h after the induction of pancreatitis and administration of E. coli. Pancreatic infection developed in eight cats with pancreatitis compared with none of the cefotaxime-treated animals and none of the controls (P < 0.05). Cefotaxime reached bactericidal levels in pancreatic tissue and juice. In conclusion, ductal administration of E. coli caused pancreatic infection only in cats with acute pancreatitis. Early administration of an appropriate antibiotic was effective in treating pancreatic infection in acute pancreatitis.

Acute Disease↗
PubMed1994

Leakage from stapled low anastomosis after total mesorectal excision for carcinoma of the rectum.

Over 14 years 276 patients with rectal cancer underwent surgery; 219 who underwent low anterior resection of the rectum with total mesorectal excision were studied. There were 24 (11.0 per cent) major anastomotic leaks associated with peritonitis or a pelvic collection and 14 (6.4 per cent) minor leaks that were asymptomatic and detected by contrast enema. All major leaks occurred at an anastomotic height of less than 6 cm (P = 0.08). The abdominoperineal excision rate was 9.1 per cent. Major leaks were associated with failure to defunction in 11 of 62 patients and with a defunctioning colostomy in 13 of 157 (P = 0.03). Of the 24 patients with major leaks seven developed peritonitis, one with a defunctioned anastomosis (P = 0.002), and three died (P = 0.02). Use of the sigmoid colon led to major leakage in seven of 32 patients compared with 17 of 187 when the splenic flexure was employed (P = 0.05). There was no increase in the local recurrence rate but only nine patients with major leakage and a temporary stoma have had these closed. Key technical factors include: a clean dry pelvic cavity, pulsatile colonic blood supply, suction drainage started during closure and mobilization of ample tissue to fill the pelvic space.

Adult↗
PubMed1994

Sources of pancreatic pathogens in acute pancreatitis in cats.

The source(s) of pancreatic pathogens is uncertain, although the colon is usually implicated. We studied whether pathogens may spread from different sites in a feline model of the disease. Acute pancreatitis was induced using a standard technique and a distinctive clinical strain of Escherichia coli as the marker bacterium. E. coli were placed in the colon, gall bladder, main pancreatic duct, or obstructed renal pelvis of control cats (no pancreatitis) and acute pancreatitis cats. Pancreases were colonized from each source, whether or not pancreatitis was present. The pancreatic colonization rate was greater in acute pancreatitis only when E. coli had been placed in the colon. In conclusion, E. coli may spread to the pancreas from different sources. The high rate of pancreatic colonization in both control and inflamed glands suggested that, clinically, bacteria may spread to the pancreas more frequently than is currently thought.

Acute Disease↗
PubMed1994

Dopamine in models of alcoholic acute pancreatitis.

Acute oedematous pancreatitis and acute haemorrhagic pancreatitis were studied using the low pressure duct perfusion models of alcoholic pancreatitis in cats. After creating either form over 24 hours, each pancreas was histologically graded and assigned an inflammatory score (0-16; absent-severe). Urinary trypsinogen activation peptide concentrations were also used as a measure of severity. Using the model of acute haemorrhagic pancreatitis, it was previously shown that low dose dopamine (5 micrograms/kg.m) reduced the inflammatory score at 24 hours and that this effect was mediated by a reduction in pancreatic microvascular permeability acting via dopaminergic and beta adrenergic receptors. Further studies were conducted and are reported here. In experiment 1 different doses of dopamine in established alcoholic acute haemorrhagic pancreatitis were studied. In group 1 control cats (no dopamine), the inflammatory score was 10.5 (interquartile range (IQR)4). In groups 2, 3, and 4, haemorrhagic pancreatitis was induced. Twelve hours later dopamine was infused for six hours, in the doses of 2 micrograms/kg.min, 5 micrograms/kg.min, and 50 micrograms/kg.min respectively. The inflammatory score in group 2 was 7 (IQR 0.5, p < 0.05 v group 1), in group 3 it was 7 (IQR 2, p < 0.05 v group 1), and in group 4 it was 7 (IQR 4, p < 0.05 v group 1). This was matched by significantly lower levels of urinary tripsinogen activation peptide at 24 hours. In experiment 2 (group 5) we tried to reduce microvascular permeability further by combining dopamine with antihistamines, but there was no improvement in the inflammatory score. As oedematous pancreatitis is the commoner and milder form of acute pancreatitis in clinical practice, in experiment 3 we looked at the effect of dopamine in this model. In group 6 control cats (no treatment), the inflammatory score was 7 (IQR 3, p < 0.05 v group 1). In group 7 cats given dopamine (5 micrograms/kg.min for six hours) from 12 hours after the onset of actue oedematous pancreatitis, the inflammatory score was reduced to 4(IQR 2, p < 0.05 v group 6). This was matched by a significant reduction in the 24 hour urinary tripsin activation peptide concentration.

Acute Disease↗
PubMed1994

Routes of spread of pathogens into the pancreas in a feline model of acute pancreatitis.

The routes of spread of pathogens into the pancreas in acute pancreatitis were investigated. Four experiments were performed: (1) cats with and without acute pancreatitis were given 10(7) Escherichia coli (E coli) intravenously, (2) in cats with acute pancreatitis 10(8) E coli was placed in the colon. In half of them the colon was then enclosed in an impermeable bag to prevent transmural spread. (3) E coli (10(4)) was placed in the pancreatic duct in cats with and without acute pancreatitis. (4) In cats with acute pancreatitis 10(5) E coli was placed in the gall bladder. In half of them the common bile duct was ligated to prevent biliary-pancreatic reflux. After 24 hours, intravenous E coli infected the pancreas in six of nine cats with acute pancreatitis and three of 10 controls. After 72 hours E coli spread to the pancreas from the colon in six of nine cats with acute pancreatitis. This was prevented by enclosing the colon in an impermeable bag (p = 0.02). In five of six cats with acute pancreatitis and five of six controls E coli placed in the pancreatic duct colonised the pancreas within 24 hours. Pancreatic colonisation from the gall bladder occurred in five of six cats with a patent common bile duct and in three of six with an obstructed common bile duct. In conclusion, in cats E coli can spread to the pancreas by the blood stream, transmurally from the colon, and by reflux into the pancreatic duct.

Acute Disease↗
PubMed1994

Histochemical and metabolic changes in functioning ileal pouches after proctocolectomy for familial adenomatous polyposis and ulcerative colitis.

Ulcerative colitis and familial adenomatous polyposis may be treated by proctocolectomy with ileal pouch reconstruction, anastomosing the pouch to the anus. We studied 24 patients who underwent this procedure, of whom 12 had ulcerative colitis and 12 had familial adenomatous polyposis. Ileal absorption was investigated and pouch histology assessed more than one year after closure of the protective defunctioning loop ileostomy. The results showed a reduction in bile acid reabsorption and vitamin B12 absorption. These observations were associated with a morphologic transformation in the small bowel mucosa to large bowel mucosa. In 10 of the 12 colitis patients one or more of the histological features of the original disease (such as active inflammation, increased regeneration, atypia) were evident. Histological examination of the biopsies taken from the polyposis patients showed areas with an excess of sialomucins.

Absorption↗
PubMed1993

Pancreatic infection complicating acute pancreatitis.

Pancreatic infection is the leading cause of death from acute pancreatitis. Patients with severe necrotizing pancreatitis are most at risk. Early computed tomography and percutaneous fine-needle aspiration microbiology of areas of pancreatic necrosis enable early diagnosis. Pancreatic infection should be treated surgically, although sterile necrosis may be managed conservatively. The role of antimicrobial drugs is uncertain.

Acute Disease↗