Experimental Pancreatitis

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 177 Experts worldwide ranked by ideXlab platform

Ofer Kaplan - One of the best experts on this subject based on the ideXlab platform.

  • Effects of delayed administration of octreotide in acute Experimental Pancreatitis
    The Journal of surgical research, 1996
    Co-Authors: Ofer Kaplan, Doron Kaplan, Eran Casif, Annette Siegal, Haim Paran, Eran Graf, Yehuda Skornick
    Abstract:

    Multiple therapeutic modalities studied for acute Pancreatitis often show a poor correlation between results obtained in Experimental studies and results of clinical trials. One of the main reasons for this discrepancy is that in most Experimental studies the drugs were administered immediately after induction of Pancreatitis, whereas in the clinical setting there is almost always a delay between the onset of the disease and initiation of the treatment. We studied the effects of a delayed treatment with octreotide, the synthetic analogue of the hormone somatostatin, on acute Experimental Pancreatitis in rats. The disease was induced by intraparenchymal injections of 0.5 ml 5% sodium taurocholate, and octreotide (10 mg/kg/day s.c.) was started either 4 or 12 hr later. Subcutaneous saline injections were used in controls. One-half of the animals of each study group was sacrificed after 36 hr, and the following parameters were examined: pancreatic weight, plasma pH, serum calcium and amylase, and histopathological damage. The same parameters, as well as survival, were assessed after 20 days in the remaining rats. Neither intrapancreatic saline injections, nor octreotide administration without the induction of Pancreatitis, caused any biochemical or histological alterations. Hypocalcemia and acidosis in Pancreatitis-induced rats were improved by octreotide, but, as expected, it had no effect on amylase levels. Octreotide ameliorated pancreatic edema, intestinal dilatation, and the histopathological injury score 36 hr after induction of Pancreatitis. Mortality was 40% in control animals, and only 20% in rats treated with octreotide. Overall, octreotide had beneficial effects in acute Experimental Pancreatitis, and was more effective when started earlier. These results indicate that octreotide may have a role in the management of acute Pancreatitis.

  • Effect of the Somatostatin Analogue Octreotide on Experimental Pancreatitis in Rats
    The Journal of surgical research, 1996
    Co-Authors: Haim Paran, Annette Siegal, Joseph M. Klausner, E. Graff, Uri Freund, Ofer Kaplan
    Abstract:

    Somatostatin and its analogue octreotide have a profound inhibitory effect on the endocrine and exocrine secretions of the pancreas, stomach, and small intestine. Previous studies have been inconclusive about the possible therapeutic effect of somatostatin and its analogues in the treatment of Pancreatitis. This study assessed the effect of the long acting somatostatin analogue, octreotide, in two models of Experimental Pancreatitis in rats. Necrotizing Pancreatitis was induced by pancreatic injection of 5 ml taurocholate, 5% in male Wistar rats. In a second model mild edematous Pancreatitis was induced by intravenous injection of caerulein at a supramaximal dose, 6 micrograms/kg/hr, for 5 hr. Compared to untreated rats, treatment with octreotide either prior to or following the induction of necrotizing Pancreatitis resulted in less hypocalcemia (P < 0.05) and acidosis (P < 0.05), and prevented the increase in pancreatic weight (P < 0.05). Amylase levels remained high. After 20 days, there was less pancreatic damage, lower mortality rates (P < 0.05), and increase in body weight (P < 0.05). In the model of milder Pancreatitis, octreotide treatment attenuated the increase in pancreatic weight (P < 0.05) and pathological damage (P < 0.05). We concluded that the somatostatin analogue octreotide has a beneficial effect in the treatment of Experimental acute Pancreatitis.

Haim Paran - One of the best experts on this subject based on the ideXlab platform.

  • Effects of delayed administration of octreotide in acute Experimental Pancreatitis
    The Journal of surgical research, 1996
    Co-Authors: Ofer Kaplan, Doron Kaplan, Eran Casif, Annette Siegal, Haim Paran, Eran Graf, Yehuda Skornick
    Abstract:

    Multiple therapeutic modalities studied for acute Pancreatitis often show a poor correlation between results obtained in Experimental studies and results of clinical trials. One of the main reasons for this discrepancy is that in most Experimental studies the drugs were administered immediately after induction of Pancreatitis, whereas in the clinical setting there is almost always a delay between the onset of the disease and initiation of the treatment. We studied the effects of a delayed treatment with octreotide, the synthetic analogue of the hormone somatostatin, on acute Experimental Pancreatitis in rats. The disease was induced by intraparenchymal injections of 0.5 ml 5% sodium taurocholate, and octreotide (10 mg/kg/day s.c.) was started either 4 or 12 hr later. Subcutaneous saline injections were used in controls. One-half of the animals of each study group was sacrificed after 36 hr, and the following parameters were examined: pancreatic weight, plasma pH, serum calcium and amylase, and histopathological damage. The same parameters, as well as survival, were assessed after 20 days in the remaining rats. Neither intrapancreatic saline injections, nor octreotide administration without the induction of Pancreatitis, caused any biochemical or histological alterations. Hypocalcemia and acidosis in Pancreatitis-induced rats were improved by octreotide, but, as expected, it had no effect on amylase levels. Octreotide ameliorated pancreatic edema, intestinal dilatation, and the histopathological injury score 36 hr after induction of Pancreatitis. Mortality was 40% in control animals, and only 20% in rats treated with octreotide. Overall, octreotide had beneficial effects in acute Experimental Pancreatitis, and was more effective when started earlier. These results indicate that octreotide may have a role in the management of acute Pancreatitis.

  • Effect of the Somatostatin Analogue Octreotide on Experimental Pancreatitis in Rats
    The Journal of surgical research, 1996
    Co-Authors: Haim Paran, Annette Siegal, Joseph M. Klausner, E. Graff, Uri Freund, Ofer Kaplan
    Abstract:

    Somatostatin and its analogue octreotide have a profound inhibitory effect on the endocrine and exocrine secretions of the pancreas, stomach, and small intestine. Previous studies have been inconclusive about the possible therapeutic effect of somatostatin and its analogues in the treatment of Pancreatitis. This study assessed the effect of the long acting somatostatin analogue, octreotide, in two models of Experimental Pancreatitis in rats. Necrotizing Pancreatitis was induced by pancreatic injection of 5 ml taurocholate, 5% in male Wistar rats. In a second model mild edematous Pancreatitis was induced by intravenous injection of caerulein at a supramaximal dose, 6 micrograms/kg/hr, for 5 hr. Compared to untreated rats, treatment with octreotide either prior to or following the induction of necrotizing Pancreatitis resulted in less hypocalcemia (P < 0.05) and acidosis (P < 0.05), and prevented the increase in pancreatic weight (P < 0.05). Amylase levels remained high. After 20 days, there was less pancreatic damage, lower mortality rates (P < 0.05), and increase in body weight (P < 0.05). In the model of milder Pancreatitis, octreotide treatment attenuated the increase in pancreatic weight (P < 0.05) and pathological damage (P < 0.05). We concluded that the somatostatin analogue octreotide has a beneficial effect in the treatment of Experimental acute Pancreatitis.

Annette Siegal - One of the best experts on this subject based on the ideXlab platform.

  • Effects of delayed administration of octreotide in acute Experimental Pancreatitis
    The Journal of surgical research, 1996
    Co-Authors: Ofer Kaplan, Doron Kaplan, Eran Casif, Annette Siegal, Haim Paran, Eran Graf, Yehuda Skornick
    Abstract:

    Multiple therapeutic modalities studied for acute Pancreatitis often show a poor correlation between results obtained in Experimental studies and results of clinical trials. One of the main reasons for this discrepancy is that in most Experimental studies the drugs were administered immediately after induction of Pancreatitis, whereas in the clinical setting there is almost always a delay between the onset of the disease and initiation of the treatment. We studied the effects of a delayed treatment with octreotide, the synthetic analogue of the hormone somatostatin, on acute Experimental Pancreatitis in rats. The disease was induced by intraparenchymal injections of 0.5 ml 5% sodium taurocholate, and octreotide (10 mg/kg/day s.c.) was started either 4 or 12 hr later. Subcutaneous saline injections were used in controls. One-half of the animals of each study group was sacrificed after 36 hr, and the following parameters were examined: pancreatic weight, plasma pH, serum calcium and amylase, and histopathological damage. The same parameters, as well as survival, were assessed after 20 days in the remaining rats. Neither intrapancreatic saline injections, nor octreotide administration without the induction of Pancreatitis, caused any biochemical or histological alterations. Hypocalcemia and acidosis in Pancreatitis-induced rats were improved by octreotide, but, as expected, it had no effect on amylase levels. Octreotide ameliorated pancreatic edema, intestinal dilatation, and the histopathological injury score 36 hr after induction of Pancreatitis. Mortality was 40% in control animals, and only 20% in rats treated with octreotide. Overall, octreotide had beneficial effects in acute Experimental Pancreatitis, and was more effective when started earlier. These results indicate that octreotide may have a role in the management of acute Pancreatitis.

  • Effect of the Somatostatin Analogue Octreotide on Experimental Pancreatitis in Rats
    The Journal of surgical research, 1996
    Co-Authors: Haim Paran, Annette Siegal, Joseph M. Klausner, E. Graff, Uri Freund, Ofer Kaplan
    Abstract:

    Somatostatin and its analogue octreotide have a profound inhibitory effect on the endocrine and exocrine secretions of the pancreas, stomach, and small intestine. Previous studies have been inconclusive about the possible therapeutic effect of somatostatin and its analogues in the treatment of Pancreatitis. This study assessed the effect of the long acting somatostatin analogue, octreotide, in two models of Experimental Pancreatitis in rats. Necrotizing Pancreatitis was induced by pancreatic injection of 5 ml taurocholate, 5% in male Wistar rats. In a second model mild edematous Pancreatitis was induced by intravenous injection of caerulein at a supramaximal dose, 6 micrograms/kg/hr, for 5 hr. Compared to untreated rats, treatment with octreotide either prior to or following the induction of necrotizing Pancreatitis resulted in less hypocalcemia (P < 0.05) and acidosis (P < 0.05), and prevented the increase in pancreatic weight (P < 0.05). Amylase levels remained high. After 20 days, there was less pancreatic damage, lower mortality rates (P < 0.05), and increase in body weight (P < 0.05). In the model of milder Pancreatitis, octreotide treatment attenuated the increase in pancreatic weight (P < 0.05) and pathological damage (P < 0.05). We concluded that the somatostatin analogue octreotide has a beneficial effect in the treatment of Experimental acute Pancreatitis.

Frank Porreca - One of the best experts on this subject based on the ideXlab platform.

  • attenuation of persistent Experimental Pancreatitis pain by a bradykinin b2 receptor antagonist
    Pancreas, 2010
    Co-Authors: Qingmin Chen, Michael H Ossipov, Louis P Veraportocarrero, Marina Vardanyan, Josephine Lai, Frank Porreca
    Abstract:

    OBJECTIVE The role of bradykinin (BK) receptors in activating and sensitizing peripheral nociceptors is well known. Recently, we showed that spinal dynorphin was pronociceptive through direct or indirect BK receptor activation. Here, we explored the potential role of BK receptors in pain associated with persistent Pancreatitis in rats. METHODS Experimental Pancreatitis and abdominal hypersensitivity were induced by intravenous administrations of dibutyltin dichloride (DBTC). [des-Arg-Leu]BK (B1 antagonist) and HOE 140 (B2 antagonist) were given by intraperitoneal or intrathecal injection. Dynorphin antiserum was given intrathecally. Reverse transcription-polymerase chain reaction was used to detect spinal mRNA for BK receptors. RESULTS Dibutyltin dichloride-induced Pancreatitis upregulated B1 and B2 mRNA in the thoracic dorsal root ganglion and B2, but not B1, in the pancreas. No changes in spinal B1 or B2 mRNA were observed. Intraperitoneal or intrathecal administration of HOE 140 dose dependently abolished DBTC-induced abdominal hypersensitivity, whereas [des-Arg-Leu]BK was without effect by either route of administration. Antiserum to dynorphin (intrathecal) abolished DBTC-induced hypersensitivity. CONCLUSIONS These results suggest that blockade of peripheral or spinal BK B2 receptors may be an effective approach for diminishing pain associated with Pancreatitis. Moreover, it is suggested that spinal dynorphin may maintain Pancreatitis pain through direct or indirect activation of BK B2 receptors in the spinal cord.

  • descending facilitation from the rostral ventromedial medulla maintains visceral pain in rats with Experimental Pancreatitis
    Gastroenterology, 2006
    Co-Authors: Louis Vera P Portocarrero, Justin Kowal, Tamara King, Michael H Ossipov, Frank Porreca
    Abstract:

    Background & Aims: Pain is a main complaint of patients with Pancreatitis. We hypothesized that such pain is mediated through ascending pathways via the nucleus gracilis (NG) and is dependent on descending facilitatory influences from the rostral ventromedial medulla (RVM). Methods: A rat model of persistent Experimental Pancreatitis was used. After establishment of Pancreatitis, rats received microinjection of lidocaine in the NG or in the RVM to determine the importance of neural activity at these supraspinal sites in the expression of abdominal hypersensitivity evoked by von Frey filaments (ie, pancreatic pain). Rats also were pretreated for 28 days before induction of Pancreatitis with a single RVM microinjection of dermorphin–saporin to eliminate cells that drive descending facilitation. Dynorphin content was measured in the spinal cord of pancreatitic rats and the effects of spinal antidynorphin antiserum in pancreatic pain were assessed. Results: Microinjection of lidocaine into either the NG or the RVM produced a time-related reversal of Pancreatitis-induced pain. Pancreatitis significantly increased thoracic spinal dynorphin content and spinal antidynorphin antiserum elicited a time-related reversal of abdominal hypersensitivity. RVM dermorphin–saporin injection prevented the maintenance, but not the expression, of Pancreatitis abdominal hypersensitivity and also prevented the increase of spinal dynorphin content in animals with Pancreatitis. Conclusions: Our findings suggest that descending facilitation from the RVM plays a critical role in the maintenance, but not the expression, of pancreatic pain. These results provide a novel insight into the role of descending pathways and spinal plasticity in the maintenance of visceral pain from Pancreatitis.

Yehuda Skornick - One of the best experts on this subject based on the ideXlab platform.

  • Effects of delayed administration of octreotide in acute Experimental Pancreatitis
    The Journal of surgical research, 1996
    Co-Authors: Ofer Kaplan, Doron Kaplan, Eran Casif, Annette Siegal, Haim Paran, Eran Graf, Yehuda Skornick
    Abstract:

    Multiple therapeutic modalities studied for acute Pancreatitis often show a poor correlation between results obtained in Experimental studies and results of clinical trials. One of the main reasons for this discrepancy is that in most Experimental studies the drugs were administered immediately after induction of Pancreatitis, whereas in the clinical setting there is almost always a delay between the onset of the disease and initiation of the treatment. We studied the effects of a delayed treatment with octreotide, the synthetic analogue of the hormone somatostatin, on acute Experimental Pancreatitis in rats. The disease was induced by intraparenchymal injections of 0.5 ml 5% sodium taurocholate, and octreotide (10 mg/kg/day s.c.) was started either 4 or 12 hr later. Subcutaneous saline injections were used in controls. One-half of the animals of each study group was sacrificed after 36 hr, and the following parameters were examined: pancreatic weight, plasma pH, serum calcium and amylase, and histopathological damage. The same parameters, as well as survival, were assessed after 20 days in the remaining rats. Neither intrapancreatic saline injections, nor octreotide administration without the induction of Pancreatitis, caused any biochemical or histological alterations. Hypocalcemia and acidosis in Pancreatitis-induced rats were improved by octreotide, but, as expected, it had no effect on amylase levels. Octreotide ameliorated pancreatic edema, intestinal dilatation, and the histopathological injury score 36 hr after induction of Pancreatitis. Mortality was 40% in control animals, and only 20% in rats treated with octreotide. Overall, octreotide had beneficial effects in acute Experimental Pancreatitis, and was more effective when started earlier. These results indicate that octreotide may have a role in the management of acute Pancreatitis.