The Experts below are selected from a list of 87 Experts worldwide ranked by ideXlab platform

Tohru Tani - One of the best experts on this subject based on the ideXlab platform.

  • A mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, W Patrick Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P

  • a mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, Patrick W Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P<0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1~70.5 ng/mL; P<0.05), hypoglycemia, lactacidemia and mortality (45%; P<0.05). Conclusion: Early development of shock following Stomach Rupture may be in part due to endotoxin translocation and endotoxemia.

Toyokazu Yoshioka - One of the best experts on this subject based on the ideXlab platform.

  • A mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, W Patrick Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P

  • a mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, Patrick W Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P<0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1~70.5 ng/mL; P<0.05), hypoglycemia, lactacidemia and mortality (45%; P<0.05). Conclusion: Early development of shock following Stomach Rupture may be in part due to endotoxin translocation and endotoxemia.

M. Goto - One of the best experts on this subject based on the ideXlab platform.

  • A mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, W Patrick Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P

  • a mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, Patrick W Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P<0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1~70.5 ng/mL; P<0.05), hypoglycemia, lactacidemia and mortality (45%; P<0.05). Conclusion: Early development of shock following Stomach Rupture may be in part due to endotoxin translocation and endotoxemia.

W Patrick Zeller - One of the best experts on this subject based on the ideXlab platform.

  • A mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, W Patrick Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P

Patrick W Zeller - One of the best experts on this subject based on the ideXlab platform.

  • a mechanism for shock following Stomach Rupture in the newborn
    Pediatrics International, 1999
    Co-Authors: M. Goto, Toyokazu Yoshioka, Takanobu Hase, Tohru Tani, Patrick W Zeller
    Abstract:

    Background: Stomach Rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating Stomach Rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. Results: Endotoxin feeding alone caused endotoxemia (0.49~0.12 ng/mL; P<0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1~70.5 ng/mL; P<0.05), hypoglycemia, lactacidemia and mortality (45%; P<0.05). Conclusion: Early development of shock following Stomach Rupture may be in part due to endotoxin translocation and endotoxemia.