Biomedical subjects

T E Emerson

Publications and source records attributed to T E Emerson.

At least 37 records · Page 2Linked to original sources

PubMed1985

Efficaciousness of immunoglobulin G prophylaxis on mortality and physiological variables in gram-negative peritonitis in rodents.

A rapidly expanding role involving the use of immunoglobulin preparations in conditions other than the classical immunodeficiency syndromes is evident in recent years. Treatment with immunoglobulin may be especially important during infection in which specific antibody to pathogens has been consumed, degraded, or not produced and in cases in which antibiotic treatment is ineffective. Recent studies in animals and humans support this concept, although further studies are needed to fully develop it. This study was completed to explore possible beneficial effects of prophylactic treatment of rodents during severe Salmonella typhimurium peritonitis with a newly developed native immunoglobulin G preparation for intravenous use (IGIV pH 4.25). This study demonstrates that IGIV pH 4.25 increases survival time and decreases absolute mortality, prevents hypotension and acidosis, and ameliorates or prevents changes in variables indicative of organ damage during S. typhimurium bacteremia in the rat. Studies in mice indicate that protection is mediated by antibody to cell surface antigen (s) of S. typhimurium.

Acidosis↗

PubMed1982

Forelimb skeletal muscle and skin glucose uptake during Escherichia coli endotoxin shock in the dog.

We previously demonstrated an increase in gracilis muscle glucose uptake during endotoxin shock in the dog. The present study was completed to investigate this phenomenon in forelimb skeletal muscle and skin. The isolated forelimb preparation was used. Mongrel dogs were anesthetized with nembutal and heparinized. Shock was induced by i.v. infusion of E. coli endotoxin. When isolated forelimb temperature was maintained at contralateral intact forelimb temperature (which was always the same as core temperature), forelimb skeletal muscle and skin glucose uptake increased by 30 minutes of shock, and remained above control for the 4 hour shock period. Total forelimb blood flow decreased and the limb became severely hypoxic (mean venous PO2 = 24 mmHg). However, when the isolated forelimb temperature was not artificially maintained at contralateral intact forelimb temperature (same as core temperature), the isolated forelimb temperature fell approximately 3 degrees C and the elevation of glucose uptake was not observed. Although forelimb blood flow decreased to the same level as in the temperature controlled group, the forelimbs were only moderately hypoxic. This study emphasizes the important influence of temperature on tissue metabolism and the recognition of its importance in experimental data interpretation, especially when metabolic variables are involved. It also demonstrates that changes in glucose uptake during shock are similar in dog forelimb skeletal muscle, provided that changes in muscle temperature are similar.

Animals↗

PubMed1982

Mechanism of forelimb skin and skeletal muscle glucose uptake during Escherichia coli endotoxin shock in the dog.

This study was undertaken to investigate mechanisms of increased glucose uptake by forelimb skin and skeletal muscle during endotoxin shock. Anesthetized mongrel dogs were used. Forelimbs were perfused at either natural or constant blood flow. Temperature of the isolated forelimb was maintained at core temperature. Shock was induced by an IV injection of 2 mg/kg Escherichia coli endotoxin. Forelimb skin and skeletal muscle glucose uptake increased by 30 minutes of shock and remained elevated in the natural flow study. In the constant flow study, glucose uptake by both skin and skeletal muscle was increased at 30 minutes of shock but thereafter returned to control. The natural flow forelimbs were ischemic and hypoxic during shock, whereas the constant flow forelimbs were neither ischemic not hypoxic. Progressive hypoglycemia developed in both endotoxin shock groups. These data support the hypothesis that the mechanism of increases in forelimb skin and skeletal muscle glucose uptake during endotoxin shock is related to local tissue hypoxia.

Animals↗

PubMed1982

Direct effects of insulin and endotoxin on glucose uptake by skeletal muscle during high cardiac index sepsis in the dog.

Experiments were completed upon unanesthetized and anesthetized dogs in the control and septic groups. Dogs that were made septic by the intraperitoneal administration of live Escherichia coli bacteria showed an elevation in cardiac index and core temperature and a decrease in total peripheral resistance index and mean arterial blood pressure. Following the seventh day of sepsis, the dogs were anesthetized and the constantly perfused gracilis muscle preparation was used for metabolic and hemodynamic determinations. Insulin stimulated muscle glucose uptake in non-septic dogs was markedly increased, whereas increases in muscle glucose uptake in the septic group of dogs was absent when challenged with local insulin infusion. Resting muscle glucose uptake of the septic group was observed to be greater than that of dogs in the nonseptic group. These data demonstrate a hyperdynamic model of sepsis in the dog which was associated with decreased muscle responsiveness or sensitivity to local insulin infusion, or both. The insulin-like activity of the endotoxin molecule in promoting muscle glucose uptake was maintained in both the septic and control group of dogs. This activity of the endotoxin molecule could explain, in part, the increased resting muscle glucose uptake observed in the septic group of dogs.

Animals↗

PubMed1981

Direct effects of gram-negative endotoxin on skeletal muscle glucose uptake.

The effect of locally infused endotoxin on gracilis muscle glucose uptake was determined in anesthetized mongrel dogs. Locally infused endotoxin consistently caused an increase in skeletal muscle glucose uptake with no alterations in any other metabolic variable. These data demonstrate that endotoxin can act locally to increase glucose uptake by skeletal muscle, independent of the action of insulin or other metabolic factors. On the other hand, when endotoxin was given systemically to induce shock, gracilis muscle glucose uptake did not increase. These differences may reflect the reduction in plasma endotoxin concentration mediated by the reticuloendothelial system (RES). However, live Escherichia coli shock was associated with an increase in glucose uptake in the constant flow perfused gracilis muscle after 4.5 h of shock. We believe this increase in muscle glucose uptake resulted from the direct effects of endotoxin, the plasma concentration of which presumably increased as the RES was overwhelmed and became less effective. The contribution of this phenomenon to the hypoglycemia of gram-negative endotoxin or septic shock cannot be evaluated from this study.

Animals↗

PubMed1981

Involvement of adenosine in cerebral hypoxic hyperemia in the dog.

Theophylline, a competitive adenosine antagonist, was used to evaluate the role of adenosine in cerebral hypoxic hyperemia. Cerebral venous outflow was measured by the Rapela-Green technique in mongrel dogs anesthetized with pentobarbital sodium and ventilated artificially. Theophylline was infused locally into the cerebral arterial system during moderate [cerebral venous O2 tension (PO2) 27-29 mmHg] or severe (cerebral venous PO2 = 10-15 mmHg) hypoxia; theophylline had no direct vascular effects at the concentration used. Cerebral hyperemia was completely reversed during moderate hypoxia, but only partially reversed during severe hypoxia when theophylline was infused during maintained hypoxia. Theophylline had no effect on cerebral; perfusion pressure, blood flow, or vascular resistance during normoxia. In another group, theophylline had no effect on the cerebral hyperemia induced by hypercapnia. In separate experiments, local cerebral arterial infusion of adenosine or AMP during normoxia had no effect on cerebral hemodynamics at any infusion rate tested (up to 100 micrograms/min). This study supports the hypothesis that adenosine is involved in the hyperemia associated with cerebral hypoxia. However, the degree of involvement may be dependent on the degree of hypoxia.

Adenosine↗

PubMed1981

Insulin-like action of E. coli endotoxin in promoting skeletal muscle glucose uptake in the dog.

The effect of locally infused endotoxin on gracilis muscle glucose uptake was determined in anesthetized mongrel dogs. The effects of infusion of small amounts of E. coli endotoxin into the artery of isolated, innervated, constant-flow-perfused gracilis muscles on glucose uptake and other metabolic variables were determined. Locally infused endotoxin consistently caused a significant and substantial increase in skeletal muscle glucose uptake with no alterations in muscle arterio-venous difference of insulin, oxygen, carbon dioxide, or pH, or in venous blood hematocrit or temperature. These data demonstrate that endotoxin can act locally to increase glucose uptake by skeletal muscle, independent of the action of insulin or other metabolic factors. On the other hand, when endotoxin was given systemically to induce shock, gracilis muscle glucose uptake was maintained for the duration of the 6-hr experiment. These differences we feel reflect the reduction in plasma endotoxin concentration mediated by the reticuloendothelial system (RES). On the other hand, live E. coli septic shock was associated with an increase in glucose uptake in the constant-flow-perfused gracilis muscle after 4.5 hr of shock. We believe this increase in muscle glucose uptake resulted from the direct effects of endotoxin, whose plasma concentration presumably increases substantially as the RES is overwhelmed and becomes less effective. The contribution of this phenomenon to the progressive hypoglycemia characteristic of gram-negative endotoxin or septic shock cannot be evaluated from this study, although it is probably substantial.

Animals↗

PubMed1981

Effects of naloxone therapy on hemodynamics and metabolism following a superlethal dosage of Escherichia coli endotoxin in dogs.

Experiments were done upon anesthetized and unanesthetized dogs given endotoxin only, endotoxin plus naloxone or naloxone only. Dogs given endotoxin and treated with naloxone showed marked hemodynamic and metabolic improvements compared with the dogs given endotoxin only. Beneficial effects of naloxone treatment following the administration of endotoxin are attentuated hypotension, hemoconcentration and acidosis and prevention of hypoglycemia. Results of mortality studies in unanesthetized dogs given endotoxin suggest that naloxone treatment increases the survival time.

Animals↗

PubMed1981

Mechanism of increased glucose uptake by skeletal muscle during E coli endotoxin shock in the dog.

Carbohydrate metabolism of skeletal muscle was studied during 2 mg/kg E coli endotoxin shock in dogs. During natural (free-flow) conditions, glucose uptake by the muscle increased markedly during 6 hours of shock. Increased glucose uptake occurred concomitant with muscle ischemia and hypoxia. However, when muscle blood flow was held constant, thereby preventing local muscle ischemia and hypoxia, glucose uptake by the gracilis muscle did not change during shock. These results implicate local muscle ischemia and/or hypoxia as the mediator(s) of the increased muscle glucose uptake during shock. Further studies demonstrated that local muscle hypoxia was the stimulus for increased glucose uptake by skeletal muscle during endotoxin shock, and muscle ischemia per se did not alter muscle glucose uptake. Since approximately 50% of body mass is composed of skeletal muscle, the contribution of this organ system in the hypoglycemia of endotoxin shock in the dog may be substantial.

Animals↗

PubMed1981

In vivo skeletal muscle insulin resistance during E coli endotoxin shock in the dog.

The ability of insulin to promote glucose diffusion into skeletal muscle before and during gram-negative endotoxin shock was studied in mongrel dogs anesthetized with sodium pentobarbital. The in vivo, isolated, innervated, constant-flow-perfused gracilis muscle preparation was used. Prior to shock induction, close intraarterial insulin infusion resulted in a 320% increase in muscle glucose uptake. However, at one, two, and three hours of endotoxin shock, gracilis muscle glucose uptake was unaltered by insulin infusion. This loss of responsiveness to insulin occurred with no alteration in gracilis muscle oxygen uptake, muscle venous PO2, or muscle blood flow. During control experiments, however, the muscle response to intraarterial infusion of insulin (increased glucose uptake) was unaltered during the three-hour control period. These data demonstrate that skeletal muscle insulin resistance develops early and is maintained during three hours of endotoxin shock in the dog.

Animals↗

PubMed1981

Skeletal muscle insulin resistance during Escherichia coli bacteremic shock in the dog.

Skeletal muscle glucose uptake during close, intra-arterial insulin infusion was studied before and during live Escherichia coli bacteremic shock in the dog. An in vivo, constant-flow perfused gracilis muscle preparation was used. Insulin infusion before shock resulted in a 395% increase in muscle glucose uptake, which was independent of changes in muscle lactate production or oxygen uptake. At 1, 2, and 3 hours of shock, insulin infusion had no effect on gracilis muscle glucose uptake. This loss of responsiveness to insulin occurred with no change in muscle oxygen uptake, muscle venous PO2, or muscle blood flow (held constant). On the other hand, during nonshock control experiments, muscle glucose uptake in response to insulin infusion was maintained during the 3-hour protocol. These data demonstrate that skeletal muscle insulin resistance develops early during bacteremic shock.

Animals↗

PubMed1979

Methylprednisolone in the prevention of cerebral hemodynamic and metabolic disorders during endotoxin shock in the dog.

These results provide evidence that steroid pretreatment and subsequent post-treatment prevent cerebral hemodynamic and metabolic alterations during four hours of Escherichia coli endotoxin shock in the dog. However, in this study, no data are provided on how the steroid prevents an increase in cerebral vascular resistance, and no clear answer is available in the literature. While active vasodilation or alpha-adrenergic blocking properties, or both, have been attributed to glucocorticoids, recent evidence does not support these findings during normal conditions or circulatory shock. If the increase in cerebral vascular resistance is passive, steroids may help by preventing platelet aggregation, cell disruption and subsequent microvascular plugging. Intravenously administered fluids, dextran-saline solution, while in themselves are probably not important to survival, may augment cerebral blood flow during shock through a blood dilutional effect. Finally, it is possible that steroids act to permit normal, long term cerebral auto-regulation, which is apparently impaired during endotoxin shock in the dog.

Animals↗

PubMed1979

Cerebrospinal fluid composition during endotoxin shock in the dog.

Cerebrospinal fluid (CSF) electrolytes, lactate, pyruvate, total proteins, and osmolality, together with arterial plasma electrolytes, total proteins, osmolarity, and systemic arterial blood pressure were monitored during 2 mg/kg and 5 mg/kg E coli endotoxin shock in spontaneously breathing dogs. During four hours of shock, Na+, K+ osmolarity, and total proteins did not change in either plasma or CSF. CSF lactate and lactate/pyruvate ratio were significantly elevated, whereas pyruvate was decreased throughout the four hours of shock. Systemic arterial blood pressure was below control during the entire shock period. Saline control experiments yielded no significant changes in all parameters monitored. These data show that during four hours of shock the brain has shifted form aerobic to anaerobic metabolism the degree of which is not sufficient to cause any detectable changes in membrane permeability or alterations in Na+/K+ active processes.

Animals↗

PubMed1978

Effects of ethanol- and saline-base PGE1 on the canine cerebral circulation.

The effects of ethanol- and saline-base prostaglandin E1 (PGE1) on systemic arterial blood pressure ((ABP), cerebral blood flow (CBF), cerebral vascular resistance (CVR), and cerebrospinal fluid (CSF) pressure were determined in anesthetized dogs. Progressively greater carotid intra-arterial infusions of ethanol-base PGE1 moderately decreased systemic ABP and CVR while perfusion of the CSF system with PGE1 moderately increased ABP and CVR; CBF was unaffected by either route of administration and CSF pressure was constant except for a slight decrease at the lowest intraventricular perfusion rate. Similar infusions of PGE1 were administered in saline base solutions in another group of dogs. Carotid intra-arterial infusion decreased ABP and CBF moderately at the highest infusion rate and caused a transient increase in CSF pressure. Cerebrospinal fluid system perfusion increased ABP moderately but did not affect the other parameters. These data indicate that PGE1 does not have a significant effect on cerebral hemodynamics when infused via the CSF system, but may produce slight cerebral vasodilation when infused into the carotid arteries in an ethanol base. This vasodilation may be due to autoregulation.

Animals↗

PubMed1978