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W M Gardiner

Publications and source records attributed to W M Gardiner.

8 recordsLinked to original sources
PubMed1989

Color-flow US imaging through the analysis of speckle motion.

Reflections obtained from moving red blood cells on an ultrasound (US) scan of the abdominal aorta were enhanced with real-time Boolean operations on sequential frames of the image, as well as with frame subtraction and motion-detection processing. The Boolean operations used were the logical AND, OR, and Exclusive OR (XOR). Through the manipulation of output color lookup tables, the pixels within the flow field were given color representations. The resulting color-flow information can then be superimposed over the gray-scale image from the US imager to create color-flow imaging without the use of traditional Doppler US technology.

Adult↗
PubMed1988

Systemic and regional hemodynamic effects of cyclo-oxygenase and thromboxane synthetase inhibition in normal and hyperdynamic endotoxemic rabbits.

We tested the hypothesis that prostaglandins (PGs) and thromboxane (Tx) A2 are important mediators of the hemodynamic derangements occurring in a rabbit model of hyperdynamic endotoxicosis. Rabbits were injected with either normal saline (NS) or Escherichia coli lipopolysaccharide (LPS; 1-3 micrograms/kg) and studied 6 hr later. Cardiac index (CI) and regional blood flow were determined using thermodilution and radioactive microspheres, respectively. Systemic and regional hemodynamics were determined before and 40 min after administering indomethacin (cyclo-oxygenase inhibitor; 5 mg/kg), UK38485 (Tx synthetase inhibitor; 10 mg/kg), or NS. LPS increased CI (P = .0024) and decreased mean arterial pressure (P = .0031) and systemic vascular resistance index (P = .0001). LPS increased flow to the heart and small intestine and decreased flow to the hepatic artery and pancreas. The systemic and regional hemodynamic effects of indomethacin were similar in NS- and LPS-treated rabbits. UK38485 decreased perfusion of skeletal muscle and diaphragm in both endotoxemic and control animals. This agent increased splenic perfusion only in NS-treated rabbits. Plasma levels of 6-keto PGF1 alpha (PGI2 metabolite) were typically undetectable in both NS- and LPS-treated rabbits. These data do not support the hypothesis that PG's or TxA2 are major determinants of the hemodynamic perturbations that occur in this endotoxicosis model.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Increased ex vivo synthesis of prostaglandin E2 by gastric tissue after hemorrhage in rats.

Endogenously synthesized prostaglandins are potential mediators of gastrointestinal mucosal protection. Some data suggest that gastric ulceration caused by stressful stimuli is due to diminished mucosal synthesis of prostaglandins. To examine this hypothesis, we determined the effect of hemorrhage, an ulcerogenic stimulus, on ex vivo production of immunoreactive prostaglandin E2 by gastric tissue in the rat. Macroscopic gastric ulcers were reproducibly observed in Sprague-Dawley rats subjected to hemorrhage (3 ml/100 g body weight). The number of ulcers was linearly related to the duration of shock. Prostaglandin E2 synthesis was significantly increased during in vitro incubation of oxyntic and nonoxyntic stomach tissue excised from rats subjected to hemorrhage for 30 minutes (p less than 0.05). These results indicate that damage to the gastric mucosa in rats subjected to hemorrhage occurs despite augmented endogenous secretion of prostaglandin E2. Mechanisms other than impaired prostaglandin biosynthesis were probably responsible for mucosal injury in this model.

Animals↗
PubMed1987

Systemic and regional hemodynamic changes after intraperitoneal endotoxin in rabbits: development of a new model of the clinical syndrome of hyperdynamic sepsis.

Rabbits were injected intraperitoneally with sterile saline or Escherichia coli endotoxin (LPS; 50 or 500 micrograms/kg). Sixteen to 18 h later, the animals were anesthetized with ketamine and instrumented to permit measurement of mean arterial pressure, cardiac output (by thermodilution), and regional blood flow (using radioactive microspheres). The animals were allowed to waken fully in a plastic restraining cage prior to measuring systemic and regional hemodynamics. LPS had similar effects regardless of dose, and results from the two dosage groups have been combined. Compared to controls, administrations of LPS resulted in a 29.3% increase in cardiac output (P = .011) and a 22.8% decrease in systemic vascular resistance (P = .0009). Injection of LPS caused significant changes in blood flow to the heart (55.3% increase), small intestine (128.3% increase), portal vein (54.7% increase), and hepatic artery (65.0% decrease). The percentage of cardiac output perfusing the kidneys and hepatic artery was significantly decreased in the endotoxemic group (P = .037 and P = .002, respectively). Injecting LPS resulted in increased relative flow to the heart (P = .024), small intestine (P = .049), and portal vein (P = .041). We conclude that this model reproduces several of the systemic hemodynamic features of the sepsis syndrome in humans. In this model, the hyperdynamic state is associated with vasodilatation in mesenteric (small intestine and colon) and coronary beds and vasoconstriction in the hepatic artery.

Animals↗
PubMed1985

Plasma levels of 6-keto PGF1 alpha but not TxB2 increase in rats with peritonitis due to cecal ligation.

Acute, overwhelming sepsis or endotoxemia in experimental animals is associated with increased circulating levels of thromboxane (Tx)B2 (stable metabolite of TxA2) and 6-keto PGF1 alpha (stable metabolite of prostacyclin). The purpose of the present investigation was to determine the plasma prostanoid response to sepsis using an animal paradigm in which the septic process evolved more slowly than in previous similar studies. Bacterial peritonitis was induced in rats by cecal ligation (group B) or cecal ligation plus puncture with a 22-gauge needle (group C). Compared to sham-operated controls (group A), levels of immunoreactive 6-keto PGF1 alpha were significantly (p less than .05) elevated in group C rats at 6, 12, and 24 hr after surgery. At 48 hr after surgery, levels of this prostanoid were significantly (p less than .05) elevated in group B animals. In contrast, TxB2 levels were never significantly increased in septic (groups B and C) as compared to control (group A) rats. These data are consistent with results from several clinical studies and emphasize an important difference between the cecal ligation model and other experimental sepsis paradigms.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Rat intraperitoneal sepsis--a clinically relevant model.

The pathologic changes in septic shock, a disease state involving several hemodynamic and metabolic parameters, are not completely understood. Because research on animals can provide information vital to treating disease in humans, and because of the increasing constraints on clinical trials with humans, a clinically relevant animal sepsis model has been developed using adult male Sprague-Dawley rats. Sepsis was induced in large numbers of rats by IP injections of discrete quantities of live E coli organisms. The following elements were measured at specific times: MAP, CO, CVP, WBC, platelets, hemoglobin, hematocrit, PT, PTT, fibrinogen, clotting factors, glucose, blood gases, Ca++, Mg++, and TSP. The study shows that the model is easily replicated and relatively inexpensive, and that it can be used for detailed study in rats of several of the pathophysiological states characteristic of sepsis in humans.

Animals↗
PubMed1983

Thromboxane synthetase inhibitors in septic shock.

Thromboxane (TX) has been reported to cause mortality in endotoxin or septic shock. Cyclooxygenase inhibition improves survival in gram-negative or gram-positive shock. The exact level in the prostaglandin system of which the protection occurs is unknown. This study was designed to compare the effects of a cyclooxygenase inhibitor (indomethacin, IND) to a thromboxane synthetase inhibitor (IMI) on survival and on the production of Tx and prostacyclin (PGI2) in a clinically relevant rat gram-negative sepsis model. Three groups were studied: 1) control (N = 35) animals received E coli only; 2) IND (N = 35) treated animals received 3 mg/kg IP; 3) IMI (N = 35) treated animals received 30 mg/kg IP. All drugs were given 1 h after an IP injection of E coli (LD70) organisms. In this model only IND significantly improved survival. IND and IMI significantly blocked the production of Tx seen in septic shock. IND blocked PGI2 production whereas IMI increased the production. These results show that Tx may not be important in the irreversible stages of shock. Shunting prostaglandin production to PGI2 with thromboxane synthetase inhibitors needs to be considered when using this group of compounds. The mechanism of protection by IND remains unknown.

Animals↗