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Biomedical subjects

D Fox

Publications and source records attributed to D Fox.

At least 73 records · Page 4Linked to original sources
PubMed1990

The superior intracapsular ligament of the sacroiliac joint: presumptive evidence for confirmation of Illi's ligament.

The existence of a superior intracapsular ligament within the sacroiliac joint has been disputed for years. This study notes that the dissection technique used to open the sacroiliac joint is of critical importance in finding this ligament. A dissection technique that emphasizes an inferior approach to the joint cavity is described. A superior intracapsular ligament of the sacroiliac joint (Illi's ligament) is noted with a 75% frequency in dissected cadavers. Illi's model for motion of the sacrum was based partially on the function of this ligament. The findings of this study suggest that current models of motion at the sacroiliac joint must include the presence of a superior intracapsular ligament.

Anthropometry↗
PubMed1989

Actions of some autacoids and peptides, including relaxin, on costo-uterine muscle from rats.

1. The actions of angiotensin II, bradykinin, oxytocin, arginine vasopressin, relaxin, serotonin and the prostaglandins E2 and F2 alpha were examined on preparations of costo-uterine muscle from stilboestrol-treated rats. 2. All the agonists, except relaxin, when used in concentrations which contract the rat uterus, also produced contractions of costo-uterine muscles. Concentration-response curves were steep and maximal responses to the agonists were comparable. The negative log molar EC50 values were: serotonin, 6.5; angiotensin II, 8.8; bradykinin, 8.4; PGE2, 8.3; PGF2 alpha, 7.1. The EC50 values (units/L) for oxytocin and vasopressin were 4.4 and 2.7 respectively. 3. Indomethacin (2.8 or 5 mumol/L) did not decrease the contractile effects of the peptides or serotonin. The effects of serotonin were reduced, but not reversed, by methysergide (0.94 mumol/L). 4. Porcine relaxin inhibited field stimulation-induced contractions of costo-uterine muscle and uterine horns from immature rats pretreated with oestradiol cypionate and from stilboestrol-treated mature rats. It was much less potent, and its effects were less clearly concentration-related, on costo-uterine muscle. 5. The inhibitory effects of relaxin on the uterus were unaffected by propranolol (1 mumol/L), confirming that on this tissue relaxin acts independently of the release of catecholamines. Progesterone (30 mumol/L) was also without effect on the action of relaxin on the uterus. 6. These results taken together indicate that the costo-uterine muscle of the rat: (i) contracts in response to serotonin and the peptides angiotensin II, arginine vasopressin, bradykinin and oxytocin independently of the release of the contractile prostaglandins F2 alpha and E2; and (ii) in contrast to the uterus, may lack a significant population of receptors for relaxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Intravenous cyclophosphamide therapy of severe SLE.

Intravenous cyclophosphamide therapy of severe systemic lupus is associated with reduction in the numbers of circulating T and B lymphocytes, suppression of T11 (CD2) receptor-mediated responses, and suppression of autoantibody production. In clinical trials, intravenous cyclophosphamide plus moderate-to low-dose daily oral prednisone appears to reduce the rate of progression of irreversible renal injury in patients who have active nephritis and definite but limited chronic changes in biopsy specimens. It may also be effective in other forms of severe lupus, although controlled trials are lacking. It may be the treatment of choice in severe lupus characterized by ongoing antibody or immune-complex mediated tissue injury.

Acute Disease↗
PubMed1988

Dapsone inhibits LTB4 binding and bioresponse at the cellular and physiologic levels.

Radioligand binding studies using human neutrophils exposed to 10-100 microM dapsone indicated that this anti-inflammatory compound antagonized association of LTB4 (leukotriene B4) with its specific receptor sites. Binding inhibition was manifested in reduced biologic response of the neutrophils as determined in LTB4-stimulated chemotaxis. In addition, a physiologic model of LTB4-dependent inflammation in mice was antagonized by systemic administration of dapsone. These data suggest that inhibition of LTB4 binding may represent the cellular mechanism of action responsible for the anti-inflammatory effects of dapsone.

Animals↗
PubMed1988

Rate of reperfusion blood flow modulates reperfusion injury in skeletal muscle.

The mechanisms of ischemia-reperfusion (I-R) injury in skeletal muscle remain controversial. We investigated the effect of the rate of reperfusion blood flow on I-R injury in an isolated in vivo canine gracilis muscle model in six anesthetized dogs. In all animals, both gracilis muscles were subjected to 6 hr of ischemia followed by 1 hr of reperfusion. During reperfusion, one gracilis artery was partially occluded to limit the rate of reperfusion blood flow to its preischemic rate (limited reperfusion, LR), while the contralateral artery was allowed to perfuse freely at a normal rate (normal reperfusion, NR). Muscle injury was quantified by histochemical staining (triphenyltetrazolium chloride, TTC) with computerized planimetry of the infarct size, and by spectrophotometric determination of technetium-99m pyrophosphate uptake. Endothelial permeability was quantified by measurement of gracilis muscle weight gain and 125I-albumin radioactivity after intravenous injection. Results are presented as the means +/- SEM, and differences are considered to be statistically significant if P less than 0.05 by Student's t test for paired data. LR resulted in significantly less blood flow (9.7 +/- 1.7 cc/min/100 g) when compared to NR (55.7 +/- 11.6 cc/min/100 g). I-R injury was significantly reduced by LR as evidenced by a decrease in TTC infarct size from 41 +/- 7% to 11 +/- 5%, and a decrease in technetium-99m pyrophosphate uptake from 512 +/- 20 to 163 +/- 44 X 10(3) counts/min/g. LR also significantly decreased the postreperfusion edema formation as evidenced by a reduction in the muscle weight gain from 27 +/- 6 to 9 +/- 1 g, and a reduction in the 125I-albumin radioactivity from 45 +/- 14 to 32 +/- 8 counts/min/g. These data suggest that the hyperemic rate of reperfusion blood flow is a significant factor in the pathophysiology of postreperfusion edema and that clinical control of reperfusion injury in skeletal muscle may be achieved by limiting the rate of reperfusion blood flow.

Animals↗
PubMed1988

Effect of increasing inspired oxygen concentration on hemodynamics and regional blood flows.

Previous reports suggest that in response to increasing FIO2, peripheral resistance increases, cardiac output falls, and regional blood flow decreases. This study examined the influence of varying FIO2 on pulmonary and systemic vascular resistances (PVR, SVR), cardiac output, ventricular work, and regional blood flows in ten anesthetized Yorkshire white pigs. Each animal served as its own control, and was exposed to varying FIO2 in random order. PCO2 was maintained at 40 +/- 5 torr and body temperature at 38.5 degrees C. Heart rate, systemic arterial pressure, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure, thermodilution cardiac output, and blood flows in the femoral, carotid, renal and superior mesenteric arteries were measured at each FIO2. SVR, PVR, left and right ventricular stroke work (LVSW, RVSW) were calculated. One-way analysis of variance-randomized block design (F-test) showed significant decreases in PAP, PVR, and RVSW with increased FIO2. No change was noted in regional flows, cardiac output, SVR, or LVSW. We conclude that in this animal model administration of oxygen up to an FIO2 of 1.0 had no adverse effect on hemodynamic performance.

Animals↗
PubMed1988

Heparinization reduces endothelial permeability and hydrogen ion accumulation in a canine skeletal muscle ischemia-reperfusion model.

Skeletal muscle injury after revascularization (ischemia-reperfusion) continues to be a major clinical problem. Although heparinization has been recommended, its action in an experimental model of I-R has not been evaluated. We investigated the ability of heparinization to decrease I-R injury in 10 anesthetized dogs (nonheparinized, n = 5; heparinized, n = 5), subjecting one gracilis muscle to 6 hours of ischemia followed by 1 hour of reperfusion while the identically prepared contralateral muscle served as a nonischemic control. Skeletal muscle infarction was determined by Tc-PYP uptake. Endothelial permeability was quantified by measurement of skeletal muscle 125I-Alb activity after intravenous injection. Interstitial hydrogen ion (H+) accumulation was determined by a miniature pH electrode inserted into the gracilis muscle. Isotopic activities from the ischemic muscle were calculated as a percentage of the contralateral nonischemic muscle (mean +/- SEM). Nonheparinized ischemic muscles had an increase in the activities of Tc-PYP and 125I-Alb of 684% +/- 149% and 742% +/- 130%, which were reduced to 218% +/- 54% and 378% +/- 85% by heparinization, respectively (p less than 0.05). During ischemia, the nonheparinized muscles accumulated 1223 +/- 121 nmol of H+ compared with 785 +/- 95 nmol in the heparinized animals (p less than 0.01). This significant reduction in I-R injury may be causally related to diminished endothelial permeability and H+ accumulation.

Animals↗