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Biomedical subjects

I Shrier

Publications and source records attributed to I Shrier.

49 records · Page 3Linked to original sources
PubMed1997

Effects of adenosine on pressure-flow relationships in an in vitro model of compartment syndrome.

Blood flow through skeletal muscle is best modeled with a vascular waterfall at the arteriolar level. Under these conditions, flow is determined by the difference between perfusion pressure (Pper) and the waterfall pressure (Pcrit), divided by the arterial resistance (Ra). By pump perfusing an isolated canine gastrocnemius muscle (n = 6) after it was placed within an airtight box, with and without adenosine infusion, we observed an interaction between the pressure surrounding a muscle (as occurs in compartment syndrome) and baseline vascular tone. We titrated adenosine concentration to double baseline flow. We measured Pcrit and Ra at box pressures (Pbox), which resulted in 100 (Pbox = 0), 90, 75, and 50% flow without adenosine; and 200, 180, 150, 100, and 50% flow with adenosine. Without adenosine, each 10% decline in flow was associated with a 5.7 mmHg increase in Pcrit (P < 0.01). With adenosine, the same decrease in flow was associated with a 2.6-mmHg increase in Pcrit (P < 0.01). Values of Pcrit at 50% of flow were almost identical. Each 10% decrease in flow was also associated with 2.2% increase in Ra with or without adenosine (P < 0.001). Ra decreased with adenosine infusion (P < 0.05), and there was no interaction between adenosine and flow (P > 0.9). We conclude that increases in pressure surrounding a muscle limit flow primarily through changes in Pcrit with and without adenosine-induced vasodilation. The interaction between Pbox and adenosine with respect to Pcrit but not Ra suggests that Pbox affects the tone of the vessels responsible for Pcrit but not Ra.

Adenosine↗
PubMed1996

Should the gap be filled between guidelines and actual practice for management of low back pain in primary care? The Quebec experience.

STUDY DESIGN: A prospective cohort study. OBJECTIVES: To describe health services utilization for low back pain in the province of Quebec, Canada, and to compare it with North American guidelines. SUMMARY OF BACKGROUND DATA: The Quebec Task Force and the Agency for Health Care Planning and Research (United States) published guidelines for the management of low back pain in 1987 and 1994, respectively. METHODS: A cohort of 2147 adults with low back pain identified at the Quebec Worker's Compensation Board were selected randomly and observed over 2 years' time for their health care utilization profile. RESULTS: During the study period, 57.8% of the workers still under active care 7 weeks after their back injury had not yet been referred to a specialist. Specialized imaging techniques were obtained by 4.5% of the patients, with a delay of 7 weeks or more in 66% of them. Surgery was performed on 1.6% of the patients. The presence of an initial specific diagnosis and proximity to a university hospital significantly increased utilization rate and reduced the delays. CONCLUSION: Health services utilization for back pain in Quebec was equal or lower to what currently is practiced elsewhere, but access to specialists was not meeting the current recommendations. This would represent a 12% net increase in new specialist contacts and a quicker access in 39% who saw a specialist. Before such an effort can be considered, health care planners will need a better definition of the role of the specialist consultation in the guidelines and scientific evidence specifically addressing their benefit in primary care, especially in the absence of a specific diagnosis.

Adolescent↗
PubMed1996

Achilles tendonitis: are corticosteroid injections useful or harmful?

OBJECTIVE: The use of local corticosteroid injections for the treatment of Achilles tendonitis is controversial. Some authors advocate their use based on efficacy in accelerating the healing process of Achilles tendonitis; others feel the associated side effects should preclude their use altogether. The purpose of this study was to comprehensively review and critically appraise the available literature in order to examine the evidence concerning this clinical dilemma. DATA SOURCES: MEDLINE was searched using MeSH and textwords for English- and French-language articles related to Achilles tendonitis and corticosteroids published since 1966. Additional references were reviewed from the bibliographies of the retrieved articles. The total number of articles reviewed was 145. STUDY SELECTION: All clinical study designs were included as well as related animal studies using experimental and quasi-experimental designs. DATA EXTRACTION AND SYNTHESIS: In reviewing the literature, particular attention was paid to the relative strengths of the different study designs. From these data, the factors associated with effectiveness and safety of injected corticosteroids were examined. MAIN RESULTS: The only rigorous studies (one randomized controlled trial, one cohort study) showed no benefit of corticosteroids over placebo. In animal studies, corticosteroid injections decrease adhesion formation, temporarily weaken the tendon if given intratendinously, but have no effect on tendon strength if injected into the paratenon. The overall incidence of side effects with locally injected corticosteroids is approximately 1%. Most side effects are temporary, but skin atrophy and depigmentation can be permanent. Although there are many case reports of Achilles tendon rupture following local corticosteroid injection, there are no published rigorous studies that evaluate the risk of rupture with or without corticosteroid injection. CONCLUSIONS: There are insufficient published data to determine the comparative risks and benefits of corticosteroid injections in Achilles tendonitis. The decreased tendon strength with intratendinous injections in animal studies suggests that rupture may be a potential complication for several weeks following injection.

Achilles Tendon↗
PubMed1995

Treatment of lateral collateral ligament sprains of the ankle: a critical appraisal of the literature.

Although sprains of the lateral collateral ligaments of the ankle are extremely common, controversy still exists over the proper treatment. Some authors recommend early mobilization of the ankle, others recommend cast immobilization for 1-6 weeks, and others insist that sprains should be treated with primary surgical repair. A critical appraisal of the literature supports the concepts of early mobilization with a proper rehabilitation program. The review of treatment is followed by a discussion of the potential causes of persistent pain and functional instability.

Adolescent↗
PubMed1995

Effects of nifedipine on vascular waterfall and arterial resistance in canine hindlimb.

Pressure-flow relations in the canine hindlimb can be well explained by a vascular waterfall at the arteriolar level. Under these conditions, P(art) = Pcrit + Q.Rart, where P(art) is the arterial pressure, Pcrit is the waterfall pressure, Q is regional flow, and Rart is the arterial resistance of the vessels upstream from the waterfall. To determine whether calcium channels in vascular smooth muscle affect Pcrit in addition to Rart, we pump perfused canine hindlimbs and measured both variables over a range of perfusion pressures (Pper) before and during the infusion of the calcium channel blocker nifedipine. Nifedipine significantly decreased Pcrit and Rart at each Pper. Increasing Pper under control conditions from 50 to 150 mmHg significantly increased Pcrit from 24.2 +/- 1.5 to 42.5 +/- 2.2 mmHg. During nifedipine infusion, increasing Pper from 25 to 100 mmHg also increased Pcrit from 14.5 +/- 1.5 to 20.2 +/- 1.9 mmHg, but the rate of increase was less. In contrast to the rise in Pcrit with increasing Pper, Rart significantly decreased from 10.7 +/- 1.1 to 8.1 +/- 1.2 mmHg.min.100 g.ml-1 before nifedipine infusion, and from 5.7 +/- 0.4 to 2.2 +/- 0.1 mmHg.min.100 g.ml-1 during nifedipine infusion. Venous resistance (Rven) significantly decreased with increases in Pper and during nifedipine infusion. The regional elastic recoil pressure (Pel, a measure of small venular pressure) increased with both an increase in Pper and nifedipine. These results suggest that nifedipine decreases Pcrit, Rart, and Rven and that at constant Pper nifedipine increases Pel.

Animals↗
PubMed1995

NG-nitro-L-arginine and phenylephrine have similar effects on the vascular waterfall in the canine hindlimb.

Hindlimb pressure-flow relationships are well characterized by modeling a vascular waterfall at the arteriolar level. Under these conditions, Q = (Pper - Pcrit)/Rart, where Q is blood flow, Pper is perfusion pressure, Pcrit is waterfall pressure, and Rart is the resistance upstream from the waterfall. To determine the effects of endothelium-derived relaxing factor (EDRF) on Pcrit, Rart, and venous resistance (Rv), we varied Pper in the canine hindlimb between 100 and 200 mmHg before and after NG-nitro-L-arginine infusion (L-NNA, an inhibitor of EDRF synthesis). Before L-NNA, Pcrit increased with increasing Pper. After L-NNA, Pcrit was higher at each Pper, and the increase in Pcrit with increases in Pper was greater than under control conditions. In contrast to Pcrit, Rart decreased with increasing Pper before L-NNA. After L-NNA, Rart was higher at each Pper and no longer decreased with increasing Pper. Rv was not affected by Pper under control conditions but decreased with increasing Pper after L-NNA. The pressure in the small venules at each Pper decreased after L-NNA. In a second group of animals, we infused phenylephrine to control for increased tone produced by L-NNA. Results were similar to those seen with L-NNA. In conclusion, blocking EDRF synthesis increases both Pcrit and Rart, but the same response was also obtained with phenylephrine.

Animals↗
PubMed1995

Pressure-flow relationships in in vitro model of compartment syndrome.

Compartment syndrome is a condition in which an increase in intramuscular pressure decreases blood flow to skeletal muscle. According to the Starling resistor (i.e., vascular waterfall) model of blood flow, the decrease in flow could occur through an increase in arterial resistance (Rart) or an increase in the critical closing pressure (Pcrit). To determine which explains the decrease in flow, we pump perfused a canine gastrocnemius muscle placed within an airtight box, controlled box pressures (Pbox) so that flow ranged from 100 to 50%, and measured Pcrit, Rart, arterial compliance, small venular pressure (measured by the double-occlusion technique), and venous pressure. An increase in Pbox limited flow mainly through an increase in Pcrit (75-85%), with only small changes in Rart (15-25%) and no change in arterial compliance. Increases in Pbox also produced a vascular waterfall in the venous circulation, but small venular transmural pressure always remained less than control levels. We conclude that increases in Pbox mostly limit blood flow through increases in Pcrit and that Rart plays a minor role. Transmural pressure across the small venules decreases with increases in intramuscular pressure, which contradicts the currently held belief that compartment syndrome is due to a cycle of swelling-ischemia-swelling.

Animals↗
PubMed1995

Maximal vasodilation does not eliminate the vascular waterfall in the canine hindlimb.

Previous studies have shown that blood flow through skeletal muscle is regulated by changes in an arteriolar vascular waterfall [critical pressure (Pcrit)] and a proximal (arterial) resistance (Ra) element. To determine whether Pcrit still exists during maximal vasodilation, we pump perfused vascularly isolated canine hindlimbs. We set outflow pressure to zero and measured Pcrit, perfusion pressure (Pper), and regional elastic recoil pressure (Pcl; by a stop-flow technique) and calculated both Ra and venous resistance before and after maximal vasodilation with adenosine and nitroprusside. Pcrit was 56.4 +/- 5.1 mmHg before vasodilation and decreased to 11.0 +/- 0.6 mmHg after vasodilation, which was less than the downstream pressure in the venous compliant region (Pel). Therefore, Pcrit should not have affected flow at normal Pper levels under vasodilated conditions. However, we could still measure Pcrit because our technique allowed Pel to decline and Pcrit becomes apparent once Pel < Pcrit. With vasodilation, Ra decreased to < 8.1 +/- 2.6% and Rv decreased to 41 +/- 6% of control values. In contrast to the nonvasodilated vasculature, increases in venous pressure during maximal vasodilation caused immediate increases in Pper. This also suggests that the vascular waterfall is inactive under conditions of maximal vasodilation. We conclude that a small arteriolar Pcrit is still present in the maximally vasodilated hindlimb but is less than the downstream pressure and does not affect flow under these conditions.

Adenosine↗
PubMed1993

Effect of carotid sinus stimulation on resistance and critical closing pressure of the canine hindlimb.

Sympathetically mediated changes in blood pressure are thought to occur through changes in arterial resistance (Ra). To test whether the critical closing pressure (Pcrit) could also play a role, we pump-perfused the vascularly isolated canine hindlimb at constant flow. Carotid sinuses were isolated and both vagus nerves cut. Carotid sinus (Pcar), arterial, perfusion (Pper), and venous (Pv) pressures and flow to the hindlimb (Q, electromagnetic flow probe) were measured. By decreasing pump flow to zero over time periods of 1-10 s and measuring the pressure at zero-flow, it was possible to estimate arterial compliance and Pcrit. Ra was calculated as (Pper - Pcrit)/Q. Venous resistance was calculated as (Pel - Pv)/Q, where Pel is the pressure in the compliant region obtained by the double-occlusion technique. Raising Pcar from 115 +/- 7 to 203 +/- 10 mmHg (n = 6) decreased Pcrit from 49.7 +/- 4.3 to 25.9 +/- 2.6 mmHg and Ra from 10.7 +/- 1.2 to 6.8 +/- 0.9 mmHg.min.100 g-1.ml-1 (P < 0.05). Lowering Pcar from 119 +/- 6 to 71 +/- 6 mmHg (n = 6) increased Pcrit from 37.0 +/- 3.3 to 61.0 +/- 8.5 mmHg and Ra from 10.0 +/- 1.6 to 14.0 +/- 2.4 mmHg.min.100 g.ml-1 (P < 0.05). Arterial compliance increased when Pcar was raised (P < 0.05) and decreased when Pcar was decreased (P < 0.1). Venous resistance did not change when Pcar was altered. In conclusion, changes in carotid sinus stimulation alters blood flow to the hindlimb through changes in both Pcrit and Ra.

Animals↗
PubMed1993

Response of arterial resistance and critical pressure to changes in perfusion pressure in canine hindlimb.

The dynamic pressure-flow relationship in the canine hindlimb at normal arterial pressure is best explained by modeling a Starling resistor (critical pressure, Pcrit) at the level of the arterioles. Regulation of flow can therefore occur at the Starling resistor through changes in Pcrit or along the length of the vessel through changes in arterial resistance (Ra). We hypothesized that increasing perfusion pressure (Pper) would increase Pcrit due to the myogenic response but would decrease Ra because of flow-mediated vasodilation and passive effects. We pump-perfused vascularly isolated hindlimbs of anesthetized dogs and then measured Pcrit and calculated Ra over Pper range of 75-175 mmHg. When Pper was increased from 75 to 175 mmHg, Pcrit increased from 33 +/- 2 to 48 +/- 6 (means +/- SE) mmHg, whereas Ra decreased from 10.1 +/- 1.2 to 7.86 +/- 0.7 mmHg.min.100 g.ml-1 (P < 0.01). Thus the responses of Pcrit and Ra to an increase in Pper were dissociated. In a second part of the study, we lowered carotid sinus pressure to determine the effects of central factors on local autoregulation. A decrease in carotid sinus pressure increased Pcrit and Ra at each Pper (P < 0.05). We conclude that an increase in Pper causes the arterial vasculature to constrict at the level of the Starling resistor and dilate more proximally. The carotid baroreflex causes an increase in tone throughout the arterial vasculature but does not alter the local response to increases in Pper.

Animals↗
PubMed1991

Failure of oxygen radical scavengers to modify fatigue in electrically stimulated muscle.

We used in situ gastrocnemius muscle of anaesthetized dogs to test the hypothesis that O2 radical production during muscle contraction contributes to fatigue. Muscle tension was measured with a force transducer and blood flow was monitored with an electromagnetic flow probe. Muscle contractions were produced by stimulating the nerve for 15 min at 20 Hz, 12 trains/min, and a duty cycle of 0.25. Three groups of seven animals were given an infusion of 0.2 mL.min-1 of either saline, low-dose oxygen radical scavengers (250 IU.mL-1 superoxide dismutase, 640 IU.mL-1 polyethylene glycol (PEG)-catalase, 0.25 mg.mL-1 deferoxamine, and 0.1 mg.mL-1 oxypurinol), or high-dose oxygen radical scavengers (3300 IU.mL-1 superoxide dismutase, 6600 IU.mL-1 PEG-catalase, 2.5 mg.mL-1 deferoxamine, and 0.1 mg.mL-1 oxypurinol). Blood flow and vascular resistance of the gastrocnemius muscle during stimulation did not differ among groups. After 15 min of stimulation, the developed tension (represented as a percentage of initial tension developed) was 66 +/- 7% in the saline treated group, 70 +/- 6% in the low-dose group, and 70 +/- 4% in the high-dose group. The change in tension during recovery was not significant in the control or low-dose groups. However, there was partial recovery in the high-dose group. In conclusion, in this preparation, oxygen radical scavengers did not delay the development of decreased muscle tension.

Animals↗