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Biomedical subjects

Sheldon Magder

Publications and source records attributed to Sheldon Magder.

10 recordsLinked to original sources
PubMed2006

Central venous pressure: A useful but not so simple measurement.

OBJECTIVE: To review the clinical use of central venous pressure measurements. DATA SOURCES: The Medline database, biographies of selected articles, and the author's personal database. DATA SYNTHESIS: Four basic principles must be considered. Pressure measurements with fluid-filled systems are made relative to an arbitrary reference point. The pressure that is important for preload of the heart is the transmural pressure, whereas the pressure relative to atmosphere still affects other vascular beds outside the thorax. The central venous pressure is dependent upon the interaction of cardiac function and return function. There is a plateau to the cardiac function curve, and once it is reached, further volume loading will not increase cardiac output. CONCLUSIONS: If careful attention is paid to proper measurement techniques, central venous pressure can be very useful clinically. However, the physiologic or pathophysiological significance of the central venous pressure should be considered only with a corresponding measurement of cardiac output or at least a surrogate measure of cardiac output.

Atrial Function, Right↗
PubMed2006

Central venous pressure monitoring.

PURPOSE OF REVIEW: The proper use of central venous pressure requires a good understanding of basic measurement techniques and features of the waveform. RECENT FINDINGS: If attention is not paid to proper leveling of the transducer and consideration of transmural pressure then major errors are made in the use of central venous pressure. Besides the information gained from the relationship of changes in central venous pressure to changes in cardiac output, there is also much information to be obtained by examining the waveforms of the central venous pressure tracing. Examples are given of rhythm disorders, tricuspid regurgitation, cardiac tamponade, cardiac restriction, and decreased thoracic compliance. SUMMARY: There is much more to the measurement of central venous pressure than the simple digital value on the monitor and the actual waveform should always be examined.

Central Venous Pressure↗
PubMed2006

Reactive oxygen species: toxic molecules or spark of life?

Increases in reactive oxygen species (ROS) and tissue evidence of oxidative injury are common in patients with inflammatory processes or tissue injury. This has led to many clinical attempts to scavenge ROS and reduce oxidative injury. However, we live in an oxygen rich environment and ROS and their chemical reactions are part of the basic chemical processes of normal metabolism. Accordingly, organisms have evolved sophisticated mechanisms to control these reactive molecules. Recently, it has become increasingly evident that ROS also play a role in the regulation of many intracellular signaling pathways that are important for normal cell growth and inflammatory responses that are essential for host defense. Thus, simply trying to scavenge ROS is likely not possible and potentially harmful. The 'normal' level of ROS will also likely vary in different tissues and even in different parts of cells. In this paper, the terminology and basic chemistry of reactive species are reviewed. Examples and mechanisms of tissue injury by ROS as well as their positive role as signaling molecules are discussed. Hopefully, a better understanding of the nature of ROS will lead to better planned therapeutic attempts to manipulate the concentrations of these important molecules. We need to regulate ROS, not eradicate them.

Animals↗
PubMed2005

Vasopressin release during endotoxaemic shock in mice lacking inducible nitric oxide synthase.

We tested the hypothesis that nitric oxide (NO) arising from the action of inducible nitric oxide synthase (iNOS) is responsible for the deficiency in vasopressin (AVP) release and consequent hypotension during endotoxaemic shock. Wild-type (WT) and iNOS knockout mice (iNOS(-/-)) were given either saline or Escherichia coli lipopolysaccharide (LPS, 1.0 mg/kg i.v., final volume 0.03 ml). Mean arterial blood pressure (MAP) was measured and plasma AVP levels determined before and after LPS or saline injection. In WT mice, MAP was significantly lower 2 h after LPS administration and remained low for the remainder of the 6-h observation period. AVP plasma levels were increased at the 2nd and 4th h of the experiment, returning thereafter to basal levels. Conversely, LPS injection in iNOS iNOS(-/-) mice elicited a sustained increase in plasma AVP concentration and attenuated the fall in blood pressure. These data indicate that NO arising from the iNOS plays an important inhibitory role in AVP release during endotoxaemia and may be responsible for the hypotension occurring during this vasodilatory shock.

Animals↗
PubMed2005

How to use central venous pressure measurements.

PURPOSE OF REVIEW: Central venous pressure is a very common clinical measurement, but it is frequently misunderstood and misused. As with all hemodynamic measurements, it is important to understand its basic principles. RECENT FINDINGS: This analysis indicates that it is best to always consider the significance of central venous pressure in the context of the corresponding cardiac output. Even more important is the use of dynamic measures to interpret the meaning of the central venous pressure. This includes the hemodynamic response to fluid load, respiratory variations in central venous pressure, and even the change in central venous pressure with changes in the patient's overall status. SUMMARY: The clinical application of central venous pressure measurement requires a good understanding of the concept of the interaction of the function of the heart with the function of the return of blood to the heart.

Cardiac Output↗
PubMed2004

Estrogen induced changes in Akt-dependent activation of endothelial nitric oxide synthase and vasodilation.

OBJECTIVES: Acute administration of estrogen results in vasodilation and increased nitric oxide (NO) production. We examined the hypothesis that this is due to activation of Akt/PKB which subsequently increases eNOS activity. METHODS AND RESULTS: Treatment of bovine microvascular and human umbilical endothelial cells (HUVEC) with 17-beta-estradiol (E2) (10(-9) to 10(-5)M) increased phosphorylation of Akt within 1 min and this was followed by phosphorylation of eNOS. These effects were blocked by wortmannin, a PI(3)K inhibitor and the upstream activator of Akt. The estrogen receptor antagonist, ICI 182,780, inhibited eNOS phosphorylation. E2 increased calcium dependent NOS activity and nitrite production and this was inhibited by wortmannin and ICI 182,780. E2 increased the vasodilatory response of aortic rings to acetylcholine and wortmannin blocked the effect. E2 (10(-9)M) dilated cerebral microvascular vessels under conditions of no flow, constant flow and increasing flow and this was blocked by wortmannin. Tamoxifen, a partial estrogen receptor antagonist, also dilated the microvessels. CONCLUSIONS: : E2 increases NO production through an Akt/PKB dependent pathway. This is associated with increased sensitivity to endothelial dependent dilation. In cerebral microvessels, E2 and tamoxifen produce significant dilation at low concentrations with and without acetylcholine induced stimulation of endothelial vasodilation.

Acetylcholine↗
PubMed2004

Treatment with 17-beta-estradiol reduces superoxide production in aorta of ovariectomized rats.

OBJECTIVE: Oxidant stress contributes to vascular injury and atherosclerosis. We hypothesized that estrogen treatment of ovariectomized rats decreases O(2)(-) by decreasing the activity of NAD(P)H oxidase and this reduction in O(2)(-) could have a vasculoprotective effect. METHODS AND RESULTS: Ovariectomized rats were treated with 17-beta-estradiol E2 (0.25mg) or oil placebo for 21 days. Aorta were removed for contractility studies and O(2)(-) production was measured by lucigenin enhanced chemiluminescence (230 and 5microM). E2 treatment decreased basal O(2)(-) production but did not alter NADH or NADPH stimulated O(2)(-) production. Total p47phox and p47phox in membrane fractions of cardiac tissue were decreased, which suggests less activation of NAD(P)H oxidase in E2 treated rats. E2 did not change expression of other components of NAD(P)H oxidase in heart, lung, spleen and diaphragm. Expression of eNOS was also lower in E2 treated rats. E2 did not affect the contractile response to phenylepherine, dilation with acetylcholine, dilation with superoxide dismutase or constriction with l-NAME. This argues against changes in bioavailable NO. CONCLUSIONS: E2 decreases activation of p47phox and O(2)(-) production by NAD(P)H oxidase. This did not affect contractile properties of the vessel, but could still potentially alter cell signaling from oxidant increasing stresses.

Animals↗