Biomedical subjects

F I Hawari

Publications and source records attributed to F I Hawari.

3 recordsLinked to original sources

PubMed2001

Diameter, pressure and compliance relationships in dorsal hand veins.

The diameter-pressure characteristics of dorsal hand veins previously have not been characterized. In this study, the effects of distending pressure with and without infused norepinephrine on diameter and compliance were observed. The elevation needed for venous collapse was measured, and the effects of baseline constriction on venous reactivity were assessed. In seven supine subjects, a brachial cuff on an elevated arm was used to generate distending pressures while a linear variable displacement transformer (LVDT) measured changes in venous diameter. Arctangent functions of distending pressure were fitted to the normalized diameter, then compliance functions were calculated. In supine subjects, 5-15 cm of elevation emptied dorsal hand veins. Norepinephrine decreased the venous diameter at any distending pressure by increasing the P50 without significantly changing the midpoint slope. Compliance was a nearly single-valued function of the normalized diameter with a maximum value at about 60% distention. Reactivity depends on distending pressure and baseline P50. Percentage constriction is a function of initial and final P50 and of distending pressure.

Blood Pressure↗

PubMed1998

Impact of angiotensin-converting enzyme inhibitor underdosing on rehospitalization rates in congestive heart failure.

In a retrospective, cohort design, clinical usage of digoxin, diuretic, and angiotensin-converting enzyme (ACE) inhibitor was assessed in all patients readmitted over a 36-month period for congestive heart failure (CHF) diagnostic-related group (DRG) 127. ACE inhibitor dose-response analysis used the discharge dose of ACE inhibitor, converted to enalapril-equivalent doses and adjusted for renal function. Principal end points were time-to-readmission and 90-day readmission rate. Of 314 total patients, digoxin was used in 72%, diuretic in 86%, and 67% received an ACE inhibitor. Only 22% of those on an ACE inhibitor received currently recommended doses of enalapril > or = 20 mg/day or equivalent, whereas 41% received enalapril < or = 5 mg/day. Time-to-readmission was increased by an ACE inhibitor (p = 0.002) but not digoxin or diuretic. An ACE inhibitor was the principal covariate of 90-day readmission rate (p <0.05). The readmission rate was not reduced with daily ACE inhibitor doses of < or = 5 mg enalapril, whereas daily doses of > or = 10 mg enalapril reduced 90-day readmission rates by 28% compared to those receiving diuretic or digoxin therapy (p <0.05). Using a dynamic model, the dose required to achieve 90% to 95% of the theoretical maximum ACE inhibitor effect exceeded 100 mg enalapril daily. Thus, CHF readmission rates are lower when daily ACE inhibitor doses exceed 5 mg enalapril or the equivalent daily, but are unaffected by digoxin or diuretic. Modeled maximum ACE inhibitor benefits require doses 8- to 10-fold higher than current usage patterns.

Aged↗

PubMed1998

Heparin attenuates norepinephrine-induced venoconstriction.

Reversal by heparin of norepinephrine-induced constriction of normal hand veins was studied. Venous size was measured using a linear variable differential transformer (LVDT) during infusions of saline, norepinephrine, insulin and norepinephrine, and graded doses of heparin with norepinephrine. Heparin reduced the venoconstrictive effects of norepinephrine (p < 0.01), with the effects beginning at 18.5 nmol/min (0.05 U/min) and reaching a maximum between 185 nmol/min and 1.85 mumol/min (0.5 and 5 U/min). Maximal heparin-induced venorelaxation correlated with the maximal insulin effect within individuals (r = 0.8, p < 0.01) and was unchanged by the addition of insulin. Methylene blue, a non-specific inhibitor of the nitric oxide cGMP cascade, reduced heparin-induced venorelaxation. In conclusion, heparin in either physiologic or pharmacologic concentration attenuated norepinephrine-induced venoconstriction. A common mechanism of venorelaxation by heparin and insulin is not excluded given the correlation and lack of additivity of maximum effects and their inhibition by methylene blue.

Adult↗