תוצאת חיפוש

Reactive Increase in Blood Pressure on Immobilization, but not Hypertension, Prevents Pressure Ulcers

Vladimir Shats, Silvio Kozacov

Geriatric Dept., Rebecca Sieff Hospital, Safed

Of 135 geriatric patients immobilized for at least 2 days, 37 (27.4%) had pressure ulcers (PU). Those without PU were the control comparison group. Gender, length of immobilization, number of blood pressure determinations and proportion with hypertension were similar in those with and without PU. Those with PU were slightly older than those in the comparison group: 75.5±8.8 and 74.7±9.6 years, respectively (p>0.05).

Of 66 patients with acute ischemic stroke, reactive increase of systolic or diastolic blood pressure to 140/90 mm Hg or above following immobilization, was seen in 60.6% and 22.7% of patients, respectively, and there were PU in 12.1%. Of 17 with recurrent ischemic stroke, corresponding figures were: 41.2%, 23.5% (p>0.05), and 47.1% (p<0.01). In 7 patients with previous ischemic stroke corresponding figures were: 14.3% and 0% (p<0.01) and 100% (p<0.001). In 36 operated for fracture of the femur, corresponding figures were: 50%, 11.1% (p>0.05), and 27.8% (p>0.05). For 9 patients with severe infections, sepsis or pneumonia, the corresponding figures were: 22.2% and 0.0% (p>0.05), and 44.4% (p<0.04).

The proportion of patients with reactive increase in systolic blood pressure on immobilization was lower in the PU group than in the controls, 27% vs 59.2%, (p<0.001). The corresponding figures for reactive increase in diastolic blood pressure were similar, 8.1% and 20.4%, respectively (p>0.05).

The mean systolic blood pressure on immobilization was higher in the control than in the PU group, 145.4±21.7 and 130.8±14.9 mm Hg, respectively (p<0.001). The corresponding figures for the mean diastolic blood pressure were similar, 81.2±10.5 and 75.7±8.9 mm Hg, respectively (p<0.01). An increase in systolic blood pressure on immobilization reduced the risk of developing PU (p<0.05).

There was no significant statistical relation between diagnosis of hypertension and proportion of patients with PU (p>0.05). Of 67 patients with hypertension, in 23.9% and 74.6% of them there was no increase in systolic or diastolic blood pressure, respectively. Statistical difference between lack of diastolic or systolic response was very significant (p<0.001).

Reactive increase of blood pressure, but not hypertension, predicts reduced risk of PU on immobilization in the hospitalized elderly. Diminished reactive increase of blood pressure in response to stress of any kind may be a criterion of frailty and reduced physiological reserves. Efforts to reduce elevated blood pressure when a patient is immobilized appear irrational.

Pulmonary Hypertension and Multi-Valvular Damage Caused by Anorectic Drugs

Serge E. Goldstein, Yair Levy, Yehuda Shoenfeld

Medical Dept. B and Institute for Immunological Disease Research, Chaim Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University

Marked obesity is an independent risk factor for multisystem morbidity. The use of anorectic drugs is an aggressive strategy for weight reduction. It appears to be an easy way of dealing with the problem, because the patient needn't change his behavior. However, such treatment is not harmless. At the end of the 60's an outbreak of pulmonary hypertension was associated with the drug aminorex, and it was soon withdrawn from the market. 30 years later it became clear that new-generation anorectic drugs (fenfluramine, dexfenfluramine, phentermine), which were being used world-wide, lead to both pulmonary hypertension and valvular damage.

We describe a woman of 70 with both these complications which developed after prolonged anorectic therapy with a fenfluramine-phentermine combination.

Mechanism of Primary Hypertension

Ludwig Kornel,* Arthur V. Prancan

Steroid Research Laboratory, Depts. of Internal Medicine and Biochemistry, and Dept. of Pharmacology, Rush Medical Center, Chicago and *Endocrinology-Diabetes Outpatient Clinic, Kupat Holim Klalit, Jerusalem

We review various theories of the pathogenetic mechanisms of steroid-induced and essential hypertension. We investigated the possibility that a pathogenetic mechanism leading to glucocorticoid (GC)-induced hypertension or to mineralocorticoid (MC)-induced hypertension, or both, may be of critical importance in primary hypertension. We studied plasma levels of corticosterone (BK) and aldosterone (Aldo), and their concentrations in arterial and renal tissues of spontaneously hypertensive rats (SHR), a model of primary hypertension, and in the antecedent strain WKY rats as a normotensive control. Plasma levels of BK and Aldo were found to be normal and identical in SHRs and WKYs. Tissue (intracellular) levels of BK were more than double in SHRs than in WKYs. Subsequently we examined the activity of 11b-hydroxy steroid dehydrogenase (11-HSD) in both aortic and renal tissues of SHRs and WKYs. 11-HSD converts BK to the corresponding 11-keto compound, 11-dehydro-corticosterone (cpd.AK), which is inactive, in view of its inability to bind to the MC receptors (and also to the GC receptors). BK, the main glucocorticoid in the rat, as well as cortisol, have high affinity for the MC-receptor (MR). Normally BK or cortisol are present in 10²-10³ times greater concentrations than Aldo in tissues possessing MR. The enzyme 11-HSD deactivates BK (or cortisol), thus protecting MC-receptors in the MC target tissues from being activated by GC. When we examined arterial and renal tissue activities of 11-HSD in SHRs, the activity of 11-HSD was only one-third that found in the WKY rats. This explained higher levels of BK in the tissues of SHR, and suggested that decreased activity of 11-HSD is a pathogenetic factor for hypertension in SHRs.

Thus, in a model of primary hypertension such as SHR, decreased activity of 11-HSD in the target tissues of MC appears to lead to glucocorticoid-induced mineralocorticoid hypertension.

Red Cell Na+/H+ Exchange and Role of Protein Kinase C in its Stimu-Lation in Diabetes Mellitus, Essential Hypertension and Nephropathy

Wladimir Koren, Robert Koldanov, Edna Peleg, Eva Izsak, Meir Berezin, Talma Rosenthal

Dept. of Medicine C, Hypertension Unit and Endocrinology Institute, Chaim Sheba Medical Center, Tel Hashomer

Na+/H+ exchange (NHE) was measured as maximal initial velocity of pH-dependent H+ efflux from red cells into an alkaline medium containing Na+ in patients with insulin-dependent or noninsulin-dependent diabetes, with and without hypertension and in normoglycemic, essential hypertensives and normal controls (50 subjects in each subgroup). Maximal velocities of NHE were found in microalbuminuric patients in all subgroups, and NHE correlated with the rate of microalbuminuria (r=0.61, p=0.02). Daily insulin requirements were greater in those with elevated NHE (84±8 vs 42±4 U/day). There was no correlation between NHE and levels of plasma glucose, HbA1 and plasma aldosterone and lipid profile and PRA. NHE was correlated with plasma prolactin (r=0.51, p=0.02) and PTH r=0.24, p=0.05). In uremic patients, NHE was inversively correlated with creatinine clearance (r=-0.48, p=0.03). Since calphostin C, a selective inhibitor of protein kinase C, lowered increased NHE in vitro, the protein kinase C-dependent pathway of the exchanger regulation was concluded to be responsible for NHE activation in diabetes mellitus and essential hypertension.