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Biomedical subjects

E D Frohlich

Publications and source records attributed to E D Frohlich.

At least 73 records · Page 4Linked to original sources
PubMed1996

Arterial and venous compliance in obese and nonobese subjects.

Arterial compliance and central blood volume were evaluated in obese and nonobese patients with and without hypertension. Arterial compliance was lower in the hypertensive group, although obese subjects, regardless of their blood pressure, had higher arterial compliance. The ratio of central blood volume to total blood volume was highest in hypertensive patients, whether obese or lean, indicating increased venoconstriction.

Adult↗
PubMed1996

Reduction in left ventricular mass in patients with systemic hypertension treated with enalapril, lisinopril, or fosenopril.

There are still conflicting data as to whether reduction in LV mass is beneficial. In the present study, no deterioration in LV systolic function occurred in patients in whom regression of LV mass was achieved. Impairment in LV compliance has been shown in hypertensive patients, even in the presence of preserved systolic function and normal LV mass. In our study, improvement in diastolic function was observed only in patients whose LV mass decreased, and it was related to reduction in mass and not to a decrease in mean arterial pressure. Therefore, we suggest that because diastolic function is the first activity to deteriorate in hypertensive patients, it may be the first activity to improve, and this improvement may be related to reduction in LV mass with ACE inhibitors.

Adult↗
PubMed1996

Effects of calcium entry blockers on distribution of blood volume.

To evaluate the effects on hemodynamics and the distribution of blood volume of various calcium entry blocker (CEB) agents, we invasively studied 24 hypertensive patients before and after treatment with isradipine, diltiazem, and verapamil. All three agents reduced arterial pressure through a significant fall in total peripheral resistance without causing reflex tachycardia, while preserving stroke volume and cardiac output. Verapamil reduced the central blood volume (CBV) and the ratio of CBV to total blood volume (TBV) in the supine position (P < .05), suggesting peripheral venodilatation. Isradipine and verapamil modified the responses to head-up tilt. The orthostatic decrease in stroke volume was accentuated following treatment, and it was associated with a greater fall in the ratio of CBV to TBV, suggesting that these two agents attenuate the reflex venoconstriction induced by postural change. In contrast to verapamil and isradipine, diltiazem did not affect volume distribution in the supine or head-up positions. These results suggest that the effect of CEBs varies in order of venodilatory effect from verapamil to isradipine to diltiazem, with verapamil having the greatest effect.

Blood Volume↗
PubMed1996

Classic papers symposium: history of medicine series: surrogate indexes of target organ involvement in hypertension.

This review of previous work provides credence that the fourth heart sound associated with electrocardiographic evidence of left atrial abnormality and hyperuricemia is an easily determined and cost-effective clinically determined functional surrogates of hypertensive heart and kidney involvement, respectively. These routinely obtained clinically measurable indexes are well established and are pathophysiologically related to the functional involvement of the heart and kidney from hypertensive cardiovascular disease. Moreover, these seemingly nonspecific findings provide strong clinical support for feasible means to determine the independent risk of hypertensive left ventricular hypertrophy and renal involvement in patients with hypertension. In these times of using routine clinical information for cost-effective outcomes, those measurements provide excellent surrogate pathophysiologic indices.

Heart Diseases↗
PubMed1996

Losartan reduces cardiac mass and improves coronary flow reserve in the spontaneously hypertensive rat.

OBJECTIVES: To evaluate the effects of losartan administration on cardiovascular mass, systemic and coronary hemodynamics (rest, maximal treadmill exercise, and dipyridamole infusion) and on resting regional hemodynamics in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. RESULTS: Although losartan administration (two doses: 10 and 30 mg/kg per day for 3 weeks by gavage) reduced left ventricular mass at the higher dose in WKY rats and with both doses in SHR, only the higher dose reduced arterial pressure in SHR. Losartan administration did not affect cardiac index, myocardial or other organ flows (radiomicrosphere) at rest in both strains. Significant increases in cardiac index and coronary flow and decreases in coronary vascular resistance were observed during exercise in both strains and these responses were not affected by losartan administration. Compared with those in WKY rats, coronary flow and flow reserve (dipyridamole) were decreased and minimal coronary vascular resistance was increased in untreated SHR. Administration of a higher losartan dose increased coronary flow reserve and decreased minimal coronary vascular resistance (measured during dipyridamole infusion) in SHR. CONCLUSIONS: These data demonstrated that losartan administration reduced left ventricular mass, a response that did not seem to be solely dependent on afterload. Furthermore, cardiac and stroke indices and coronary flow reserve were not changed in SHR during maximal treadmill exercise after hypertrophy reversal, even with the lower dose of losartan and when the ventricular afterload was similar to that of untreated SHR.

Angiotensin II↗
PubMed1996

Hydrochlorothiazide exacerbates nitric oxide-blockade nephrosclerosis with glomerular hypertension in spontaneously hypertensive rats.

OBJECTIVE: To determine whether a diuretic can also reverse the clinical, systemic, renal and glomerular haemodynamic and pathological changes caused by nephrosclerosis. METHODS: Three groups of 20-week-old spontaneously hypertensive rats (SHR) were investigated: control male SHR; a similar group, administered 50 mg/l NG-nitro-L-arginine methyl ester (L-NAME) for 3 weeks; and SHR treated similarly with L-NAME but also with 80 mg/kg per day hydrochlorothiazide (HCTZ) by gavage for 3 weeks. RESULTS: The mean arterial pressure, cardiac output, effective renal plasma flow and glomerular filtration rate decreased as urinary volume increased in the SHR treated with HCTZ and L-NAME. A micropuncture study demonstrated increased glomerular capillary pressure (PG, 56 +/- 1 versus 68 +/- 3 mmHg) associated with increased efferent (2.1 +/- 0.2 versus 2.9 +/- 0.3 u) but no change in afferent arteriolar resistances compared with the SHR group treated with L-NAME only. In addition, HCTZ administration increased the juxtamedullary glomerular injury score (47 +/- 13 versus 114 +/- 29) associated with elevated urinary protein excretion (35 +/- 1 versus 53 +/- 13 mg/100 g body weight per 24 h) The afferent arteriolar injury score was not changed. The PG elevation was related not only to severe glomerulosclerosis but also to increased fibronectin and alpha-smooth muscle actin deposition. CONCLUSION: HCTZ administration exacerbated the changes in renal and micropuncture dynamics, proteinuria and histopathological nephrosclerosis produced by L-NAME in SHR.

Animals↗
PubMed1996

ACE inhibition prevents and reverses L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats.

Chronic nitric oxide inhibition exacerbates hypertension and nephrosclerosis in spontaneously hypertensive rats (SHRs). In this study, we determined whether angiotensin-converting enzyme (ACE) inhibition could prevent or reverse the systemic, renal, and glomerular hemodynamic alterations and the pathological changes of nephrosclerosis. Four groups of 20-week-old SHRs were studied: group 1, untreated controls; group 2, treated with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/L for 3 weeks); group 3, L-NAME cotreated with quinapril (3 mg.kg-1.d-1 for 3 weeks); and group 4, L-NAME for 3 weeks followed by quinapril for 3 weeks (same doses). The results of this study demonstrated that both cotreatment (group 3) and posttreatment (group 4) with quinapril reduced mean arterial pressure (186 +/- 9 and 192 +/- 9 mm Hg, respectively, compared with group 2 SHRs, 221 +/- 5 mm Hg) and total peripheral resistance index associated with significant reductions in afferent and efferent arteriolar resistances; nephrosclerosis pathological scores; and urinary protein excretion (all at least P < .01). ACE inhibition also significantly increased stroke index, single-nephron glomerular filtration rate, and ultrafiltration coefficient compared with the L-NAME SHRs. Most notable were the findings that cotreatment with quinapril completely prevented the renal glomerular hemodynamic alterations with reduced glomerular capillary hydrostatic pressure and efferent arteriolar resistance compared with both the untreated and the L-NAME-treated SHRs (all at least P < .01). Posttreatment with quinapril also reversed the glomerular injury (subcapsular, -83%; juxtamedullary, -56%) and arteriolar (-87%) injury scores obtained from renal biopsy specimens (P < .005 and P < .0001, respectively). These changes were associated with decreased periarteriolar fibronectin and increased afferent arteriolar alpha-smooth muscle actin deposition (immunohistochemistry). These data, therefore, demonstrate that ACE inhibition not only prevents but also reverses L-NAME-exacerbated severe nephrosclerosis in SHRs, as indicated by improved systemic, renal, and glomerular hemodynamic changes, proteinuria, and histological alterations.

Analysis of Variance↗
PubMed1996

Angiotensin II increases left ventricular mass without affecting myosin isoform mRNAs.

We studied the effect of chronic (7 days) angiotensin II (Ang II) infusion in nonpressor and pressor doses on cardiovascular mass and expression of alpha- and beta-myosin heavy chain genes in the left ventricle in normotensive Wistar rats. An increased left ventricular mass was observed in rats receiving non-pressor and pressor doses of Ang II, but only high doses increased arterial pressure. Normalization of arterial pressure during Ang II infusion by losartan, a specific Ang II receptor antagonist, or hydralazine had different effects on left ventricular mass. Losartan prevented the increased left ventricular mass, and hydralazine did not affect left ventricular mass. Northern blot analysis showed that the switch in left ventricular myosin isoform mRNA from the adult to the fetal pattern occurred only in rats given the pressor Ang II dose. Both losartan and hydralazine, in parallel with the normalization of arterial pressure, prevented this myosin isoform switch. Thus, these data suggest that the Ang II-induced increase in left ventricular mass was not dependent on pressure overload, but the switch in myosin isoform mRNA from the adult to the fetal pattern was dependent on pressure overload.

Angiotensin II↗
PubMed1996

Impact and interpretation of multiple guidelines and consensus documents.

The US National High Blood Pressure Education Program (NHBPEP) was established in 1972, shortly after publication of the initial landmark reports of the Veterans Administration Cooperative study reports demonstrating safety and efficacy in reducing abnormally elevated arterial pressure with antihypertensive drugs. Over the ensuing 23 years, this program was responsible for the formulation of periodic guidelines on the general approach to the patient with hypertension as well as on a number of more specific considerations by more specialized working groups that deal with other concerns relative to the diagnosis, treatment and other aspects of hypertensive cardiovascular disease.

Clinical Trials as Topic↗
PubMed1995

Pharmacologic support with high-energy phosphate preservation in the postischemic neonatal heart.

Milrinone improves function in failing adult hearts. This study examined its effect on immature myocardium. Using an isolated working neonatal rabbit heart preparation, we measured myocardial function, high-energy compounds, and cyclic adenosine monophosphate. Hearts were subjected to 1 hour of normothermic ischemia, 10 minutes of reperfusion with Ringer's solution, and 30 minutes of reperfusion with either unaltered Ringer's, Ringer's with dobutamine (0.1 microgram/mL), or Ringer's with milrinone (1 microgram/mL). These hearts were compared with each other, with a control group continuously perfused for 70 minutes, and with a group of hearts that were made ischemic and reperfused for only 10 minutes. There was a progressive decline in adenosine triphosphate levels measured in hearts from the groups receiving 10 and 40 minutes of reperfusion with unaltered perfusate, and cardiac output fell to 82% +/- 4% of preischemic control in the latter group. When either dobutamine or milrinone was added to the reperfusion solution, postischemic myocardial function was restored completely, and the loss of adenosine triphosphate with reperfusion was halted. Cyclic adenosine monophosphate level was highest in ischemic/40-minute reperfused hearts, and there was no measurable increase in cyclic adenosine monophosphate level in the group of hearts receiving milrinone. The mechanism of preservation of high-energy stores with inotropic agents is not known but may involve potentiation of mitochondrial oxidative phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1995

Continuing advances in hypertension: the Joint National Committee's fifth report.

This report focuses on the new features of the Joint National Committee's most recent report (JNC-5) on the detection, evaluation and treatment of hypertension. It highlights the new classification of hypertension based on stages of the disease, and the recent demonstration that primary prevention of hypertension is feasible and practicable, and it provides a rationale for its recommendations on the selection of initial therapy for the treatment of hypertension. The latter discussion also provides a reasoned response to certain related issues that have engendered controversy relating to these recommendations.

Humans↗
PubMed1995

Reversal of hypertrophy: an active biologic process.

Evidence from in vivo, in vitro, and genetic studies suggests that the reversal as well as the development of left ventricular hypertrophy do not depend solely on hemodynamic load; other factors are involved. Several humoral agents that may affect mitogenesis of cardiac myocytes and nonmyocitic elements have been identified, including the local renin-angiotensin system, norepinephrine, endothelins, transforming growth factor beta, insulin-like growth factor, bradykinin, prostaglandins, and nitric oxide. Animal studies using various models of left ventricular hypertrophy are beginning to suggest that reversal of hypertrophy may decrease mortality, improve coronary flow reserve, and maintain cardiac performance. Studies in humans are less supportive, and more are needed before it may be concluded that reduction of left ventricular mass decreases the cardiovascular morbidity and mortality associated with cardiac hypertrophy.

Animals↗