Use of a newly-developed portable capillary electrophoresis analyser to detect drugs of abuse in oral fluid: A case study.

The aim of the current study was to develop and validate an analytical method to determine whether drugs of abuse (DOA) were present in oral fluid (OF) using a newly-developed, portable capillary electrophoresis (CE) instrument coupled to a deep ultra-violet fluorescence detector (FD). The performance of this portable CE-FD DOA analyser was tested at the Weekend Festival Baltic (Pärnu, Estonia) between 2016 and 2018 as well as on the roadside OF samples collected by the police. The study reported 128 analysed cases in which persons were allegedly found to have been under the influence of DOA.

Effects of ACE inhibition versus non-ACE inhibitor antihypertensive treatment on myocardial fibrosis in patients with arterial hypertension. Retrospective analysis of 120 patients with left ventricular endomyocardial biopsies.

Background And Purpose: In experimental arterial hypertension, left ventricular hypertrophy (LVH) becomes pathologic with impaired myocardial function if myocardial fibrosis occurs. Myocardial fibrosis is associated with activated circulating or local renin-angiotensin-aldosterone systems. The primary objective of this retrospective study was to determine whether patients with arterial hypertension treated with angiotensin-converting enzyme inhibitors (ACEI) have less myocardial fibrosis than patients on non-ACEI treatment.

Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease.

Background: In arterial hypertension, left ventricular hypertrophy (LVH) includes myocyte hypertrophy and fibrosis, which leads to LV diastolic dysfunction and, finally, heart failure. In spontaneously hypertensive rats, myocardial fibrosis was regressed and LV diastolic function was improved by treatment with the angiotensin-converting enzyme inhibitor lisinopril. Whether this holds true for patients with hypertensive heart disease was addressed in this prospective, randomized, double-blind trial.

Aldosterone and myocardial fibrosis in heart failure.

Cardiac fibroblasts are known to have high affinity corticoid receptors for aldosterone and account for the accumulation of collagen within the interstitium of the rat myocardium in acquired and genetic hypertension. This interstitial fibrosis is an important determinant of pathologic hypertrophy in chronic heart failure. To examine the relationship between aldosterone and myocardial fibrosis, collagen volume fraction of the left and right ventricles were analyzed by videodensitometry of sirius red stained tissue in the following rat models: 2 kidney/1 clip model of renovascular hypertension; continuous aldosterone administration via osmotic minipumps (0.

Regression of myocardial fibrosis in hypertensive heart disease: diverse effects of various antihypertensive drugs.

Objective: In left ventricular hypertrophy (LVH) due to systemic hypertension, myocardial fibrosis is an important determinant of pathologic hypertrophy. Therefore, it is most relevant to utilize an antihypertensive regimen that permits a regression in myocardial fibrosis along with blood pressure normalization and regression of LVH.

Methods: To address this issue we examined 60 Sprague-Dawley rats.

Intrapericardial treatment of inflammatory and neoplastic pericarditis guided by pericardioscopy and epicardial biopsy--results from a pilot study.

From a registry of 136 patients undergoing pericardiocentesis, 14 patients with autoimmune and 15 patients with neoplastic effusions were selected. All underwent pericardioscopy, epicardial and pericardial biopsy with histologic, immunohistologic, and polymerase chain reaction/or in situ hybridization analysis for microbial DNAs and RNA. Pericardioscopy identified neoplastic effusions by the high occurrence of protrusions.

Angiotensin II and intracellular calcium of adult cardiac fibroblasts.

In various cardiovascular disorders, circulating or myocardial angiotensin II (Ang II) levels are increased, leading to excess collagen synthesis of cardiac fibroblasts. To characterize signal transduction mechanisms of Ang II, we examined changes in intracellular Ca2+ concentration ([Ca2+]i) of fura-2-loaded cultured adult rat cardiac fibroblasts by fluorescence photometry. [Ca2+]i was increased by Ang II via AT1 receptors in a dose-dependent manner (EC50 = 2.

Renin-angiotensin system and myocardial collagen matrix: modulation of cardiac fibroblast function by angiotensin II type 1 receptor antagonism.

Background: Left ventricular hypertrophy is an adaptive process to increased loading of the left ventricle. This condition becomes pathologic with impaired myocardial function if the various tissue compartments of the myocardium (myocyte, interstitial and vascular compartments) are inhomogeneously altered, particularly if myocardial fibrosis occurs. In arterial hypertension, myocardial fibrosis is known to occur in association with activated circulating or local renin-angiotensin systems and includes reactive perivascular and interstitial fibrosis in both the pressure-overloaded hypertrophied left ventricle and the normotensive non-hypertrophied right ventricle.

[Heart failure after myocardial infarct in decompensated diabetes mellitus. Acute therapy with catecholamines--long-term therapy with ACE inhibitor-loop diuretic combination].

In a 63-year-old woman with longstanding type I diabetes mellitus, CAD and chronic heart failure, a subacute myocardial infarction developed, together with decompensation of cardiac function and diabetes and concurrent pneumonia. Acute heart failure with acute renal failure on top of diabetic nephropathy, and interstitial pulmonary edema was initially treated with hemofiltration and catechol amines together with antibiotic and perfusor-regulated insulin therapy, and systemic heparinization. Subsequent chronic treatment with digitalis, acetyl salicylic acid, insulin and a combination of an ACE inhibitor and a loop diuretic resulted in an improvement of heart failure to NYHA functional class II where PTCA of coronary multi-vessel disease could be performed with low risk.

[Transmyocardial laser revascularization--an innovative pathophysiologic concept].

In patients with coronary artery disease where standard revascularization procedures are not appropriate, transmyocardial laser revascularization (TMLR) represents an innovative technique which is currently validated worldwide. Initially, it has been assumed that myocardial perfusion of ischemic regions could be instantly improved by inducing TMLR channels, which, however, might not be confirmed in ongoing studies. Indeed, the gain in O2 diffusion surface obtained by 20 patent TMLR channels is only 6 cm2 which accounts for just 0.

[Spironolactone: renaissance of anti-aldosterone therapy in heart failure?].

Mortality of patients with severe congestive heart failure (CHF) is still high despite combined treatment with angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis. Further therapeutic regimens are needed which include reversal of adverse myocardial remodeling and subsequent ventricular dysfunction. One third of all patients with CHF have diastolic left ventricular (LV) dysfunction with preserved systolic function.

Schedule-induced psychological stress and molecular structures of cardiomyocytes.

To establish a psychological stress model, we characterized in rats the effects of chronic (5-6 wk) scheduled food pellet feeding (35 mg/80 s for 8 h/day). Because the scheduled intake of pellets required that rats have access to 80% of ad libitum intake, the effect of food restriction was also examined by withholding food intermittently for 24 or 48 h each, followed by 24 h free access to food. Cardiac norepinephrine concentration was significantly increased (1,076 +/- 169 vs.

Regulation and role of myocardial collagen matrix remodeling in hypertensive heart disease.

In hypertensive heart disease, reactive myocardial fibrosis represents as an excessive accumulation of fibrillar collagen within the normal connective tissue structures of the myocardium. The fact, that the myocardium of both ventricles is involved, irrespective of ventricular loading conditions, suggests that circulating factors, and not the hemodynamic load are primary responsible for this adverse response of the myocardial fibrous tissue. In various experimental in vivo models, it has been shown that myocardial fibrosis is always associated with activation of circulating or local renin-angiotensin-aldosterone systems (RAAS).

Dietary linolenic acid-mediated increase in vascular prostacyclin formation.

To define vascular effects of an enhanced dietary alpha-linolenic acid intake, 28 spontaneously hypertensive rats were fed a 3% sunflowerseed oil (44% linoleic acid) diet; in 3 groups (7 rats each), the diet was supplemented with 1, 2.5 or 5% linseed oil containing 62% alpha-linolenic acid. alpha-Linolenic acid was incorporated up to 12% in the aorta of the 5% linseed oil group.

[Hypertension and alcohol: central and peripheral mechanisms].

Despite intense research efforts, the etiology of primary hypertension remains ill-defined. During our work on molecular influences of lifestyle factors on hypertension, the question arose to what extent cellular and molecular events could be involved in alcohol-induced hypertension. There is increasing evidence that alcohol initiates central as well as peripheral reactions which in a synergistic manner have a hypertensive action.

Advanced hypertensive heart disease in spontaneously hypertensive rats. Lisinopril-mediated regression of myocardial fibrosis.

Left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR) is accompanied by a structural remodeling of the myocardium that includes myocyte hypertrophy and interstitial and perivascular fibrosis of intramyocardial coronary arteries. The structural abnormalities related to fibrous tissue accumulation lead to increased myocardial diastolic stiffness and ultimately impaired systolic function of the left ventricle. It has been shown in 14-week-old SHR with early hypertensive heart disease that myocardial fibrosis could be reversed and myocardial diastolic stiffness normalized by 12-week treatment with the angiotensin-converting enzyme inhibitor lisinopril.

The concept of cardioreparation: Part 1. Pathophysiology of remodelling.

Purpose: Left ventricular hypertrophy is common in patients with hypertension or congestive heart failure and in survivors of myocardial infarction. It is associated with increased risks of adverse cardiovascular events, including angina, myocardial infarction and congestive heart failure. We aimed to explain these observations in terms of changes in the structure of the heart, collectively described as remodelling.

Drug withdrawal and rebound hypertension: differential action of the central antihypertensive drugs moxonidine and clonidine.

To examine the antihypertensive action of the centrally acting antiadrenergic drugs moxonidine and clonidine, systolic and diastolic blood pressure as well as heart rate were monitored by radio telemetry in spontaneously hypertensive rats (SHR) with established high blood pressure. Increasing doses were administered with regular rat chow for 6-8 day periods. Moxonidine reduced (p < 0.

Effect of the renin-angiotensin-aldosterone system on the cardiac interstitium in heart failure.

The interaction of the renin-angiotensin-aldosterone system (RAAS) and cardiac growth is of great interest in chronic heart failure. The pressure or volume overloaded heart shows a hypertrophic growth of the myocardium, i.e.

The renin-angiotensin-aldosterone system and myocardial collagen matrix remodelling in congestive heart failure.

In chronic heart failure, various regulatory systems including the Frank-Starling mechanism, the neuro-hormonal response, cardiac growth and peripheral oxygen delivery may be operative. Recently, the inter-relationship of the renin-angiotensin-aldosterone system (RAAS) and cardiac growth has drawn clinical interest. In the pressure-or volume-overloaded heart, the development of myocyte growth is primarily dependent on ventricular loading.

[Retrospective studies and prospects of therapy for hypertension].

Future trends in hypertensive treatment have to rely on our past and present experience with antihypertensive drugs as well as on emerging concepts of blood pressure regulation, on which some new drugs in the "pipeline" are based. Early detection of hypertension, before organ manifestations particularly in the heart, the kidney and the vessels occur, remain mandatory since in most of the patients with mild and moderate hypertension the high blood pressure is not diagnosed at all or treated inadequately. Prevention of cardiac, vascular, renal or metabolic complications has always been better for the patient and less costly than their repair or reparation.