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Biomedical subjects

S Jern

Publications and source records attributed to S Jern.

At least 55 records · Page 3Linked to original sources
PubMed1997

Sympathoadrenal activation and muscarinic receptor stimulation induce acute release of tissue-type plasminogen activator but not von Willebrand factor across the human forearm.

We have previously shown that both mental stress and administration of the muscarinic receptor agonist methacholine induce an acute release of tissue-type plasminogen activator (t-PA) across the human forearm. There are data indicating that the regulated acute release of t-PA from the endothelium is closely interrelated with release of von Willebrand factor (vWF). The aim of the present study was to simultaneously determine basal and stimulated in vivo release rates of t-PA and vWF in an intact human muscle vascular bed. Eighteen healthy young males were studied at rest and during 10 min of mental stress (forced arithmetic). A subsample of ten subjects also received a step-wise i.a. infusion of methacholine (0.1-0.8-4.0 microg/min). Forearm blood flow was determined by venous occlusion plethysmography and interconverted to forearm plasma flow (FPF) using individual hematocrits. Net release/uptake rates of t-PA and vWF were calculated as the product of the arteriovenous concentration gradient and FPF. At rest there was a net release of both t-PA antigen and activity. In contrast, there was no significant local net release of vWF antigen across the forearm. Net release rates of t-PA roughly doubled in response to the stress test (0.4 to 0.8 and 0.2 to 0.5 ng x min(-1) x 100 ml(-1) for t-PA antigen and activity, respectively, p <0.05 for both). Local administration of methacholine induced a more than 10-fold increase in the net release rates of t-PA (0.6 to 9.6 and 0.3 to 6.6 ng x min(-1) x 100 ml(-1) at the highest dose step for antigen and activity respectively, p <0.01 for both). In contrast, neither mental stress nor local administration of methacholine induced a significant net release of vWF antigen across the forearm. The results demonstrate that the processes of acute release of t-PA and vWF are not necessarily linked in vivo in man.

Adrenal Glands↗
PubMed1997

An experimental multiple-organ model for the study of regional net release/uptake rates of tissue-type plasminogen activator in the intact pig.

Experimental data indicate large between-organs variations in rates of synthesis of tissue-type plasminogen activator (t-PA), which may reflect important differences in the capacity for constitutive and stimulated t-PA release from the vascular endothelium. In this report we describe a new multiple-organ experimental in vivo model for simultaneous determinations of net release/uptake rates of t-PA across the coronary, splanchnic, pulmonary, and hepatic vascular beds. In eleven intact anesthetized pigs, blood samples were obtained simultaneously from the proximal aorta, coronary sinus, pulmonary artery, and portal and hepatic veins. Plasma flows were monitored separately for each vascular region. Total plasma t-PA was determined by ELISA with a porcine t-PA standard. Regional net release/uptake rates were defined as the product of arteriovenous concentration gradients and local plasma flows. The net release of t-PA across the splanchnic vascular bed was very high, with a mean output of 1,919 ng total t-PA x min(-1) (corresponding to 90 ng per min and 100 g tissue). The net coronary t-PA release was 68 ng x min(-1) (30 ng x min(-1) X 100 g(-1)). Pulmonary net fluxes of t-PA were variable without any significant net t-PA release. The net hepatic uptake rate was 4,855 ng x min(-1) (436 ng x min(-1) x 100 g(-1)). Net trans-organ changes of active t-PA mirrored those of total t-PA. The results demonstrate marked regional differences in net release rates of t-PA in vivo. The experimental model we present offers new possibilities for evaluation of regional secretion patterns in the intact animal.

Animals↗
PubMed1997

Assessment of left ventricular hypertrophy in patients with essential hypertension.

By virtue of its potency as a cardiovascular risk indicator, the presence of left ventricular hypertrophy (LVH) in a patient with hypertension deserves serious attention and make its diagnosis a clinical priority. In view of its prognostic impact, an argument could be made for routine assessment of this intermediate endpoint in each patient with essential hypertension. Two diagnostic approaches are available for screening evaluation of hypertensive patients; either a limited echocardiographic examination or an ECG-based LVH assessment. Recently developed new or combined criteria have significantly improved the diagnostic performance of ECG criteria, and evolving data show that accurate estimation of LVH can be performed by ECG screening in a majority of patients. At present, ECG evaluation based either on sex-specific orthogonal-lead time-voltage criteria or on the combined standard 12-lead criteria of Sokolow-Lyon (sum of S in V1 and R in V5 or V6) or Cornell Product (product of sum of R in aVL and S in V3 + 6 mm in females and QRS duration) demonstrates the best overall diagnostic accuracy. With orthogonal criteria, the sensitivity is 81% in women and 71% in men at a matched 98% specificity. The corresponding overall sensitivity of the combined Cornell Product or Sokolow-Lyon criteria is reported to be 68% at a specificity of 96.6%. What speaks in favour of the echocardiographic approach is its superior sensitivity and the possibility of gaining additional potential risk information associated with the geometric pattern of the LVH. However, its general availability makes electrocardiography a cost-effective diagnostic alternative with which to follow the progression or regression of LVH in hypertensive patients.

Echocardiography↗
PubMed1996

Estrogen and progestagen modify the hemodynamic response to mental stress in young women.

OBJECTIVE: To evaluate separately the effects of estrogen and progestagen on the cardiovascular response to a standardized mental stress test. METHODS: Seven women were studied during the early follicular phase (day 1-4) of three different menstrual cycles after randomized oral administration of either 6 mg estradiol valerate or 15 mg norethisterone acetate or placebo. Heart rate and blood pressure were recorded at rest for 2 hours after administration and throughout the stress test. Forearm plethysmography was recorded at rest and during stress. RESULTS: Estrogen had no effect on heart rate or blood pressure at rest. After estrogen administration the increases in heart rate (delta 14 bpm/10 bpm; p < 0.01) and diastolic blood pressure (delta 14 mmHg/9 mmHg: p = 0.06) from baseline to stress were augmented compared to those observed after placebo administration. Heart rate, systolic and diastolic blood pressures reached higher levels during stress after estrogen administration compared to placebo (delta 5 bpm, and delta 7 mmHg and delta 5 mmHg respectively; p < 0.05). Estrogen administration also caused a prolongation of the diastolic blood pressure response to stress. Progestagen compared to placebo induced an increase in heart rate already at rest (delta 4 bpm; p < 0.01), and heart rate was maintained on a higher level throughout the stress test (p < 0.05). Blood pressure at rest and pressor responses to stress were not significantly changed after progestagen administration. CONCLUSIONS: The results indicate that estrogen is responsible for the enhanced cardiovascular responses to stress, whereas progestagen provokes a parallel upward shift of basal heart rate which is independent of level of activation.

Adult↗
PubMed1996

Impaired glucose tolerance at five-year follow-up of young men with borderline hypertension.

BACKGROUND: Recent studies suggest that patients with essential hypertension have impaired glucose tolerance and are hyperinsulinemic compared with normotensive subjects. The aims of the study were (1) to follow blood pressures of 56 young men with borderline hypertension for 5 years, (2) to investigate glucose tolerance in these subjects, and (3) to determine the relation of insulin/glucose metabolism to structural vascular changes and hemodynamic patterns in borderline hypertension. METHODS: Thirty-nine young (age 22-34 years) male subjects with borderline hypertension (SBP 140-160 and or DBP 85-95 mmHg initially) and 17 normotensive control subjects (SBP 110-130 and DBP 60-80 mmHg) participated in the study. Blood pressure was measured, a standard oral glucose tolerance test (OGTT) was performed, and glucose, insulin and C-peptide were determined before and 30, 60, 90 and 120 minutes after a standard 75-g glucose load. Post-ischemic forearm vasodilatory responses were examined by plethysmography. RESULTS: At follow-up, the borderline hypertensives had maintained significantly higher blood pressures than control subjects. Borderline hypertensives also had significantly impaired glucose tolerance compared to control subjects. The insulin response had a somewhat more sluggish descent, but did not differ significantly from the response of normotensives. The C-peptide response pattern resembled that of insulin, but C-peptide was significantly elevated after 120 min. On the whole group level, there were only weak relations of insulin to blood pressure. By contrast, fasting insulin and post-load insulin levels were strongly correlated with body mass index, the waist-hip circumference ratio, triglyceride, and both total and LDL cholesterol. Across the whole group, there were significant correlations between forearm minimal vascular resistance and fasting insulin (r = +0.37 p = 0.007) and insulin area-under-the-curve (r = +0.28 p = 0.044). However, Rmin was even more strongly correlated with body mass index, suggesting that this relationship was related to degree of obesity. CONCLUSION: Borderline hypertension in young men is a persistent condition which is associated with impaired glucose tolerance without hyperinsulinemia. This finding suggests that impaired glucose tolerance might be a more primary phenomenon in early hypertension devoid of lipid metabolic aberrations.

Adult↗
PubMed1995

Long-term stability of blood pressure and pressor reactivity to mental stress in borderline hypertension.

Borderline hypertension is characterized by pressor hyperreactivity to mental stress. However, it has not been shown whether blood pressure hyperresponsiveness is a temporary phenomenon due to situational anxiety or a stable feature of the borderline hypertensive state. We therefore evaluated the long-term stability of invasively assessed blood pressure and central hemodynamic responses to mental stress in 10 young male subjects with borderline hypertension recruited from a population screening. Two identical 10-min mental arithmetic stress tests were performed 50 to 62 months apart (median, 4 years 8 months). Intraarterial blood pressure was monitored continuously before, during, and after stress. Cardiac output was measured by the indocyanine green dye dilution technique and indexed for body surface area. Total peripheral resistance index was computed from cardiac index and mean arterial pressure. During the 4-year follow-up period, none of the central hemodynamic parameters had changed significantly, either with respect to rest or stress levels. Test-retest variability of blood pressure measures was low, and errors of measurement ranged between 4.8 and 8.2 mm Hg for blood pressure levels at rest and during stress. Mental arithmetic induced highly significant blood pressure increments on both occasions (ANOVA, P < .0001 throughout). Pressor responses were somewhat but not significantly lower during the second test. Errors of measurement for absolute blood pressure reactivity ranged between 3.9 and 7.1 mm Hg. Intersession correlation coefficients for blood pressure levels attained during stress were above r = 0.75 throughout (P < or = .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Enhanced levels of tissue-type plasminogen activator in borderline hypertension.

Despite effective antihypertensive therapy, essential hypertension is still associated with considerable residual risk of cardiovascular complications. The aim of the present study was to investigate the state of the endogenous fibrinolytic system in young subjects with borderline hypertension. Thirty-nine young (age, 24 to 34 years) male subjects with borderline hypertension (systolic BP [SBP] 140 to 160 mm Hg and/or diastolic BP [DBP] 85 to 95 mm Hg) and 17 normotensive control subjects (age, 22 to 31 years; SBP 110 to 130 and DBP 60 to 80 mm Hg) were recruited from a population screening. Plasma levels of tissue-type plasminogen activator (t-PA) antigen and activity and plasminogen activator inhibitor 1 (PAI-1) antigen were determined at rest and in response to a venous occlusion test. Borderline-hypertensive subjects had metabolic and anthropometric characteristics similar to normotensive individuals. In comparison with normotensive subjects, borderline-hypertensive subjects had higher plasma concentration of t-PA antigen both at rest and after venous occlusion but similar levels of t-PA activity or PAI-1 antigen. The increase in t-PA antigen and activity in response to venous occlusion was significantly greater in borderline-hypertensive subjects than in normotensive control subjects (P < .0001 and P = .003, respectively). In stepwise regression analyses, 24-hour mean arterial pressure emerged as the single most powerful predictor of t-PA antigen levels, but body mass index was the most important determinant of t-PA activity and PAI-1 antigen. However, PAI-1 was explained by both body mass index (partial r = .48, P < .001) and 24-hour mean arterial pressure (partial r = .29, P < .05). Thus, early hypertension may be associated with significant alterations in endogenous fibrinolysis.

Adult↗