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Biomedical subjects

K Lande

Publications and source records attributed to K Lande.

At least 37 records · Page 2Linked to original sources
PubMed1988

Hyper-responsiveness to low-dose epinephrine infusion in mild essential hypertension.

The present study was undertaken to evaluate the effects of intravenous infusion of small amounts of epinephrine on haemodynamics, renal electrolyte excretion and blood platelets in essential hypertension. Arterial plasma epinephrine concentrations were increased during the infusion to approximately 2.5 nmol/l both in a group of 40-year-old men with untreated mild essential hypertension (blood pressure 154 +/- 3/100 +/- 3 mmHg, n = 12) and in a group of age-matched male controls (124 +/- 3/78 +/- 2 mmHg, n = 11). In the hypertensive group only, mean blood pressure decreased, forearm blood flow increased, forearm vascular resistance decreased (P less than 0.001 for all) and the urinary excretion of sodium and potassium increased (P less than 0.01 for both). The hypertensive group also responded with an increase in plasma beta-thromboglobulin (P less than 0.05), blood platelet size (P less than 0.05) and a higher increase in platelet counts than in the normotensive group (P less than 0.05). Thus, in several ways the hypertensive patients showed a hyper-responsiveness to amounts of epinephrine which corresponds well to the plasma concentration achieved during psychological and physical activity.

Adult↗
PubMed1988

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 +/- 11 (SE) to 24 +/- 5 and 19 +/- 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 +/- 2.9 to 39.6 +/- 4.7 pg/mg (p less than 0.005) and venous plasma norepinephrine increased from 3.7 +/- 0.4 to 5.6 +/- 0.5 pg/ml (p less than 0.005), and venous plasma dopamine increased from 26 +/- 4 to 41 +/- 5 pg/ml (p less than 0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p less than 0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion.

Blood Platelets↗
PubMed1987

Does increased platelet release normalize during anti-hypertensive treatment?

Blood platelet function was evaluated in 10 men, all 50 years old, with untreated, mild hypertension. Each patient was examined four times: At the beginning of the study, after 5 weeks on placebo treatment, after the following 5 weeks on propranolol 160 mg daily, and finally after a second period of 5 weeks on placebo. At baseline the plasma level of the platelet release product beta-thromboglobulin (BTG) was 41.6 (30.5-57.0) micrograms/l (median and 95% confidence interval). During the first placebo period BTG was normalized to 21.0 (14.1-25.9) micrograms/l. While systolic blood pressure and heart rate fell during beta-adrenergic receptor blockade, BTG remained unchanged throughout the rest of the observation periods. Platelet size increased significantly during treatment with beta-blocker. The present study indicates that the normalization of elevated platelet function which previously has been reported to occur during anti-hypertensive drug therapy, may be explained by patient adaptation to the blood sampling procedure.

Blood Platelets↗
PubMed1987

Increased platelet release reaction in 50-year-old men with essential hypertension: correlation with atherogenic cholesterol fractions.

Beta-thromboglobulin (BTG) is a platelet-specific release product. Plasma BTG was significantly increased (p less than 0.01) in 50-year-old, untreated essential hypertensive men (1.22 +/- 0.13 nmol/L, n = 39, mean +/- SE) compared to 50-year-old, healthy normotensive control men (0.82 +/- 0.07 nmol/L, n = 31). Plasma BTG in the hypertensive group correlated significantly with the total serum cholesterol concentration (r = 0.47, p less than 0.01) and with the atherogenic cholesterol fractions low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol (r = 0.50, p less than 0.01). In the normotensive group, no significant correlation was observed between plasma BTG and total serum cholesterol (r = 0.14) or between plasma BTG and LDL + VLDL cholesterol (r = 0.08). Neither was any significant correlation found between plasma BTG and serum high-density lipoprotein (HDL) cholesterol or total triglycerides in either group. Thus, middle-aged men with untreated essential hypertension have an increased blood platelet release reaction related to their concentrations of atherogenic blood lipids. This relationship may be of pathogenetic importance for atherogenesis in hypertension.

Blood Platelets↗
PubMed1987

Cardiac adjustments to left-side inotropic stimulation of in situ pig hearts.

Cardiac adjustments to inotropic stimulation of the left side of the heart by continuous infusions of isoproterenol (0.6-0.8 microgram/min) and calcium chloride (240 mumol/min) into the left coronary artery were examined in open-chest pigs (17-36 kg) anesthetized with pentobarbital sodium. Both agents caused a reduction in the left ventricular (LV) preload and preejection segment length (PESL). Stroke volume (SV) rose by only 1.2 ml from 15.9 ml (P less than 0.01) during isoproterenol infusion, but when the reduction in LV PESL of 3.2% (P less than 0.01) was restored by saline infusion, SV increased by 27%. The LV PESL reduction was less at hypervolemia than at normovolemia. A computer-based model of the circulation predicted most of these changes and suggested redistribution of blood from the pulmonary to the systemic circulation. During isoproterenol infusion, the pulmonary arterial pressure fell, and the right ventricular end-ejection segment length declined. Reduced right ventricular afterload thus appears to be an important mechanism by which right ventricular output is increased during a selective increase in LV inotropy.

Animals↗
PubMed1987

Increased platelet size and release reaction in essential hypertension.

Basal platelet function was measured in 35 40-year-old men with untreated mild essential hypertension and compared with 44 age-matched normotensive men. The groups differed significantly with respect to platelet size in venous blood (hypertensive, 7.46 +/- 0.10 X 10(-15) l versus normotensive, 7.11 +/- 0.09 X 10(-15) l; P = 0.01) and arterial concentration of the platelet-specific protein beta-thromboglobulin (hypertensive, 1.11 +/- 0.23 nmol/l versus normotensive, 0.59 +/- 0.04 nmol/l; P = 0.02). The normotensive subjects had significantly higher beta-thromboglobulin (BTG) in venous than in arterial blood (P less than 0.01). The hypertensive men showed no such difference. In contrast to the normotensive subjects, the hypertensive group had reduced arterial compared with venous platelet count (P less than 0.01). This may reflect an increased liability in the hypertensive subjects to lose platelets through adherence to the cannula during arterial blood sampling. The above findings point to increased platelet activity in essential hypertension, particularly in arterial blood.

Adult↗
PubMed1987

Endocrine and haemodynamic responses to graded dopamine infusion in essential hypertension.

Hormonal, mean arterial blood pressure, forearm blood flow and heart rate responses to graded dopamine infusion (0.5-2.0 micrograms/kg/min) were examined in 10 men with untreated essential hypertension WHO group I (147 +/- 4/100 +/- 1 mmHg, means +/- SE), and in 10 normotensive men (129 +/- 2/85 +/- 1 mmHg), all 40 years old. Another 12 normotensive men (126 +/- 3/80 +/- 2 mmHg) were given only saline infusion. Dopamine increased heart rate significantly in the hypertensive group (8 +/- 2 beats/min, p less than 0.001), but the heart rate remained unchanged in the normotensive group (1 +/- 1 beats/min, NS). Although dopamine infusion tended to decrease mean blood pressure, the changes were not significantly different from those observed in the control group. No change in forearm blood flow was observed in either group. In the groups given dopamine, prolactin levels decreased only slightly compared to the control group given saline, the decrement tending to be more pronounced in the hypertensive group. Plasma vasopressin remained unchanged in both groups during dopamine infusion. These results indicate that hypertensive patients exhibit increased sensitivity to the cardiovascular effects of dopamine.

Adult↗
PubMed1986

Increased plasma noradrenaline during severe sodium restriction does not stimulate platelet release in essential hypertension.

Seventeen 50-year old hypertensive men, previously untreated with blood pressure 157 +/- 4/110 +/- 2 mmHg (means +/- SE) were given a low sodium diet for 2 weeks. During the second week, the diet was supplemented with potassium. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:4 and 1:11, respectively. Sympathetic noradrenergic tone increased considerably during the first week. Thus, venous plasma noradrenaline increased from 254 +/- 22 to 347 +/- 28 pg/ml (p less than 0.001) and arterial concentration from 253 +/- 36 to 317 +/- 42 pg/ml (n = 10, p less than 0.001). No significant change was observed in sympathetic adrenal tone as reflected by normal plasma adrenaline in venous (42 +/- 5 vs 43 +/- 6 pg/ml, ns) or arterial blood (71 +/- 10 vs 82 +/- 15 pg/ml, n = 10, ns) or in venous plasma concentration of the blood platelet release product beta-thromboglobulin (BTG) (50 +/- 8 vs 43 +/- 5 ng/ml, ns). During the second week sympathetic noradrenergic tone remained highly significantly elevated compared to baseline but still no change in plasma adrenaline or plasma BTG was found. Thus, whereas sodium depletion did increase plasma noradrenaline concentration markedly in these hypertensive men, no change in adrenaline concentration was observed, and blood platelet release reaction was unchanged. Plasma noradrenaline within the physiological concentration range does not seem to serve as a regulator of in vivo platelet function.

Blood Platelets↗
PubMed1986

Blood platelet release correlates with serum lipids in 50 year old men with essential hypertension.

50 year old men with moderate, essential hypertension (n = 39) were compared to normotensive males of similar age (n = 31). The hypertensive men were heavier (10 kg in average, p less than 0.01), and had a higher pulse rate (5 beats per minute (p less than 0.05). Plasma beta-thromboglobulin, a marker of platelet release reaction, was 49% higher in the hypertensive group (p less than 0.01). Total cholesterol, LDL + VLDL cholesterol and serum triglycerides were not significantly different between the groups. In the hypertensive group, plasma beta-thromboglobulin concentration correlated significantly with total cholesterol (r = 0.47, p less than 0.01) as well as with LDL + VLDL cholesterol (r = 0.50, p less than 0.01). In the normotensive group no such correlation was found. The results suggest activation of platelets in hypertension, and suggest that in hypertension, even a normal cholesterol concentration may influence platelet function.

Blood Platelets↗
PubMed1986

Platelet volume, platelet release reaction and platelet response to infused adrenaline are increased in essential hypertension.

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.

Adult↗
PubMed1986

Enhanced platelet release reaction related to arterial plasma adrenaline and blood pressure in pre-eclampsia.

The platelet release product beta-thromboglobulin (BTG) in venous plasma, and arterial and venous catecholamines were measured in 13 severe pre-eclamptic and 13 normotensive pregnant women. In the pre-eclamptic group, BTG was significantly higher and the platelet count significantly lower than in the normotensive pregnant group. In the pre-eclamptic group, arterial concentrations were significantly higher for adrenaline, noradrenaline and dopamine, whereas in venous plasma only adrenaline and dopamine were higher. Significant positive correlations appeared in the pre-eclamptic patients between venous BTG and arterial adrenaline (r = 0.82), arterial noradrenaline (r = 0.76) and venous adrenaline (r = 0.55). In the pre-eclamptic group, BTG also highly correlated with systolic (r = 0.84) and diastolic blood pressure (r = 0.77) and heart rate (r = 0.67). These findings indicate that sympathetic nervous tone, as measured by arterial and venous plasma catecholamines, is a good predictor of in-vivo blood platelet activation. In pre-eclampsia, increased sympathetic tone may play a key role in platelet activation and consumption and thus in the activation of the coagulation system.

Adult↗
PubMed1986

Increased plasma vasopressin in low renin essential hypertension.

Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 +/- 2.2 [SE] vs 7.5 +/- 1.0 pg/ml; p less than 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 +/- 0.04 vs 0.46 +/- 0.06 Goldblatt units X 10(-4)/ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 +/- 12 vs 68 +/- 6 pg/ml; p less than 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 +/- 0.8 vs 3.5 +/- 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective beta-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 +/- 6.4 to 13.5 +/- 4.2 pg/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1985

Effects of adrenaline infusion on platelet number, volume and release reaction.

At the end of a diagnostic right heart catheterization ten patients received an intravenous infusion of l-adrenaline which gradually increased the arterial plasma adrenaline concentration from resting physiological values to high values as seen during myocardial infarction, pheochromocytoma and hypoglycemia. Blood was sampled from the brachial artery, femoral vein and hepatic vein. During the adrenaline infusion venous beta-thromboglobulin concentrations increased 23% from 61 +/- 5 to 80 +/- 7 micrograms/l (mean +/- SE), arterial platelet counts 20% from 212 +/- 17 to 253 +/- 25 X 10(9)/l and arterial platelet volume 4% from 7.25 +/- 0.20 to 7.56 +/- 0.21 femtoliter. All changes were significant at the 5% level. Thus, acute increments of arterial plasma adrenaline significantly stimulated the blood platelet parameters studied.

Adult↗
PubMed1985

Increased arterial adrenaline is highly correlated to blood pressure and in vivo platelet function in pre-eclampsia.

Compared with normotensive pregnant women (n = 13), patients with severe pre-eclampsia (n = 13) had increased arterial plasma adrenaline (P < 0.001), peripheral venous adrenaline (P < 0.01), arterio-venous differences of adrenaline (P < 0.001) and venous concentration of the platelet release product beta-thromboglobulin (P < 0.001). In the pre-eclamptic group, arterial adrenaline correlated with mean blood pressure (r = 0.90, P < 0.001), heart rate (r = 0.78, P < 0.01) and beta-thromboglobulin (r = 0.82, P < 0.001), while in the normotensives adrenaline correlated only with beta-thromboglobulin (r = 0.76, P < 0.01). According to these results, sympathetic adrenal tone is increased in pre-eclampsia and may play a role in the pathogenesis of high blood pressure and platelet activation in this disease.

Adult↗