PubMed Health⌕ Search

Biomedical subjects

L Lind

Publications and source records attributed to L Lind.

At least 73 records · Page 4Linked to original sources

Divergent effects of different beta-blocking agents on endothelium-dependent vasodilatation in the human forearm.

OBJECTIVE: The aim of this study was to evaluate the direct effect of three principally different beta-receptor blocking agents on endothelium-dependent vasodilatation (EDV) in the human forearm. METHODS: In 27 young normotensive subjects forearm blood flow (FBF) was measured with venous occlusion plethysmography during local intra-arterial infusions of methacholine (MCh), evaluating EDV, and sodium nitroprusside (SNP), evaluating endothelium-independent vasodilatation (EIDV). The measurements of EDV and EIDV were undertaken at baseline conditions and repeated after 1 h of concomitant intra-arterial infusion of atenolol (n = 8, 1.2 mg/h), propranolol (n = 7, 1.2 mg/h), labetalol (n = 7, 16 mg/h) or saline (n = 5). RESULTS: The selective beta-blocker atenolol showed a tendency to improve the FBF response to MCh (from 28.8 +/- 9.2 to 32.6 +/- 8.7 ml/min/ml tissue, p < 0.05). The nonselective beta-blocker propranolol attenuated the FBF response to MCh significantly (from 30.5 +/- 6.7 to 22.8 +/- 4.5 ml/min/ml tissue, p < 0.01). In these groups baseline FBF and EIDV were unchanged. Labetalol, a combined non-selective beta-blocker and selective alpha-1-blocker, increased baseline FBF and increased the response to both MCh and SNP in parallel (p < 0.05 for MCh and p = 0.07 for SNP). Saline did not change baseline FBF, EDV or EIDV. CONCLUSIONS: This study showed that local infusion of different beta-blocking agents in normotensive subjects affects endothelial vasodilatory function differently. This technique could be used to evaluate the direct effect of vasoactive drugs on EDV.

Adrenergic alpha-Antagonists↗

Ambulatory blood pressure and endothelium-dependent vasodilation in hypertensive patients.

Endothelial function is important for local vascular regulation and an abnormal endothelium-dependent vasodilatation (EDV) has been observed in subjects with essential hypertension. As ambulatory blood pressure (ABP) is more closely related to target organ damage than office blood pressure, this study investigated also if 24-h ABP is more closely related to an impaired EDV than office blood pressure recordings. In a group of 25 untreated patients with essential hypertension and an age- and sex-matched control group (n = 21) endothelial function was evaluated by measurements of forearm blood flow (FBF) during local intra-arterial infusions of metacholine (evaluating EDV) and sodium nitroprusside (evaluating endothelium independent vasodilation, EIDV). FBF was measured with venous occlusion plethysmography. Both office mean artery pressure (MAP; r= -0.57, p < 0.001) and 24-h ABP (r = 0.40, p < 0.01) were related to the endothelial vasodilator function (EDV to EIDV ratio) in an inverse way, but ABP was not superior to office blood pressure recordings. Within the hypertensive group, pronounced white-coat effect (office minus daytime ABP) was associated with a reduced,EDV (r= 0.41, p < 0.05). The degree of night-time decline in blood pressure ("dipping") showed no correlation to EDV. In conclusion, the finding that ABP was no more closely related to the endothelial vasodilator function than office blood pressure recordings might be due to an increased mental alertness affecting EDV in some hypertensive subjects, as suggested by the finding of a reduced EDV in those with a pronounced white-coat effect.

Blood Pressure↗

Blood pressure changes in relation to sodium and calcium status in induced hyperinsulinemia.

Insulin increases renal sodium reabsorption which may contribute to hypertension. However, acute insulin administration may result in vasodilation. The aim of the present study was to investigate effects on blood pressure and alterations in ion status during hyperinsulinemia. Blood pressure and serum sodium and ionized calcium concentrations were measured before and at the end of euglycemic hyperinsulinemic clamp tests performed in 45 patients with essential hypertension. Both the systolic and the diastolic blood pressure decreased, by 4% (p < 0.05) and 3% (p < 0.05), respectively. Circulating ionized calcium concentration increased by 2% (p < 0.001), and the ratio between circulating sodium and ionized calcium concentrations decreased. The changes in circulating sodium concentration correlated to changes in systolic blood pressure (SBP; r = 0.36, p = 0.05). Both ionized calcium concentrations and the ratio between circulating sodium and ionized calcium concentrations correlated to changes in SBP during hyperinsulinemia (r = -0.41, p = 0.03, r = 0.56, p < 0.01, respectively). The changes in ion status were not significantly correlated to age, body mass index or insulin sensitivity. In conclusion, a more pronounced increase in circulating ionized calcium concentration and reduction in the ratio between sodium and ionized calcium concentrations was associated with a greater blood pressure decline during the hyperinsulinemic clamp test when performed in hypertensive patients.

Aged↗

Hypocalcemia and parathyroid hormone secretion in critically ill patients.

OBJECTIVE: To investigate possible causes of hypocalcemia and to assess parathyroid hormone (PTH) secretion in intensive care unit (ICU) patients. DESIGN: Combined cross-sectional and prospective study. SETTING: ICU in a university hospital. PATIENTS: Thirteen patients with sepsis and 13 patients who underwent major surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Calcium metabolic indices were investigated during the first 24 hrs in the ICU and after 2 days. Eight of the surgical patients and five of the septic patients were subjected to a citrate/calcium infusion on day 1 in the ICU, to study the dynamics of PTH secretion. The blood ionized calcium (Ca2+) concentration was generally low in the septic patients (mean +/- SD, 1.03+/-0.08 mmol/L; reference value, 1.10-1.30) and increased, but not normalized, after 2 days. Hypocalcemia was only occasionally seen in the surgical patients. In the septic patients, urinary excretion of calcium was low; and, in both patient groups, elevated concentrations of two markers of bone resorption, deoxypyridinoline and ICTP (serum carboxy-terminal cross-linked telopeptide of type I collagen), were found. In cases of sepsis, the concentrations of proinflammatory cytokines were high (394+/-536 pg/mL for tumor necrosis factor-alpha and 5676+/-5190 pg/mL for interleukin-6, both normally <10-20). The Ca2+ concentration was inversely related to tumor necrosis factor-alpha and interleukin-6 (r2 = .35-.42; p<.01), as well as to procalcitonin (r2 = .71; p<.01). Despite normocalcemia in the surgical patients, serum PTH concentrations were elevated in both patient groups (97 and 109 ng/L) (reference value, <55 ng/L), both on day 1 and day 3 in the ICU. The citrate/calcium infusion revealed an increased secretory response of PTH to lowered Ca2+ concentrations in both groups of patients (p<.05), when compared with matched healthy controls. CONCLUSION: Hypocalcemia was common in septic ICU patients and was not the result of an increased urinary excretion of calcium or of an attenuated bone resorption, but seemed related to the inflammatory response. An increased PTH secretion was found in both patient groups.

APACHE↗

Hypocalcemia during porcine endotoxemic shock: effects of calcium administration.

OBJECTIVE: To evaluate the pathophysiology involved in hypocalcemia in septic shock and to investigate the value of calcium administration. DESIGN: Prospective, randomized placebo-controlled trial with parallel groups. SETTING: Animal research laboratory at the University Hospital of Uppsala. SUBJECTS: Twenty-four pigs aged 12-14 wks receiving general anesthesia. INTERVENTIONS: Twenty pigs received endotoxin infusion (10 microg/kg/hr) for 6 hrs. Ten of these pigs also received a calcium infusion (20 mmol total) in parallel. Four control pigs received only saline. MEASUREMENTS AND MAIN RESULTS: At the end of the study, blood ionized calcium (Ca2+) had declined from 1.32+/-0.04 mmol/L (mean +/- SD) to 1.09+/-0.06 mmol/L in pigs receiving endotoxin (p < .05 vs. controls) compared with 1.38+/-0.04 mmol/L to 1.25+/-0.07 mmol/L in controls and 1.39+/-0.03 mmol/L to 1.24+/-0.07 mmol/L in endotoxemic pigs receiving calcium. In both endotoxemic groups, total calcium levels in ascites were increased by 56% (p < .005 vs. controls), and an accumulation of calcium in the liver was mainly seen in the endotoxemic group receiving calcium (p < .008 vs. controls). Total Ca2+ levels in adiposal tissue and skeletal muscle were similar in all groups. Calcium administration did not significantly alter systemic hemodynamics or survival in this model of septic shock (four survivors in the endotoxemic group and five in the calcium administration group). CONCLUSIONS: Endotoxemia in the pig rapidly induced hypocalcemia. Calcium accumulation was found in ascites and in the liver, but not in other examined tissues. Calcium administration, restoring the Ca2+ concentration, did not improve hemodynamics or survival in this model of hypodynamic sepsis. Porcine endotoxemic shock, which replicates human septic shock, seems to be suitable for evaluating calcium turnover.

Animals↗

Short-term effects of smoking and nicotine chewing gum on endothelium-dependent vasodilation in young healthy habitual smokers.

Smoking is a major risk factor for coronary and peripheral vascular disease. This study was designed to investigate the short-term effects of smoking and nicotine gum on endothelium-dependent (EDV) and -independent (EIDV) vasodilation in the forearm of young habitual smokers. In 10 subjects, forearm blood flow (FBF) during local infusion of metacholine (4 microg/min, evaluating EDV) and sodium nitroprusside (10 microg/min, evaluating EIDV) was assessed before and at 10 min (early phase) and 30-50 min (plateau phase) after the initiation of smoking, using forearm venous occlusion plethysmography. Six subjects underwent similar measurements of FBF before and 30 min after chewing a nicotine gum (4 mg). As a change in blood pressure was expected, forearm vascular resistance (FVR) was used to calculate EDV and EIDV. FVR during metacholine infusion increased from 4.6 +/- 1.4 SD to 5.9 +/- 2.1 mm Hg/ml/min/100 ml tissue during the early and to 5.0 +/- 1.6 mm Hg/ml/min/100 ml tissue at the plateau phase of smoking (p < 0.01 for both vs. baseline) and from 4.5 +/- 1.6 to 5.2 +/- 1.6 mm Hg/ml/min/100 ml tissue after chewing the nicotine gum (p < 0.01). No significant changes in EIDV were seen after smoking or the nicotine gum. When all data were analyzed together, plasma nicotine levels and blood pressure were both independent predictors of endothelial function (p < 0.001 for both). In conclusion, cigarette smoking induced a dose-dependent attenuation in EDV, being maximal shortly after initiation of smoking and persisting up to 30-50 min. Nicotine chewing gum induced a similar impairment in EDV.

Adult↗

Endothelium-dependent vasodilation in hypertension: a review.

Using both in vitro and in vivo techniques, it has repeatedly been shown that endothelium-dependent vasodilation (EDV) is impaired in different forms of experimental hypertension (SHR, Dahl salt-sensitive rat, DOCA-salt rat and renovascular hypertension). EDV has also been found to be impaired in primary, as well as in secondary forms of human hypertension. Although impaired EDV is a general finding in hypertension, the pathophysiological mechanisms might differ between different forms of hypertension and between different types of vessels and vascular beds. Impaired activity of nitric oxide synthase, increased release of endothelin-1, increased production of a prostanoid-derived contracting factor, decreased generation of endothelium-derived hyperpolarizing factor/s and impairment caused by superoxide ions have all been shown to contribute to the impairment of EDV during different conditions. While most antihypertensive treatments improve EDV in experimental hypertension, no uniform picture has been seen in human hypertension, possibly because different antihypertensive drugs have different direct actions on EDV. This review shows that while impaired EDV has been found to be a general feature of hypertension, the mechanisms involved and the therapeutic opportunities have still to be established.

Animals↗

Interleukin-6 induced suppression of bovine parathyroid hormone secretion.

Calcium disturbances in the critically ill coincide with elevations of proinflammatory cytokines. The effects of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) on parathyroid hormone (PTH) secretion were investigated. IL-6 and TNF-alpha had no acute effect on PTH secretion in extracellular Ca2+ concentrations of 0.5, 1.25 and 3.0 mM. In contrast to TNF-alpha, cultures for 24 h in the presence of 10 ng/mL of IL-6 showed decreased PTH secretion by 51% and 29% in 0.5 mM and 1.25 mM Ca2+ respectively. Neither IL-6 nor TNF-alpha, affected cytoplasmic Ca2+ of the cells. We conclude that PTH secretion in vitro can be suppressed by IL-6 at clinically relevant concentrations. This suppression may aggravate hypocalcemia of the critically ill and attenuate the conventionally strong stimulation of the PTH release by reduction in serum calcium.

Animals↗

The haemodynamic response to hyperinsulinaemia in hypertensive subjects.

In order to study if the vasodilatory action of insulin is impaired in essential hypertension, 24 untreated patients were challenged with a 2 h euglycaemic hyperinsulinaemic clamp (56 E/m2). Cardiac index (CI) was measured by thoracic impedance cardiography and leg blood flow (LBF) by Doppler ultrasound. During the clamp procedure a significant decline in blood pressure was seen (3.0-5.6% over 120 min, P < 0.001). However, no significant effects on ejection fraction (+6 +/- 8 s.d.%), CI (-1 +/- 2%), heart rate (+2 +/- 1%) or total peripheral resistance (TPRI, -0.5 +/- 2%) were found. LBF increased by 22 +/- 35% (P < 0.005). These haemodynamic effects of insulin were not related to age, sex, body mass index, blood pressure or the insulin-mediated glucose uptake during the clamp. In conclusion, insulin increased LBF, but no changes in CI and TPRI were seen in the hypertensive patients. Furthermore, no association between the ability of insulin to induce vasodilatation and to promote glucose uptake was seen.

Fasting↗

The influence of different antihypertensive drugs on left ventricular hypertrophy in a population sample of elderly men.

AIMS AND METHODS: To evaluate if the effects of long-term treatment with different antihypertensive drugs on left ventricular (LV) hypertrophy seen in meta-analysis could also be found in a cross-sectional study of elderly men, we investigated 584 70-year-old men with echocardiography of which 179 were treated for hypertension. RESULTS: Men on antihypertensive treatment showed a significantly higher LV mass than normotensive men (143 +/- 29 vs 132 +/- 28 g/m2, P < 0.01), but no significant difference in LV mass was seen between men on one antihypertensive drug (n = 129) and those on two drugs (n = 47). Among the men on monotherapy, no differences in LV mass between the subjects who were treated with calcium-antagonists (142 +/- 27 g/m2, n = 37), beta-blockers (140 +/- 29 g/m2, n = 66) or ACE-inhibitors (142 +/- 33 g/m2, n = 20) were found. Neither did blood pressure differ between these groups. Excluding subjects with coronary heart disease did not alter the results. Thiazides as monotherapy was uncommon in this population (n = 4) and therefore not evaluated. CONCLUSION: In a population sample of elderly men with hypertension, no differences in LV mass or blood pressure could be seen between subjects treated with ACE-inhibitors, calcium-antagonists or beta-blockers as monotherapy. In meta-analysis of the effects of different antihypertensive therapies on regression of LV hypertrophy, ACE-inhibitors have shown the best results.

Adrenergic beta-Antagonists↗

Endothelium-dependent vasodilation and structural and functional changes in the cardiovascular system are dependent on age in healthy subjects.

The aim of this study was to evaluate possible associations between endothelium-dependent vasodilatation (EDV) and cardiovascular structure and function. EDV could influence peripheral resistance and be affected by atherosclerosis and might thereby influence indices of cardiovascular structure and function. In a group of 31 apparently healthy men and 25 women (age range 20-69 years), EDV was evaluated by infusion of metacholine (4 micrograms min-1), and endothelium-independent vasodilatation (EIDV) was assessed by nitroprusside infusion (SNP, 10 micrograms min-1) in the brachial artery. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. Left ventricular (LV) geometry and function and the intima-media thickness in the carotid artery were assessed by ultrasonography. The stroke index to pulse pressure ratio was used to evaluate arterial compliance. Several indices of cardiovascular structure and function were found to be related to an index of endothelial function, the EDV to EIDV ratio. Furthermore, left ventricular mass (LVM), the atrio-ventricular plane displacement, E/A ratio, IVRT, the intima-media thickness of the carotid artery and arterial compliance were all significantly related to both EDV and EIDV in women. However, most indices of cardiovascular structure and function, as well as endothelial function, change with age and only the relation between LV diastolic function and endothelial function in men remained significant (P < 0.05) after including age in multiple regression analysis. Age was related to both cardiovascular structure and function, as well as to endothelial function. Multiple regression analysis showed that ageing generally affects cardiovascular characteristics and endothelial function in parallel in these healthy subjects.

Adult↗

Effects of age, gender and metabolic factors on endothelium-dependent vasodilation: a population-based study.

OBJECTIVES: A progressive decline in endothelium-dependent vasodilation (EDV) in the human forearm with age has previously been reported. The aim of this study was to evaluate the interplay between age, gender and metabolic factors on EDV in healthy subjects in a population-based study. SETTING: Tertiary university hospital. SUBJECTS AND DESIGN: Thirty-six healthy men and 30 women, aged 20-69 years, underwent measurements of forearm blood flow (FBF) at rest and during local infusions of 2 and 4 microg min-1 of metacholine (evaluating EDV) and 5 and 10 microg min-1 of sodium nitroprusside (evaluating endothelium-independent vasodilation, EIDV) and during reactive hyperaemia by venous occlusion plethysmography. RESULTS: Age was inversely related to EDV (r = - 0.41, P < 0.05 in men; r = - 0.61, P < 0.01 in women) and maximal FBF during reactive hyperaemia in both men and women. EIDV was significantly related to age in an inverse way in women only. EDV was more pronounced in females than in males before menopause (48 +/- 3 SD years, 635 +/- 186 vs. 502 +/- 269% in males, P < 0.05), but similar in women and men thereafter (374 +/- 141 vs. 370 +/- 185% in men). The slope of the regression line for the relationship between age and EDV was flatter in premenopausal than in postmenopausal women (- 2.3 vs. - 6.4), whilst this slope was similar in younger and older men (- 5.5 vs. - 5.3). In multiple regression analysis, fasting blood glucose levels and the waist/hip ratio remained the only significant predictors of EDV in men (P < 0.01 for both), whilst age was the only significant independent predictor of EDV in women (P < 0.01). CONCLUSION: The interplay between age and metabolic factors as determinants of endothelial function is different in healthy men and women.

Adult↗

Insulin-mediated vasodilation and glucose uptake are independently related to fasting serum nonesterified fatty acids in elderly men.

OBJECTIVES: To investigate candidate predictors for insulin sensitivity in healthy elderly males, with special reference to the influence of insulin-mediated skeletal muscle blood flow and serum nonesterified fatty acids (NEFA). SUBJECTS: From the participants in a health survey of 70-year-old males, focusing on cardiovascular risk factors, a subgroup of 46 men was sampled. Only men who declared themselves healthy and without medication were included. INTERVENTIONS: Insulin sensitivity was measured with the euglycaemic hyperinsulinaemic clamp. Leg blood flow was measured before and during the clamp, using the Doppler ultrasound technique. RESULTS: Hyperinsulinaemia [steady-state plasma insulin 105(15) mU L-1] increased leg blood flow by 10% (P < 0.004). When tested in bivariate analysis incremental leg blood flow was only significantly related to the serum NEFA concentration (r = - 0.38, P < 0.01) amongst a number of measured variables. Insulin-mediated glucose disposal was related to body mass index (BMI) (r = -0.49, P = 0. 0006), waist/hip ratio (r = - 0.31, P = 0.036), NEFA (r = - 0.50, P = 0.0004) and heart rate (r = - 0.34, P = 0.02). In multivariate analysis only BMI and NEFA remained significantly related to whole-body glucose uptake. CONCLUSIONS: The study demonstrates that in elderly men BMI and fasting serum NEFA but not insulin-induced vasodilation are related to insulin sensitivity. High fasting levels of NEFA relate to both impaired insulin-mediated vasodilation and impaired glucose disposal, respectively. These two insulin actions were not interrelated, however, a finding which may indicate dissociated mechanisms.

Aged↗

Endothelial vasodilatory dysfunction in primary hyperparathyroidism is reversed after parathyroidectomy.

BACKGROUND: Primary hyperparathyroidism (HPT) is accompanied by hypertension and a cardiovascular mortality. Impaired endothelium-dependent vasodilatation (EDV) occurs in hypertension but has not been fully investigated in HPT despite the vasoactive influences of parathyroid hormone. METHODS: Twenty-five HPT patients and 25 normocalcemic control subjects, matched for age and gender, underwent forearm venous occlusion plethysmography. EDV and endothelium-independent vasodilatation (EIDV) were evaluated during local infusion of metacholine (2 and 4 micrograms/min) and nitroprusside (5 and 10 micrograms/min), respectively. The endothelial function index was calculated as the ratio of forearm blood flows during the high doses of metacholine and nitroprusside. Ambulatory 24-hour blood pressures and thickness of the intima-media complex of the carotid arteries were also measured; the latter is considered an early marker of atherosclerosis. RESULTS: Endothelial function index was lower in the HPT patients compared with control subjects (1.01 +/- 0.26 vs 1.27 +/- 0.31, P = .003). Reinvestigation 10 months after parathyroidectomy showed normalization of the index (1.31 +/- 0.39, P = .01) due to a numeric increase in EDV and decrease in EIDV. The carotid intima-media thickness and blood pressure were similar in the groups and unaltered postoperatively. CONCLUSIONS: Endothelial vasodilatory dysfunction is another indicator of the vascular disturbance of HPT and can be normalized by parathyroidectomy.

Aged↗

Endothelin plays an important role in the endothelium-dependent vasodilatation in the human forearm.

UNLABELLED: Endothelium-dependent vasodilatation (EDV) in humans has been evaluated mainly by local infusion of a muscarinic-receptor agonists in the forearm. It has been postulated that the function of the vasodilator nitric oxide (NO) can be evaluated with this technique. However, the role of the vasoconstrictor endothelin in this model has not been investigated. METHODS: Ten male hypertensive and seven male normotensive subjects were subjected to measurements of forearm blood flow (FBF) by venous occlusion plethysmography during local intra-arterial infusion of metacholine (4 microg/min) or nitroprusside (10 microg/min). In parallel, forearm venous plasma endothelin (ir-ET) was determined. RESULTS: Metacholine and nitroprusside increased FBF 2.3 and 2.2 times the baseline level (6.6+/-2.8 SD ml/min/100 ml tissue) in hypertensive subjects and 5.1 times the baseline level (2.7+/-3.0 ml/min/100 ml tissue) for both drugs in the normotensive subjects. None of the drugs induced any significant changes in ir-ET levels in any of the groups (baseline 1.5+/-0.4 pmol/l in hypertensive and 1.1+/-1.2 pmol/l in normotensive subjects). However, in the hypertensive subjects, the individual change in venous ir-ET levels during infusion with metacholine, but not with nitroprusside, was inversely related to the degree of vasodilatation induced by this agent (r = -0.71, p < 0.02). A similar correlation coefficient (r=-0.69) was found in healthy subjects. CONCLUSION: Muscarinic-receptor-agonist-stimulated vasodilatation in the human forearm, thought mainly to reflect NO synthesis, was inversely related to the change in endothelin levels, suggesting an important role for this endothelium-derived vasoconstrictor in this model of EDV.

Adult↗

Circulating ionized calcium and parathyroid hormone levels following coronary artery by-pass surgery.

In critically ill patients, hypocalcaemia is a common finding. Also variable derangements in the normally tight Ca2+-mediated control of the parathyroid hormone (PTH) secretion have been found. Utilizing coronary artery by-pass grafting (CABG) as a standardized model of severe trauma, 18 patients underwent determinations of blood levels of calcium, magnesium (Mg), ionized calcium (Ca2+), serum levels of intact PTH, procalcitonin (PCT) and the proinflammatory cytokines tumour necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6). Samples were collected before, directly after, the morning after and 5 days after surgery. A significant, but minor, decrease in blood Ca2+ levels (mean 0.04 mmol/L, p<0.05) was seen shortly after CABG, not accompanied by any significant change of serum PTH levels. This alteration of the Ca2+ control of the steady-state PTH levels contrasted with the maintenance of the PTH secretory response to a sequential citrate and calcium infusion (CiCa clamp), which was normal in two patients evaluated in the morning following surgery. Serum Mg levels were transiently increased after operation (+0.25 mmol/L, p<0.001) and correlated to the TNF-alpha (r=0.62, p <0.01) and PCT (r=0.67, p < 0.006) levels in the morning after surgery. Serum levels of IL-6 and TNF-alpha were significantly (p < 0.0001) increased immediately after surgery, while the peak in serum PCT levels (p < 0.001) occurred in the morning after CABG. Serum PTH levels correlated positively with IL-6 (r=0.68, p<0.008) 5 days after surgery. In conclusion, CABG caused a decrease in ionized calcium levels without a rise in steady-state PTH levels, but rapid changes in Ca2+ during CiCa clamping revealed a normal PTH secretory response. These findings might relate to elevated serum Mg levels, while a direct action of TNF-alpha or IL-6 on the PTH release seem less possible.

Aged↗