Non-invasive measurement of the haemodynamic effects of inhaled salbutamol, intravenous L-arginine and sublingual nitroglycerin.

AIMS: To examine the effects of salbutamol and L-arginine, two compounds acting largely on the endothelium, and the endothelium-independent agent nitroglycerin on blood pressure, arterial compliance, cardiac function and vascular resistance. METHODS: Continuous radial pulse wave analysis, whole-body impedance cardiography, and plethysmographic blood pressure from fingers in the supine position and during head-up tilt were recorded in nine healthy subjects. Data were captured before and after L-arginine (10 mg mg(-1) min(-1)) or saline infusion, salbutamol (400 microg) or placebo inhalation, and sublingual nitroglycerin (0.25 mg) or placebo resoriblet. RESULTS: The results of all measurements were comparable before drug administration. The effects of inhaled salbutamol were apparent in the supine position: systemic vascular resistance (-9.2 +/- 2.6%) and augmentation index (-4.0 +/- 1.5%) decreased, and heart rate (8.6 +/- 2.5%) and cardiac output (8.8 +/- 3.1%) increased. L-arginine had no clear effects on supine haemodynamics, but during head-up tilt blood pressure was moderately decreased and reduction in aortic reflection time prevented, indicating improved large arterial compliance. Nitroglycerin reduced supine vascular resistance (-6.7 +/- 1.8%) and augmentation index (-7.4 +/- 1.6%), and increased cardiac output (+9.2 +/- 2.7%). During head-up tilt, nitroglycerin increased cardiac output (+10.6 +/- 5.6%) and heart rate (+40 +/- 7.5%), decreased vascular resistance (-7.8 +/- 5.8%) and augmentation index (-18.7 +/- 3.2%), and prevented the decrease in aortic reflection time. CONCLUSIONS: Inhaled salbutamol predominantly changed supine haemodynamics, whereas the moderate effects of L-arginine were observed during the head-up tilt. In contrast, small doses of nitroglycerin induced major changes in haemodynamics both supine and during the head-up tilt. Altogether, these results emphasize the importance of haemodynamic measurements in both the supine and upright positions.

Pituitary apoplexy following endoscopic nasal surgery: A case report.

Pituitary apoplexy develops as a consequence of acute haemorrhage and/or infarction in a pre-existing pituitary adenoma. Typical symptoms include sudden onset headache, visual acuity/field defects, and ocular palsies. We report a male patient with a known pituitary macroadenoma who underwent a right-sided endoscopic nasal surgery. Preoperatively, thickening of sphenoid mucosa was seen in computed tomography and magnetic resonance imaging. The patient developed pituitary apoplexy postoperatively. The presented report indicates that in patients with a pituitary adenoma, nasal surgery - like any other kind of surgery - is a possible precipitating factor for pituitary apoplexy. Isolated thickening of sphenoid mucosa is associated with pituitary apoplexy. It may also precede an apoplectic event.

Prostacyclin and thromboxane A2 production in nitric oxide-deficient hypertension in vivo. Effects of high calcium diet and angiotensin receptor blockade.

The effects of chronic nitric oxide deficiency on prostacyclin and thromboxane A(2) production in vivo are unknown. Therefore, we treated rats with N(G)-nitro-L-arginine methyl ester (L-NAME), and used losartan and high calcium diet as antihypertensive treatments. Forty eight Wistar rats were divided into six groups: control; losartan (20mgkg(-1)day(-1)); high calcium diet (dietary calcium elevated from 1.1% to 3%); L-NAME (20mgkg(-1)day(-1)); losartan+L-NAME and high calcium diet+L-NAME. Prostacyclin and thromboxane A(2) production were measured after eight weeks as urinary 2,3-dinor-6-keto-PGF(1alpha) and 11-dehydro-TXB(2), respectively. Both the high calcium diet and losartan reduced blood pressure in L-NAME hypertension. Chronic nitric oxide deficiency did not modulate prostacyclin production but it nearly doubled thromboxane A(2) production in vivo. This effect was not influenced by lowering of blood pressure by blockade of angiotensin II type 1 receptors. Independent of the level of blood pressure and blockade of nitric oxide synthesis the high calcium diet decreased prostacyclin production by one third and increased thromboxane A(2) production almost two-fold in vivo.