Development of neurogenic pulmonary edema at different grades of intracranial pressure in cats.

Development of neurogenic pulmonary edema (NPE) subsequent to increased intracranial pressure (ICP) was evaluated in an experimental model in cats. Experiments were conducted in chloralose anaesthetised animals, either on spontaneous respiration or on intermittent positive pressure ventilation. Hemodynamic parameters i.e., mean arterial pressure (MAP) and heart rate (HR) were continuously monitored. Pulmonary artery/right ventricular systolic pressure was recorded in cats on spontaneous respiration. Increase in ICP for 180 minutes caused an increase in extravascular lung water (EVLW) content in both spontaneously breathing and artificially ventilated animals. In spontaneously breathing animals EVLW to blood free dry weight ratio (EVLW/BFDW) was 3.95 +/- 0.16 and 4.96 +/- 0.16 at ICP 40 and 80 mm Hg respectively while in animals on artificial ventilation, at 40, 60, 80 and 100 mm Hg ICP, it was 3.88 +/- 0.11, 4.09 +/- 0.10, 4.50 +/- 0.13 and 5.03 +/- 0.17 respectively. These values were significantly greater (P < 0.05) as compared to that in sham operated animals (3.43 +/- 0.10). This was accompanied by rise in MAP, HR and pulmonary artery pressure. The study establishes the graded development of NPE, the severity of which is proportional to the levels of ICP.

Changes in circulatory biogenic amines during head-up tilt testing in neurocardiogenic syncope.

The pathogenesis of neurocardiogenic syncope is not completely understood. To examine the possible role of biogenic amines in patients with neurocardiogenic syncope, 18 consecutive patients (age 30 +/- 13 years, 15 males, 3 females) of unexplained syncope were subjected to Head-Up Tilt Testing (HUTT). Blood was sampled by an indwelling cannula at baseline, end of tilt test (or at syncope) and 1 min after returning to the supine position. Biogenic amines, epinephrine (E), norepinephrine (NE), serotonin (5-HT) and their metabolites, homovanillic acid (HVA) and 5-hydroxy indole acetic acid (5-HIAA), were measured in the serum after serial organic phase extraction by high-performance liquid chromatography (HPLC) using ultraviolet detection at a wavelength of 280 nm. Twelve patients were found to be HUTT negative while 6 patients were HUTT positive. Baseline E, NE and 5-HT levels were significantly greater in the HUTT positive patients [E 510 +/- 154 versus 302 +/- 96 pg/ml (p < 0.01), NE 253 +/- 99 versus 159 +/- 62 pg/ml (p < 0.05), 5-HT 174 +/- 32 versus 118 +/- 22 pg/ml (p < 0.01)]. E and HVA levels at the end of the test were significantly higher in HUTT positive patients [E 788 +/- 268 versus 465 +/- 119 pg/ml (p < 0.01), HVA 308 +/- 91 versus 112 +/- 12 pg/ml (p < 0.001)]. A significantly greater rise of E from the baseline was observed in HUTT positive patients (510 +/- 154 versus 112 +/- 12 pg/ml (p < 0.01)]. The increase in the levels of E and HVA both at baseline and after the tilt test, without a corresponding rise in NE levels indicates enhanced activity of the adrenomedullary axis which is not paralleled by NE release from sympathetic nerve endings in patients of neurocardiogenic syncope.