Upper extremity peripheral venous pressure measurements accurately reflect pulmonary artery pressures in patients with cavopulmonary or Fontan connections.

After the bidirectional cavopulmonary or Fontan operation, the physiologic consequence is passive flow of the systemic venous return to the pulmonary arteries. Knowledge of pulmonary artery pressure (PA) is valuable in the management of these patients, and obtaining this information without the need for a central line or cardiac catheterization would be advantageous. The aim of this study was to evaluate the correlation between upper extremity peripheral venous (PV) pressures and PA or superior vena cava (SVC) pressures in patients who have undergone cavopulmonary or Fontan connections. During cardiac catheterization, 19 patients with complex cyanotic heart disease who had undergone a cavopulmonary shunt or Fontan procedure were studied. Simultaneous pressure measurements were obtained from the peripheral intravenous line placed prior to the procedure and the SVC or PA. The mean pressures were compared. The mean PV pressure was 17.5 +/- 5.6 mmHg. The mean SVC or PA pressure was 16.1 +/- 5.4 mmHg. The mean difference was 1.5 +/- 1.5 mmHg ( p < 0.001). The correlation coefficient PV to SVC or PA pressure was 0.97 ( p < 0.001). PV pressure measurements taken from an upper extremity accurately reflect PA pressures in patients who have undergone a cavopulmonary shunt or Fontan procedure.

Beneficial effect of SPM-5185, a cysteine-containing nitric oxide donor, in rat carotid artery intimal injury.

We studied the effects of an organic nitric oxide (NO) donor SPM-5185 in a rat carotid artery intimal injury model. Seven days after injury, the two end segments of the injured carotid arteries were studied for endothelial release of NO, and the middle segments were used for histological measurement of the intimal-to-medial (I/M) ratio and scanning electron microscopy of the luminal surface. The NO donor SPM-5185 or its non-NO-donating control compound SPM-5267 were infused intravenously at 30 micrograms/d. Full vasorelaxant responses of rat carotid arterial rings were obtained with the endothelium-dependent vasodilators acetylcholine (ACh), A23187, and the endothelium-independent vasodilator acidified NaNO2 in sham-operated control rings. Impaired relaxation occurred with 10 mumol/L ACh and 1 mumol/L A23187 in injured rings but not in rings infused with SPM-5185 for 7 days. Relaxation to 100 mumol/L acidified NaNO2 was not significantly different among any of the groups, indicating a normal vascular smooth muscle response after intimal injury. Morphometric analysis of injured carotid arteries given vehicle and SPM-5267 showed marked intimal thickening with an average I/M ratio of 0.78 +/- 0.03 and 0.74 +/- 0.05, respectively. SPM-5185 markedly attenuated intimal thickening, resulting in an I/M ratio of 0.13 +/- 0.03 (P < .01 from vehicle), representing an approximately 82% inhibition of intimal thickening. SPM-5185 infusion resulted in accelerated regeneration of endothelial cells on the intimal surface at 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxia induces endothelial cells to increase their adherence for neutrophils: role of PAF.

We investigated the interactions of polymorphonuclear neutrophils (PMN) and endothelial cells in myocardial ischemia using a hypoxia model. We exposed porcine aortic (PAEC) and porcine coronary microvessel (PCMEC) endothelial cells to 2% O2 for 2 h (PO2 = 53 mmHg) and measured the adherence of unstimulated neutrophils (PMN) to both control and hypoxia-conditioned endothelial cell monolayers. Hypoxia conditioning increased PMN adherence to PAEC and PCMEC by 51 and 101%, respectively, above control levels. The increase in PMN adhesion to PAEC was associated with a threefold increase in endothelial cell-associated platelet-activating factor (PAF) compared with control PAEC. The conditioned media from PAEC exposed to hypoxia also contained sixfold more PAF than control conditioned media, and it activated PMN to become adherent to untreated PAEC. The hypoxia-induced PAEC adhesion response was inhibited by preincubating PMN with the specific PAF receptor antagonist, L-659,989. We conclude that PAF is produced by cultured endothelial cells in response to hypoxia and that PAF generation is chiefly responsible for the increased adherence properties of hypoxia-conditioned endothelial cells. This response may play a major role in regulating PMN margination during myocardial ischemia.