Hemodynamic effects, nitric oxide

Hoeper MM, Olschewski H, Ghofrani HA, Wilkens H, Winkler J, Borst MM, Niedermeyer J, Fabel H, Seeger W, Grimminger F, et al. A comparison of the acute hemodynamic effects of inhaled nitric oxide and... 

In another study the acute response to inhaled nitric oxide and high doses of oral nifedipine or verapamil was assessed in 33 consecutive patients with primary pulmonary hypertension (2). Ten patients responded acutely to nitric oxide, nine of whom responded acutely to calcium channel blockers, without any complications. The other 23 patients failed to respond to nitric oxide and calcium channel blockers. In these non-responders there were nine serious adverse effects with calcium channel blockers. There was no clinical or baseline hemodynamic feature that predicted the acute vasodilator response. Long-term oral treatment with calcium channel blockers was restricted to the nine acute responders, and there was a sustained clinical and hemodynamic improvement in only six patients. It was concluded that nitric oxide may be used as a screening agent for safely identifying patients with primary pulmonary hypertension who may benefit from long-term treatment with calcium channel blockers. 

Cases A, Haas J, Burnett JC, Romero JC Hemodynamic and renal effects of acute and progressive nitric oxide synthesis inhibition in anesthetized dogs. Am.J.Physiol Regul.Integr.Comp Physiol 280 R143-R148, 2001... 

The mechanism of the acute kidney injury is thought to be multifactorial and similar to other cases of myoglobinuric renal failure [118, 121-126]. These factors include obstruction of tubules, toxic effects of the pigment or iron on renal tubular cells and altered hemodynamics in association with inhibition of the vasodilator nitric oxide by myoglobin. Experimental animals exposed to heme pigment have increases in the renal synthesis of both heme oxidase and ferritin [125]. This allows for more rapid heme degradation and greater sequestration of potentially toxic iron by the tubular cells [125]. Whether narcotics or the hypotensive, hypoxic environment associated with rhabdomyolysis interfere with these protective effects of the kidney is unknown. 

Bradykinin plays an important role in the regulation of renal hemodynamics. The effects of bradykinin on isolated perfused rabbit afferent arterioles and the mechanisms of action of bradykinin was studied [275]. It was concluded that 1) bradykinin has a biphasic effect on afferent arterioles 2) both dilation and constriction may be mediated by bradykinin B2 receptors and 3) the mechanisms of vasodilation and vasoconstriction are due to cyclooxygenase products, not nitric oxide. 

Robertson, F. M., Offner, P. ]., Ciceri, D. P., Becker, W. K., and Pruitt, B. A., Jr. (1994). Detrimental hemodynamic effects of nitric oxide synthase inhihition in septic shock. Arch. Surg. 129, 149-156. 

Bigatello, L. M., Hurford, W. E., Kacmarek, R. M., Roberts, J. D., and Zapol, W. M. (1994). Prolonged inhalation of low levels of nitric oxide in patients with severe ARDS Effects on pulmonary hemodynamics and oxygenation. Anesthesiology 80, 761-770. 

Rovira, L, Chen, T.-Y., Winkler, M., Kawai, N., Bloch, K. L., and Zapol, W. M. (1994). Effects of inhaled nitric oxide on pulmonary hemodynamics and gas exchange in an ovine model of ARDS. J. Appl. Physiol. 76, 345-355. 

Kinsella, J. P., McQueston, J. A., Rosenberg, A. A., and Abman, S. H. (1992). Hemodynamic effects of exogenous nitric oxide in ovine transitional pulmonary circulation. Am. J. Physiol. 263, H875-H880. 

FIGURE 7 Percentage changes in hemodynamic variables from baseline values during a 15-rain administration of inhaled nitric oxide in postoperative neonates with no residual anatomic obstruction to pulmonary blood flow. There was a marked pulmonary vasodilating effect. HR, Heart rate Cl, cardiac index BP, systemic artery pressure SVR, systemic vascular resistance PAP, mean pulmonary artery pressure PVR, pulmonary vascular resistance. 

---