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PubMedDate not supplied

Effects of lidocaine on pulmonary circulation during hyperoxia and hypoxia in the dog.

BACKGROUND AND OBJECTIVES: High concentrations of lidocaine have been found to cause pulmonary vasoconstriction and low concentrations (0.5-0.9 microgram/mL) to cause reversal of nitrous oxide-induced depression of hypoxic pulmonary vasoconstriction. This study was undertaken to examine the effects of high concentrations of lidocaine on pulmonary circulation during hyperoxic and hypoxic ventilation. METHODS: With use of cross-circulation consisting of ventilation and constant-flow perfusion of the left lower lobe (LLL) independently of all other lobes of the dog lung under nitrous oxide and halothane anesthesia, lidocaine was infused into the inflow system, so that plasma lidocaine concentrations in the inflow blood were maintained at either 5, 10, 20, 40, 70, or 140 micrograms/mL during ventilation with 50% oxygen or 3% oxygen. Mean arterial and venous pressures in the LLL (PAPLLL and PVPLLL), airway pressure of the LLL, and blood gas in LLL inflow and outflow were measured. RESULTS: High plasma concentration of lidocaine (140 micrograms/mL) in the LLL inflow produced a significant increase in PAPLLL during hyperoxia, while PAPLLL did not change significantly at the 5-70-micrograms/mL lidocaine concentration. In LLL outflow blood, PO2 increased significantly following a 140 micrograms/mL lidocaine infusion during hyperoxia, while in LLL inflow blood, PO2 did not change. The airway pressure of LLL also did not change. During hypoxia, hypoxic pulmonary vasoconstriction did not occur, and lower plasma concentrations of lidocaine (40-70 micrograms/mL) significantly constricted the lobar vessels. In addition, lidocaine at the 140-micrograms/mL concentration constricted the upstream vessels (presumably the lobar arteries) more strongly than the lobar veins during hypoxia. CONCLUSIONS: Extremely high concentrations (140 micrograms/mL) but not low concentrations (5-70 micrograms/mL) of lidocaine produced pulmonary vasoconstriction and reduced shunt. Lower concentrations of lidocaine constricted the hypoxic lobar vessels.

Anesthetics, Local↗
PubMed1984

Prostaglandins and related compounds in the perinatal pulmonary circulation.

It is clear that the products of arachidonate metabolism (prostaglandins, leukotrienes, thromboxanes, etc) are involved in both normal and pathophysiologic pulmonary vascular responses. However, the precise roles of these compounds in the various pulmonary vasoregulatory processes remain unclear. This paper reviews the synthetic pathways for these compounds and summarizes the current state of knowledge regarding their involvement in the perinatal pulmonary circulation. Data regarding endogenous compounds as well as the effects of exogenously administered agents are presented.

Animals↗
PubMed2005

Role of endothelins and nitric oxide in the pulmonary circulation of perinatal lambs during hyperoxia and hypoxia.

Endothelins (ET) have opposite vascular effects mediated through different receptors: ET(A) receptors mediating vasoconstriction and ET(B) receptors mediating vasoconstriction as well as vasodilation. The role of ET in acute hypoxic pulmonary vasoconstriction (HPV) was studied after dual ET receptor blockade with bosentan and nitric oxide (NO) synthase inhibition with nitro-L-arginine (L-NA). We started from the hypothesis that ET antagonism may inhibit HPV but, if not, would do so after NO synthase inhibition. HPV was evaluated in anesthetized lambs, with an intact pulmonary circulation, by the increase in the mean pulmonary artery pressure (Ppa) minus occluded Ppa (Ppao) gradient in response to hypoxia (inspiratory oxygen fraction of 0.1) at different levels of pulmonary flow (multipoint pressure/flow relationships). ET receptor antagonism decreased pulmonary and systemic vascular tone both in hyperoxia and hypoxia. ET antagonism had no effect on HPV. NO synthase inhibition increased pulmonary vascular tone more in hypoxia than in hyperoxia so that HPV was enhanced. After L-NA, bosentan still decreased pulmonary vascular tone in hypoxia but did not affect the magnitude of HPV. The present results suggest that ET and NO are involved in the regulation of basal pulmonary vascular tone. Furthermore, the vasodilator effect of bosentan persisted in the presence of NO synthase inhibition, suggesting a non NO-dependent vasodilator mechanism. The results from these experiments are in agreement with the idea that ET do not play a major role in HPV in the perinatal lamb, even when it is enhanced by NO synthase inhibition.

Animals↗
PubMed1989

Purinoceptors in the pulmonary circulation of the rat and their role in hypoxic vasoconstriction.

1. P2-purinoceptors have been characterized in the systemic circulation of a variety of species but little is known about their nature in the pulmonary vasculature. 2. In the isolated, blood perfused and ventilated lung of the rat the P2x selective analogues alpha,beta-methylene ATP(alpha,beta-meATP) (25 micrograms) and beta,gamma-methylene ATP (400 micrograms) caused a rise in pulmonary artery pressure (127 +/- 32% and 110 +/- 23% increase respectively, n = 6), demonstrating the existence of vasoconstrictor P2 receptors in the pulmonary circulation. 3. Repeated boluses of alpha,beta-meATP resulted in complete desensitization of the constrictor response to beta,gamma-meATP, but a small vasodilator response remained indicating unopposed stimulation of P2y receptors. The desensitization by alpha,beta-meATP had no effect on angiotensin II-induced vasoconstriction. 4. After desensitization of the vasoconstrictor P2 receptors with alpha, beta-meATP, hypoxic pulmonary vasoconstriction remained intact, indicating that these receptors are not involved in this response.

Adenosine Triphosphate↗
PubMed1987

Myocardium as emboli in the systemic and pulmonary circulation.

Myocardium as emboli is a decidedly rare phenomenon. Only three such examples were identified among 8033 consecutive autopsies performed over a ten-year period, 1976 to 1985, an incidence of 0.037%. In two of these three cases, myocardial emboli occurred in the systemic (coronary) circulation. The source of emboli was attributed to postinfarction ruptured ventricular septum in one patient, and to traumatized myocardium during surgical reconstruction of a univentricular heart (single ventricle) in the other. In the third case, myocardial emboli occurred in the pulmonary circulation, originating from excavation of the infundibulum at surgical correction of pulmonary atresia. A literature search has uncovered only five previously reported cases of myocardium as emboli, all occurring in the systemic circulation. To my knowledge, there has not been any previous report of myocardial emboli in the pulmonary circulation.

Adult↗
PubMed1988

[Hemodynamics of pulmonary circulation in hypertension based on data from radionuclide studies].

The authors presented the results of a combined radionuclide study of the state of pulmonary hemodynamics in patients with essential hypertension. Altogether 132 patients were investigated. Radiocardiography, perfusion scintigraphy and a study of the regional pulmonary blood flow using radioactive Xe were conducted. An analysis of the results has shown that in some patients pulmonary hypertension develops even at early stages of the disease and is particularly marked in stages IIB-III. The mechanism of development of pulmonary hypertension depended at each stage on the interrelationship and time course of indices that characterized pulmonary circulation, and was of different nature. Hemodynamic disorder was manifested in blood mass redistribution from the lower lung regions to the upper ones, slowing down of rate parameters and a raise of pulmonary vascular resistance.

Hemodynamics↗
PubMed1992

Hemodynamic effects of ibopamine on the pulmonary circulation and right ventricular performance in patients with chronic obstructive pulmonary disease.

We have studied the effects of ibopamine, an oral dopamine derivative, on pulmonary hemodynamics and blood gas values when given as a single oral dose (100 mg) to patients with severe hypoxic chronic obstructive pulmonary disease. A small but significant increase in mean pulmonary arterial pressure from 29 +/- 8 to 32 +/- 7 mm Hg (p < 0.01) was noted 30 min after ibopamine was given associated with a small increase in cardiac index. No other consistent hemodynamic changes were observed, and no alteration in blood gas values or oxygen saturation occurred. These results do not indicate a role for ibopamine in the treatment of patients with hypoxic chronic obstructive pulmonary disease and pulmonary hypertension, but, in addition, do not indicate any major deleterious effects of ibopamine on pulmonary hemodynamics or blood gas values in such patients.

Administration, Oral↗