Pulmonary vasoregulation by arginine vasopressin in conscious, halothane-anesthetized, and pentobarbital-anesthetized dogs with increased vasomotor tone.

BACKGROUND: Arginine vasopressin (AVP) is an important "stress" hormone that is known to play a key role in cardiovascular homeostasis of the systemic circulation. In contrast, the effects of AVP on the pulmonary circulation have not been extensively investigated, and the extent to which general anesthesia alters the pulmonary vascular response to AVP is entirely unknown. Our first objective was to assess the effects of AVP on the pulmonary vascular pressure-flow relation in chronically instrumented conscious dogs in the setting of an acute elevation in pulmonary vasomotor tone. Our second objective was to investigate the effects of halothane and pentobarbital anesthesia on the pulmonary vascular response to AVP after inducing the same degree of pulmonary preconstriction achieved in the conscious state. METHODS: Conditioned, mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relation. LPQ plots were generated by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure minus left atrial pressure) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder around the right pulmonary artery, which directed total pulmonary blood flow through the left pulmonary circulation. LPQ plots were generated in conscious (n = 10), halothane-anesthetized (n = 9) and pentobarbital-anesthetized (n = 7) dogs. In each condition, LPQ plots were measured at baseline, during the intravenous administration of the thromboxane analog U46619 and during the cumulative administration of AVP (2-19 ng.kg-1.min-1, intravenous) in the presence of U46619 preconstriction. RESULTS: U46619 caused acute pulmonary vasoconstriction (P < 0.01) in conscious dogs. In this setting of U46619 preconstriction, AVP caused pulmonary vasodilation (P < 0.05) in the conscious state. In contrast, despite identical levels of U46619 preconstriction, the pulmonary vasodilator response to AVP was either reversed to vasoconstriction (P < 0.05) or abolished during halothane and pentobarbital anesthesia. CONCLUSIONS: These results indicate that AVP exerts a significant pulmonary vasodilator response in the setting of acute pulmonary vasoconstriction in conscious dogs. However, the pulmonary vascular response to this stress hormone is markedly altered during halothane and pentobarbital anesthesia.

Neurohumoral regulation of the pulmonary circulation during circulatory hypotension in conscious dogs.

We investigated the effects of circulatory hypotension (HYPO) on the left pulmonary vascular pressure-flow relationship in chronically instrumented conscious dogs and the role of five neurohumoral mechanisms in either mediating or modulating the response to this stimulus. HYPO was induced by acute (approximately 15-min) inflation of a hydraulic occluder implanted around the thoracic inferior vena cava, which decreased systemic arterial pressure to approximately 55 mmHg. HYPO resulted in active pulmonary vasoconstriction (53-66%; P < 0.01) in intact conscious dogs. Sympathetic alpha 1-adrenoreceptor block reduced (P < 0.01) the magnitude of HYPO-induced pulmonary vasoconstriction by 91-99%. Neither sympathetic beta-adrenoreceptor block nor cholinergic muscarinic receptor block had any significant effect on the magnitude of HYPO-induced pulmonary vasoconstriction. Surprisingly, angiotensin II receptor block increased (P < 0.05) HYPO-induced pulmonary vasoconstriction by 69-91%. In contrast, arginine vasopressin V1-receptor block reduced (P < 0.05) HYPO-induced pulmonary vasoconstriction by 34-41%. These results indicate that the pulmonary circulation of intact conscious dogs is actively regulated by three distinct neurohumoral mechanisms during HYPO. Sympathetic alpha 1-adrenoreceptor activation is the primary mediator of HYPO-induced pulmonary vasoconstriction. Angiotensin II and arginine vasopressin exert opposing pulmonary vasodilator and vasoconstrictor effects during HYPO, whereas sympathetic beta-adrenoreceptor and cholinergic muscarinic receptor activation do not appear to modulate the pulmonary vascular response to HYPO.

Amrinone and the pulmonary vascular pressure-flow relationship in conscious control dogs and following left lung autotransplantation.

BACKGROUND: Amrinone, a bipyridine compound, is known to improve left ventricular function via its positive inotropic and afterload-reducing effects. The goal of this study was to assess the efficacy of amrinone as a pulmonary vasodilator, an effect that could be beneficial in the setting of right heart failure associated with pulmonary hypertension. METHODS: Investigated were the effects of intravenous amrinone (750 micrograms/kg loading dose plus 1-20 micrograms.kg-1.min-1 maintenance dose) on the left pulmonary vascular pressure-flow (LPQ) relationship in chronically instrumented, conscious dogs. The effects of amrinone on the LPQ relationship were assessed in a series of conscious control dogs with (n = 10) and without (n = 9) acute preconstriction with the thromboxane analog U46619 and in a series of conscious dogs 2-4 weeks after left lung autotransplantation (LLA) with (n = 8) and without (n = 8) acute U46619 preconstriction. Left pulmonary vascular pressure-flow plots were generated by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure/left atrial pressure [PAP/LAP]) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder implanted around the right pulmonary artery. RESULTS: Amrinone had no effect on the baseline LPQ relationship in control dogs. U46619 caused acute pulmonary vasoconstriction. For example, PAP/LAP at left pulmonary blood flow of 70 ml.min-1.kg-1 was increased (P < 0.01) from 16 +/- 2 to 37 +/- 2 mmHg during U46619 administration. In this setting of acute preconstriction, amrinone caused pulmonary vasodilation, i.e., PAP/LAP was decreased (P < 0.05) from 37 +/- 2 to 32 +/- 2 mmHg. Left lung autotransplantation was associated with a marked shift in the LPQ relationship, indicating a chronic increase in pulmonary vascular resistance, i.e., PAP/LAP was increased (P < 0.01) from 15 +/- 2 to 32 +/- 3 mmHg. Despite the chronic increase in pulmonary vascular resistance after LLA, amrinone had no effect on the baseline LPQ relationship. However, after acute preconstriction with U46619 after LLA, amrinone caused pulmonary vasodilation, i.e., PAP/LAP was decreased (P < 0.05) from 45 +/- 4 to 39 +/- 4 mmHg. CONCLUSIONS: These results indicate that amrinone exerts a significant, although relatively modest pulmonary vasodilator influence in the setting of acute pulmonary vasoconstriction in conscious control dogs and in conscious dogs after LLA. However, amrinone did not reverse the chronic increase in pulmonary vascular resistance associated with LLA.

Anesthetic management of a morbidly obese woman with a massive ovarian cyst.

Morbid obesity affects 3% to 5% of the U.S. population and poses challenging problems to the anesthesiologist during the perioperative period. We present a unique case of the management of a morbidly obese woman complicated by a massive ovarian cyst. The major cardiopulmonary, metabolic, and technical features special to this patient population are discussed.

The difficult airway: mechanisms for effective dissemination of critical information.

The perioperative management and dissemination of critical information regarding a patient with an unexpected difficult intubation, including successful application of a difficult airway algorithm (Figure 1), are described. Documentation and dissemination of critical information include entry of patient data into an in-hospital computerized Difficult Airway/Intubation Registry, simultaneous application of a highly visible Difficult Airway/Intubation Patient Wrist Band (coded for access to computer registry), summary reports distributed to health care providers, and enrollment of the patient in the Medic Alert Foundation International's newly established category difficult airway/intubation for 24-hour access. We postulate that the widespread use of the procedures described in this report may reduce the contribution of unexpected difficult airway/intubation to anesthetic morbidity and mortality.