Medical Inspection – Health Blog

The benefits of lung transplantation are compro­mised by two common acute complications: acute lung rejection, and opportunistic infection. The lungs are a common site for these disorders. Chronic lung rejection appears to cause obliterative bronchio­litis, which has been reported to cause disability and death in up to 50 percent of long-term heart-lung transplant (HLT) recipients.

Various clinical investigations have been used to monitor the lungs for acute rejection and infection. They include chest radiology, measurement of “”Tc- DTPA clearance of the lung, pulmonary function testing, and more recently transbronchial lung biopsy (TBB). Transbronchial lung biopsy is currently the most sensitive and specific test for lung rejection and allows the distinction between infection and rejection to be made. However, it required fiberoptic bron­choscopy which, while easily repeated, is not a pro­cedure that can be undertaken daily.

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Role of HPV During Exercise

At rest, nifedipine diverted blood flow to poorly ventilated lung units (Fig 1 and 3). This observation strongly suggests release of HPV and is in keeping with previous reports in COPD. After releasing HPV, the increase in Ppa seen during exercise was blunted and the severity of pulmonary hypertension was lowered (Fig 2), again in accordance with former investigations. To our knowledge, however, the ef­fects of this lowered vascular tone on the adaptation of Va/Q mismatching to exercise in COPD have not been previously investigated. Our results show that the dispersion of the blood flow distribution (Logs_D Q) was always higher after than before nifedipine, either at rest or during exercise (Table 2 and Fig 3). Read More…

Our study documents that exercise can improve Va/Q mismatching in COPD. In addition, it confirms that nifedipine releases HPV in these patients and lowers right ventricular afterload during exercise. To our knowledge, however, no previous information regarding the role of HPV in modulating gas exchange during exercise in COPD has yet been raised. Our results show that the release of HPV induced by nifedipine clearly interferes with the ability of the pulmonary circulation to distribute blood flow more efficiently both at rest and during exercise (Fig 3). However, the latter has a small functional effect since, even after nifedipine, exercise reduced the overall amount of Va/Q mismatch. This observation suggests that the role of HPV in modulating gas exchange during exercise in COPD is probably minor, and that most of the Va/Q improvement seen under these conditions is due to improvement in the ventilation distribution. To clarify the more relevant aspects of this investigation, the effects of exercise on gas ex­change at baseline (before nifedipine) and the role of HPV in modulating gas exchange during exercise will be discussed separately.

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Exercise Before Nifedipine (vs Rest Before Nifedipine)

Exercise Vo₂ (872 ml/min) averaged 53 ±5 percent of maximal predicted. This represented a substantial level of exercise for these patients, as it is shown by the significant decrease in arterial pH and base excess (BE) (Table 2). During exercise, pulmonary hyperten­sion became severe and both TPVR (Table 2) and RVSWI increased (8.2±0.5 to 23.0±1.7 g-m/m², p<0.001). Even though Pa0₂ showed a trend to fall (76 to 68 mm Hg, p = 0.07), because PaC0₂ increased simultaneously (39 to 43 mm Hg, p<0.001), P(A-a)0₂ did not change (28 to 31 mm Hg). The Vd/Vt fell from 50 to 42 percent (p<0.001). Exercise reduced Va/Q mismatching as estimated either by the significant decreases in Log Q and Log V or DISP R-E* (Table 2 and Fig 1 and 3). The Q shifted toward higher values (p<0.005) but V did not change.

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Airflow obstruction was severe in all but patient 8, and all but one subject (patient 2) showed marked air trapping (Table 1). Hyperinflation was noticed only in patient 5. The Deo was reduced in four subjects (patients 2, 3, 5, and 6) (Table 1). Table 2 provides the metabolic, hemodynamic, and gas exchange data at rest and during exercise, before and after nifedipine. Nifedipine was well tolerated by all the patients and did not produce any symptomatic adverse side effect.

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Protocol

The protocol was approved by the Hospital Clinic-Facultat de Medicina Research Committee on Human Investigations. Patients were allowed to continue taking their usual steroid regimen (if any), but treatment with all oral or inhaled bronchodilators was withdrawn 24 hours before the study. Specifically, patients were not receiving additional medication that could have either vasoactive or bron- choactive effects. After the patient had fasted overnight and without premedication, pulmonary and systemic arterial catheterization were performed. Forty-five minutes after starting the inert gas infusion, measurements of pulmonary and systemic hemodynamic variables and respiratory and inert gas exchange parameters were taken at rest. Then, exercise was begun on a cycle ergometer (E. Jaeger) at a power output (33 ±8 W) equivalent to 50 to 60 percent of their maximal tolerated work load (which had been quantified on a previous day), and a second set of hemodynamic and gas exchange measurements was obtained approximately ten minutes later. The patients were allowed to rest for 15 to 30 minutes until pulmonary and systemic hemodynamic variables and respira­tory gas exchange parameters had returned to resting conditions. Nifedipine (20 mg) was then given sublingualis and resting and exercise measurements were repeated as before (at 45 minutes and 1 h after nifedipine, respectively). Read More…