Using an X-ray TV system, we analyzed responses in the internal diameter (ID), flow velocity, and volume flow in small pulmonary vessels (100-600 microns ID) during unilobar hypoxia and hypercapnia in cats. In the hypoxic and hypercapnic lobes, the ID reduced in proportion to the degree of hypoxia and hypercapnia, respectively. The ID reduction was larger in the arteries than in the veins for a given stimulus. In the arteries, the ID reduced nonuniformly in the series-arranged vessels in response to both stimuli. The percentage ID reduction was maximal in the arteries of 200-300 microns ID, in which it was 21, 26, 28, and 36% with 5% O2, 0% O2, 5% CO2, and 10% CO2 inhalations, respectively. On the other hand, in the veins, uniform ID reduction occurred for a given stimulus. In the contralateral normoxic lobe, the ID did not change significantly. In both hypoxic and hypercapnic lobes, the flow velocity and volume flow of the small arteries decreased, with 5% O2, by 18 and 40%, respectively, and, with 5% CO2, by 23 and 50%, respectively. In contrast, in the normoxic lobe, they increased significantly during 5% O2 and 5% CO2 inhalations. We concluded that regional alveolar hypoxia and hypercapnia induced a local vasoconstriction particularly in the small arteries of 200-300 microns ID and decreased the flow velocity and volume flow in the same lung region.
We developed a new system that consists of 1) a specially designed X-ray apparatus, 2) an X-ray-sensitive 1-in. Vidicon camera, and 3) a digital image-processing device. The picture element is approximately 20 micron in size, and the time required for one frame is 1/30 s. Using this system, we measured the internal diameter (ID), the cross-sectional area, flow velocity, volume flow, and transit time of small pulmonary vessels of approximately 100-500 micron at control and with serotonin in anesthetized cats. Flow velocity and volume flow from large [458 +/- 22 (SE) micron] to small (340 +/- 32 micron) arteries were 5.4 +/- 0.4 cm/s and 0.53 +/- 0.06 ml/min, respectively. Transit times of the contrast medium from large to small arteries (Ta) and to large veins (Tv) were 0.68 +/- 0.04 and 3.71 +/- 0.25 s, respectively. Serotonin injection (20-30 micrograms/kg iv) decreased ID, flow velocity, and volume flow of arteries by 8-48, 32, and 76%, respectively, whereas Ta and Tv increased by 91 and 69%, respectively. The system can provide useful information regarding the local circulation in the lung.
Acute elevations in left atrial pressure (LAP) were induced by altering the volume of air within a balloon inserted into the left atrium; the changes in internal diameter (ID) of small muscular pulmonary arteries (100-600 microns ID) in response to the associated rises of pulmonary arterial pressure (PAP) were measured using an X-ray TV system on the in vivo cat lung. When LAP was elevated to 14 +/- 1, 24 +/- 1, and 30 +/- 1 mmHg, PAP was increased to 21 +/- 1, 30 +/- 1, and 37 +/- 1 mmHg, respectively. With PAP ranging from 16 (control value) to 21 mmHg the ID did not dilate significantly. With PAP of 30-37 mmHg significant ID dilation occurred. The magnitude of the ID dilation (16%) with PAP of 37 mmHg, however, was significantly smaller than that (20%) with PAP of 30 mmHg despite the greater pressure rise. When the elevated PAP of 30-37 mmHg was quickly returned to the control level by rapid balloon deflation, the ID constricted significantly below the control level. The magnitude of the ID constriction was proportional to the degree of the preceding PAP rise and was maximal in the arteries of 200-400 microns ID. A papaverine hydrochloride injection combined with the balloon deflation completely abolished the ID constriction. A phentolamine injection, on the other hand, significantly attenuated the constriction with approximately half of the constriction persisting. The results indicate that an increase in vascular smooth muscle tone occurred in the small muscular pulmonary arteries, particularly those of 200-400 microns ID, in response to the acute rise of PAP above 30 mmHg during the LAP elevation. In addition, the data suggest the partial participation of catecholamines in the active contraction of vascular smooth muscle. The arterial contraction may serve to protect the pulmonary capillaries from an excessive hydrostatic pressure and pulmonary edema.
We have developed a new wireless breathing-training support system for kinesitherapy. The system consists of an optical sensor, an accelerometer, a microcontroller, a Bluetooth module and a laptop computer. The optical sensor, which is attached to the patient's chest, measures chest circumference. The low frequency components of circumference are mainly generated by breathing. The optical sensor outputs the circumference as serial digital data. The accelerometer measures the dynamic acceleration force produced by exercise, such as walking. The microcontroller sequentially samples this force. The acceleration force and chest circumference are sent sequentially via Bluetooth to a physical therapist's laptop computer, which receives and stores the data. The computer simultaneously displays these data so that the physical therapist can monitor the patient's breathing and acceleration waveforms and give instructions to the patient in real time during exercise. Moreover, the system enables a quantitative training evaluation and calculation the volume of air inspired and expired by the lungs.
It is important for nurses to train older patients to turn on the light and perform standing pattern B, when going to the bathroom at night. In addition, it is advisable to confirm the placement of distinct visual markers on the way to the bathroom.
In in vivo cat lung, using an X-ray TV system, we analyzed responses in internal diameter (ID), flow velocity, and volume flow of arteries and veins (100-500 microns ID) to histamine (8-15 micrograms/kg iv) under three conditions. With histamine alone, three types of ID response (constriction, dilatation, and no change) occurred in parallel-arranged arteries. Relative frequency and magnitude of constriction were maximum in arteries of 300-400 micron ID, whereas those of dilatation were maximum in arteries of 100-200 micron ID. In veins, relatively uniform constriction occurred. Under H2-blockade, histamine caused greater constriction than that with histamine alone in arteries and veins of 300-500 micron ID. Under beta-blockade, with histamine, ID of all vessels decreased significantly below the ID sizes under the above two conditions, and no dilatation occurred. In two parallel arteries that showed opposite ID changes to histamine, flow velocity increased, but volume flow decreased in a constricted artery while it increased in a dilated one. Those data indicated that, with histamine, qualitatively and quantitatively nonuniform ID response was induced in both parallel- and series-arranged small pulmonary arteries and, in turn, produced heterogeneous flow distribution. Factors to cause the nonuniformity may be partly explained by difference in density of H2- and beta-receptors in vascular walls.
Using a new X-ray TV system, we analyzed effects of vagal nerve stimulation (VNS; 1–30 Hz) and intravenous injection of acetylcholine (Ach; 0.3–0.9 microgram) on the internal diameter (ID; 100–1,500 microns) of small pulmonary arteries and veins in anesthetized rabbits. In selective segments of the arteries, ID decreased abruptly and maximally by 50–70% in a specific stimulus frequency to the vagal nerve and a dose of ACh. The vasoconstrictor sites were distributed near the branching points of the arteries, particularly those downstream, and their numbers increased with an increase in the stimulus frequencies and ACh doses. The relative frequencies of occurrences were 15.3% with VNS (30 Hz) and 5.3% with ACh (0.9 microgram). In nonselective segments with VNS, ID decreased frequency dependently by 0, 4, 12, and 26% at 1, 4, 15, and 30 Hz, respectively, and with ACh, decreased dose dependently by 21 and 35% with 0.3 and 0.9 microgram, respectively. The vasoconstriction in response to VNS and ACh was attenuated by atropine, enhanced by eserine, and not affected by phentolamine. That vasoconstriction to VNS was abolished by hexamethonium. No selective constriction was found in veins and the ID was decreased uniformly by 1–2% with VNS and ACh.
The pulmonary vascular bed was embolized with glass beads in small doses that induced no significant changes in pulmonary arterial pressure in anesthetized cats. We analyzed changes in internal diameter (ID), flow velocity, and volume flow of embolized and nonembolized arteries simultaneously with ID changes of small veins. In embolized arteries, with 180-, 300-, and 500-microns beads, ID constricted maximally in just proximal portions of the plug by 22, 23, and 17%, respectively, but with 840-microns beads, no ID constriction occurred. With 50-microns beads, the maximum ID constriction occurred in arteries of 200-300 microns but not in those of 100-200 microns. The constriction decreased in the upstream larger arteries and disappeared in those greater than 800 microns ID. In the nonembolized arteries no ID change occurred. Veins constricted slightly compared with arteries. By heparin pretreatment, ID constriction was slightly attenuated in arteries and was almost abolished in veins, whereas it was not affected with hexamethonium bromide. At a branching site, volume flow to an embolized artery decreased because of a decrease in ID and flow velocity, whereas volume flow to a nonembolized artery increased because of an increase in flow velocity. We concluded that pulmonary microembolization induced a vasoconstriction chiefly in small pulmonary arteries upstream to the plug. After embolization, blood flow was locally redistributed from an embolized to a nonembolized artery at a branching site. Arterial vasoconstriction may be mediated chiefly by local mechanical factors.
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