An anatomical study of the full-length phrenic nerve and its blood supply: clinical implications for endoscopic dissection.

For surgeries aimed at the dissection of full-length phrenic nerve, a full appreciation of its trajectory, blood supply and correlation with adjacent anatomical structures is necessary, especially for endoscopic manipulations. A fresh cadaver study was conducted with the purpose of avoiding surgical complications and ensuring further efficacy and efficiency of endoscopic manipulations. Ten fresh adult cadavers were dissected. Special attention was paid to the topography of the origin, the trajectory of the phrenic nerve, and its anatomic communication with the surrounding vessels and organs. In the second side of the cadavers, thoracic endoscopic manipulations and observations were also performed. The full length of the phrenic nerve was 24.6 ± 1.7 and 30.6 ± 1.8 cm on the right and left side, respectively; the blood supply of the phrenic nerve in the thoracic cavity came exclusively from the pericardiacophrenic artery; the distance between the origin of the pericardiacophrenic artery and that of the internal thoracic artery ranged from 0.5 to 5.2 cm on the right side, and from 1.4 to 5.6 cm on the left; most of the pericardiacophrenic veins intermingled with small vessels of pericardium and pleura, forming a venous network and joining the innominate vein. Endoscopic dissection of the thoracic phrenic nerve together with the accompanying pericardiacophrenic artery can be performed. Extreme attention should be paid during surgery to a section of about 6 cm in length of the artery originating from the internal thoracic artery, while the accompanying veins do not require to be spared.

Considerations on the phrenic ganglia.

UNLABELLED: The phrenic ganglion is described as a small ganglion located at the junction of the right phrenic nerve and branches of the celiac plexus, on the diaphragm. The descriptions of this ganglion are few and incomplete and justify the present study which has been performed macroscopically by dissection and microscopically using silver stained (the method of Bielschowsky) drawn pieces. Dissections of 10 human adult specimens showed one or more ganglia located at the level of the terminal division of the right diaphragmatic artery; these ganglia belong to a trunk linking the right phrenic nerve and the celiac ganglion. In some specimens that nervous trunk was replaced by a ganglionated plexus. That trunk--the diaphragmatic nerve--attaches to a distinctive projection of the celiac ganglion; it may be double, but there is one ganglionated component. No left phrenic ganglia were detected. The macroscopic phrenic ganglia are distributed as follows: the lower to the adrenal gland and the upper to the diaphragm. Microscopically, the ganglia had autonomic characteristics; intrinsic microganglia were also detected within the diaphragmatic nerve. Moreover, periadventitial nervous cells were detected on the right inferior phrenic artery. IN CONCLUSION: (1) the phrenic ganglia seem to be constant structures on the right-hand side; (2) their number is variable--it may be the result of individual fragmentation or coalescence during development; (3) these ganglia may be either adrenal vasomotor or diaphragmatic vasomotor, and functionally belong to the celiac plexus; (4) intrinsic neural and periarterial locations are also possible for macroscopically undetectable populations of autonomic nervous cells.

[Clinical comparison of vascularized and non-vascularized full-length phrenic nerve].

OBJECTIVE: To investigate the clinical effect of vascularized and non-vascularized full-length phrenic nerve transfer on treating brachial plexus injury. METHODS: From August 1999 to March 2000, full-length phrenic nerve transfer to musculocutaneous nerve was conducted with the technique of Video-Assisted-Thoracic-Surgery in 15 patients (M 13, F 2) that all suffered from avulsion. Three kinds of procedures were carried out. The first was retaining initial point of phrenic nerve and dissecting full-length distal nerve (group A). The second was keeping cervical segment and isolating thoracic segment of phrenic nerve (group B). The last was vascularized phrenic nerve transfer (group C). All these phrenic nerves were sutured to musculocutaneous nerves. The results of electrophysiology and function of biceps brachii muscle were compared. RESULTS: The length of the dissecting full-length distal nerves in group A, group B and group C compared with that of conventional operation increased by 17.8 +/- 1.1 cm, 10.2 +/- 1.0 cm and 8.8 +/- 0.5 cm respectively. There was significant difference when group A was compared with group B and group C, when group B was compared with group C. All three procedures had no significant difference and led to the same function recovery of biceps brachii muscle to grade II about 6 months later. CONCLUSION: There is no difference in treating effect between vascularized and non-vascularized full-length phrenic nerve transfer, when the recipient bed has normal vascularity.

Comparative clinic study on vascularized and nonvascularized full-length phrenic nerve transfer.

In order to understand whether the vascularizing procedure has any clinical value in nerve transfer and grafting, we compared nonvascularized and vascularized full-length phrenic never transfers in patients with a brachial plexus injury. Full-length phrenic nerve transfer to the musculocutaneous nerve had been conducted by the technique of video-assisted thoracic surgery in 15 patients. Three kinds of procedures were carried out. The first involved retaining the initial point of the phrenic nerve and dissecting the full-length distal nerve. The second involved keeping the cervical segment and isolating the thoracic segment of the phrenic nerve. The last involved vascularized phrenic nerve transfer. All these phrenic nerves were sutured to musculocutaneous nerves. After 28-35 months, the results of electrophysiology and function of the biceps brachii muscle were compared. All three procedures had no significant differences and led to the same functional recovery of the biceps brachii muscle after at least 28 months of follow-up. In conclusion, the vascularizing procedure had little clinical value, not only in full-length phrenic nerve transfer, but also in nerve grafting irrespective of the length of the gap, when the recipient bed had normal vascularity.

The phrenic ganglion in man.

During educational dissections we observed a phrenic ganglion on the nerve of the phrenic artery originating from the upper pole of the right coeliac ganglion, which accompanied the right inferior phrenic artery on a female cadaver at the age of 34. In our case the left coeliac ganglion, the inferior phrenic artery, the right and left greater, lesser and least splanchnic nerves were present and normal. However, the left nerve of the phrenic artery and the phrenic ganglion were absent. We consider that this rarely reported neural formation may be of importance for anatomists and clinicians.

Unilateral diaphragmatic paralysis following bronchial artery embolization for hemoptysis.

Bronchial artery embolization is an effective treatment for patients with hemoptysis. Serious complications are rare, but may occur if the arterial supply to other structures is compromised. We present a case of unilateral diaphragmatic paralysis following bronchial artery embolization in a patient with cystic fibrosis. We believe that the diaphragmatic paralysis was due to the inadvertent obstruction of the left pericardiacophrenic artery during the embolization procedure, with compromise of the phrenic nerve blood supply. This resulted in a significant loss of lung function in our patient, who did not recover despite the subsequent return of diaphragmatic function.

Activity of nitric oxide synthase in the ventilatory muscle vasculature.

We evaluated in the in situ vascularly isolated canine diaphragm the role of nitric oxide (NO) in the regulation of basal vascular resistance and vascular responses to increased muscle activity (active hyperemia), brief occlusions of the phrenic artery (reactive hyperemia), and changes in arterial pressure. The vasculature of the left hemidiaphragm was either pump-perfused at a fixed flow rate or autoperfused with arterial blood from the femoral artery. Endothelial nitric oxide synthase (NOS) activity was inhibited by intraphrenic infusion of L-arginine analogues such as N(G)-nitro-L-arginine, N(G)-nitro-L-arginine methyl ester and argininosuccinic acid. Active hyperemia was produced by low (2 Hz) frequency stimulation of the left phrenic nerve. Reactive hyperemia was measured in response to 10, 20, 30, 60, and 120 sec duration occlusions of the left phrenic artery and was quantified in terms of postocclusive blood flow, vascular resistance, hyperemic duration, and hyperemic volume. Infusion of NOS inhibitors into the vasculature of the resting diaphragm increased phrenic vascular resistance significantly and to a similar extent. Reactive hyperemic volume and reactive hyperemic duration were also significantly attenuated after NOS inhibition, however, peak reactive hyperemic dilation was not influenced by NOS inhibition. It was also found that enhanced NO release contribute by about 41% to active dilation elicited by continuous 2 Hz stimulation. In addition, NOS inhibition had no effect on O2 consumption of the resting diaphragm, but significantly attenuated the rise in diaphragmatic O2 consumption during during 2 Hz stimulation. The decline in diaphragmatic O2 consumption was due to reduction in blood flow. These results indicate that NO release plays a significant role in the regulation of diaphragmatic vascular tone and O2 consumption.

An ATP-sensitive potassium channel blocker decreases diaphragmatic circulation in anesthetized dogs.

The goal of this study was to determine whether in the dog ATP-sensitive K+ channels blocked with glibenclamide affect diaphragmatic blood flow [phrenic arterial blood flow (Qpa)] during both spontaneous breathing at rest and increased diaphragmatic activity. A control group (no glibenclamide; n = 4) and an experimental group (50 mg/kg of glibenclamide; n = 5) were studied. During spontaneous breathing at rest, Qpa was 15.0 ml.min-1 x 100 g-1 and decreased by 5% in the presence of glibenclamide. Diaphragmatic pacing (30 min-1) generated by phrenic nerve pacing produced an initial diaphragmatic tension-time index of 0.25 in both groups. A 50% decay in transdiaphragmatic pressure was reached at 165 s in the experimental group compared with 421 s in the control group. Diaphragmatic pacing increased Qpa by 46% in the experimental group and 65% in the control group, yielding a 63% greater vascular resistance in the experimental group. Phrenic vein K+ content at rest was unchanged by the presence of glibenclamide, being 3.6 +/- 0.16 mmol/l compared with 3.5 +/- 0.19 mmol/l in the control group. Phrenic nerve pacing in the control group produced a 13% increase in phrenic vein K+ content, whereas in the experimental group a 16% decrease was observed. We suggest that ATP-sensitive K+ channels play an important role in the modulation of Qpa.

Regulation of diaphragmatic oxygen uptake by endothelium-derived relaxing factor.

The role of endogenous nitric oxide (NO) in the regulation of phrenic blood flow (Qphr) and O2 consumption (VO2) of the in situ isolated left hemidiaphragms was assessed in two groups of anesthetized, mechanically ventilated dogs. Saline was infused into the phrenic artery for 20 min in one group, whereas N omega-nitro-L-arginine (L-NNA, 6 x 10(-4) M) was infused in the other (L-NNA) group. Qphr and diaphragmatic VO2 were measured at rest and during 2 min of continuous 3-Hz stimulation of the left phrenic nerve. The animals were progressively hemorrhaged, and the measurements were repeated at various arterial pressures (Pa). For the resting diaphragm, Qphr at a mean Pa of 145 mmHg was lower in the L-NNA group than in the saline group; however, diaphragmatic VO2 values were similar in both groups. Qphr decreased with the decline in Pa in both groups, but O2 extraction ratios obtained at mean Pa of 25-45 mmHg were similar in both groups (71 vs. 73%). For the contracting diaphragm, Qphr and diaphragmatic VO2 values at a given Pa were lower in the L-NNA group than in the saline group (except at mean Pa < 75 mmHg). O2 extraction ratios obtained at a given Pa were similar in both groups. We concluded that 1) EDRF inhibition limits diaphragmatic blood flow both at rest and during 3-Hz stimulation; 2) diaphragmatic O2 extraction is unaffected by EDRF inhibition; and 3) the effect of EDRF release on diaphragmatic VO2 is dependent on the level of metabolic demands.

Effects of internal mammary artery dissection on phrenic nerve perfusion and function.

The effects of left internal mammary artery (LIMA) dissection and distal division on phrenic nerve perfusion and function were examined in an adult swine model. Phrenic nerve perfusion was determined by left atrial injection of radioactively labeled microspheres. Phrenic nerve function was determined by measuring nerve and diaphragm potentials evoked by bilateral phrenic nerve stimulation. In the first group of animals (n = 9), the LIMA was dissected with ligation of all its branches. Left phrenic nerve perfusion and function decreased after LIMA dissection in every animal studied, whereas only minimal changes were observed on the right. Sixty minutes after LIMA dissection, left phrenic nerve mean perfusion decreased 71%. Left phrenic nerve and left diaphragm mean action potential amplitudes decreased 54% and 80%, respectively. In the second group of animals (n = 4), the LIMA dissection was performed without division of the pericardiacophrenic artery, a small proximal branch of the internal mammary artery that supplies the phrenic nerve. Sixty minutes after LIMA dissection, left phrenic nerve perfusion had decreased by 21% from control values, with a corresponding decrease in left phrenic nerve and diaphragm mean action potential amplitudes of 19% and 23%, respectively. These results indicate that LIMA dissection with division of all its branches in this model is associated with a significant impairment in left phrenic nerve perfusion and function and suggests a causal relationship. These results may also explain the apparent increased phrenic nerve cold sensitivity and increased incidence of phrenic nerve dysfunction associated with LIMA grafting.(ABSTRACT TRUNCATED AT 250 WORDS)