Philip A.M. Rogers MRCVS

AP and the Cardiovascular System


Chen_FP; Hwang SJ; Lee HP; Yang HY; Chung C (1990) Clinical study of syncope during AP treatment. AETRIJ 15(2):107-119. Dept of Med, Veterans General Hospital, Taipei, Taiwan, ROC. From Aug 1988 to Apr 1989, we observed 52 patients who developed so-called "needle fainting" (or what the Chinese call "Yun-Cheng" phenomenon) 55 times among a total sample of 28285 procedures of AP therapy at the Centre for Traditional Med of Veterans General Hospital in Taipei. Of these syncopal patients, 35 were male and 17 were female. Their mean age was 45 (range 11-72) yr. All patients were in an upright position when needle fainting occurred. Their usual manifestations were pallor, cold sweating, nausea, and bradycardia. They all recovered soon after lying down; no one developed a complete loss of consciousness. No mortality was noted. When comparing the patients who experienced syncope during their first visit to our Clinic (Group I, n=27) with the patients who experienced syncope in a follow-up treatment (Group II, n=25; 3 patients had 2 episodes in sequential treatments), we found a significantly higher incidence of needle fainting (p <.0001) in Group I patients (27/2,855 or 0.94%) than in Group II patients (28/25430 or 0.11%). The mean age of Group I patients (39+15.4 yr) was significantly less than that of Group II patients (51.6+18.0 yr) (p <.001). The coexistence of other medical problems was significantly higher in Group II patients (72%) than in Group I patients (18.5%) (p <.0001).

Deng_S (1990) AP treatment of syncope based on differentiation of signs and symptoms. Inst of AP, Sichuan Acad of TCM. JTCM Sep 10(3):182-188. The 3 typical cases reported above were syncopic patients of different types. Case 1 was a Yin Xu (Deficiency Syndrome), case 2 was a Yang Xu (Deficiency Syndrome), and case 3 was a Jue Syndrome due to disturbance between Qi and Xue (Energy and Blood) induced by Qi Xu and Phlegm Stasis. All of the 3 cases were satisfactorily cured with AP and moxibustion though they did not respond to western medicines. The rationale of AP treatment for syncope includes: 1) Regulate Yin and Yang: For Yin Xu (Deficiency Syndrome), Bu (Reinforcing method) is mainly used to nourish Water to promote reproduction of the Body Fluids and replenish Yin to restore Yang; in case of Yang Xu (Deficiency Syndrome), moxibustion and needle-warming methods are mainly used to nourish the depleted Yang to rescue the patient from collapse and restore Yin. 2) Resuscitate the patient by regulating Qi-Xue and dredging the Channels to activate the circulation of Qi-Xue. After a successful resuscitation, the patient should be radically treated with appropriate herbal medicines so as to consolidate the therapeutic efficacy. 3. An emergency treatment for syncopal patients with AP and moxibustion must be based on a conscientious differentiation of the signs and symptoms. The treatment should strictly follow the therapeutic principles: Bu (reinforce) for Xu (Deficiency), Xie (Reduce) for Shi (Excess), Cool the Heat and Warm the Cold.

Hou_Z; Song X; Tang Z (1995) [An observation of protective effect of AP on the cardiac function and anti-haemorrhagic shock]. Chen Tzu Yen Chiu 20(1):44-47. Inst of AP and Channel, Anhui college of TCM, Hefei. This paper reports the study of the effect of the cardiac function and arterial pressure on rabbits with haemorrhagic shock by EAP PC06 point. PEP was shortened, ET was lengthened, SV, CO and Map were raised by needling PC06 and the each index was significantly different (p <.001). AP strengthened myocardial contractile force, protected the cardiac pump function, raised the blood pressure and had a positive role against haemorrhagic shock.

Huang_K; Zhang X; Cai H (1992) [Observations on the changes in plasma pH and K level and the effect of AP on them in rats with haemorrhagic shock]. Chen Tzu Yen Chiu 17(2):133-135. Inst of AP and Moxibustion, Chinese Acad of TCM, Beijing, PRC. The effects of AP at GV26 were studied in rats with haemorrhagic shock in relation to changes of pH and K-level of the blood. Experimental rats were assigned at random to 3 groups: 1=Controls undergoing surgery; 2=Controls in haemorrhagic shock; 3=AP in haemorrhagic shock. Blood pH and K-level did not change significantly in the surgical control group (n=15). Haemorrhagic shock, maintained for 1 h, significantly decreased blood pH (n=30, p <.01) and increased K-level (n=26). As the shock time increased, blood pH decreased continually (n=14) and blood K-level increased significantly (n=12), but pH tended to increase again after AP at GV26 for 15 min (n=16), while K-level continued to increase (n=14, p <.05). AP slightly rectified the acidosis in haemorrhagic shock in rats, possibly via modulating the respiratory function and reducing the acidic metabolites in blood. AP did not significantly correct shock-induced hyperkalaemia.

Kumar_A2; Bihari A (1996) EAP for Resuscitation in Canine. Indian Vet J May 73(5):573-575. Govind Ballabh Pant Univ Agr & Technol, Coll Vet Sci, Dept Surg & Radiol, Pantnagar 263145, Uttar Pradesh, India.

Smith_FW Jr (1992) AP for cardiovascular disorders. Prob in Vet Med Mar 4(1):125-131. Cardiopet, Inc., Floral Park, New York, NY, USA. AP had significant effects on cardiovascular function and was effective therapy for many cardiovascular ailments in experimental studies in animals and clinical studies in humans. In Vet practice, AP should be considered as adjunctive therapy in cases of shock and cardiac arrest. AP may also help as adjunctive or sole therapy in the management of congestive heart failure, arrhythmia and systemic hypertension.

Song_X; Tang Z; Hou Z; Shan H; Chen Y (1990) [The anti-haemorrhagic shock of AP on PC06 and its effect on the cardiac pump function and the blood viscosity]. Chen Tzu Yen Chiu 15(1):30-34. Inst of AP and Channel, Anhui Coll of TCM, Hefei, PRC. The purpose of this paper is to study and analyze the effects of the cardiac pump function and the blood viscosity on rabbits with haemorrhagic shock by puncturing PC06. 30 rabbits were assigned to 2 groups: 1=Experimental haemorrhage + EAP (EA, n=15) and; 2=Experimental haemorrhage Control (untreated, n=15). Cardiac pump function, blood pressure and blood viscosity were recorded pretreatment and during haemorrhagic shock phase. Results: 1. AP at PC06 raised the mean arterial blood pressure (MAP) of rabbits in haemorrhagic shock from 43+8 to 87+15 mm Hg (p <.001). 2. AP at PC06 reinforced cardiac pump function on all indices measured; SV increased from 0.41+0.46 (before EA) to 0.73+0.12 ml (p <.0001). CO, SI, CI and WL all improved to some degree with different statistical significance. In all cases, indices of cardiac pump function were significantly higher in the EAP group than in the control group. 3. AP at PC06 tended to normalise blood viscosity; plasma viscosity increased. Differences between EAP- and control- changes were significant (p <.05). AP at PC06 protected the function of the cardiac pump, raised blood pressure and had a positive role in combatting haemorrhagic shock.

Song_X2; Tang Z; Hou Z; Zhu S (1993) An experimental study on AP anti-haemorrhagic shock. Chung i tsa chih (JTCM) Sep 13(3):207-210. Inst of AP and Channels, Anhui Coll of TCM, Hefei, PRC. The effect of AP at PC06 on regulating haemorrhagic shock was studied in 90 rabbits. AP at PC06 raised blood pressure, protected cardiac pump function, corrected the disturbance of secretion and metabolism of humoral factors and reduced blood adhesion to normal level. These effects provide a scientific basis for the effects of AP at PC06 in countering haemorrhagic shock.

Tang_Z; Song X (1990) [The effect of AP on the changes of ANP and AII in plasma of rabbits with haemorrhagic shock]. Chen Tzu Yen Chiu 15(2):140-142. Inst of AP and Channels, Anhui Coll of TCM Hefei, PRC. RIA was used to measure the changes of atrial natriuretic polypeptide, (ANP) and angiotensin (AII) in plasma of normal and haemorrhagic shock rabbits. The effect of AP on the changes of ANP and AII in plasma of haemorrhagic shock rabbits was noted. ANP and AII levels in plasma increased in haemorrhagic shock extended. AP at PC06 had anti-shock effect by increasing blood pressure and decreasing the ANP and AII in plasma. Shock may promote the secretion and reduce the disintegration of ANP. AP has anti-shock effect by increasing blood pressure and correcting the disturbance of secretion and metabolism of ANP and AII during shock.

Ying_S; Cheng J (1994) [Effects of EAP on EEG during transient global ischemia and reperfusion in gerbils]. Chen Tzu Yen Chiu 19(1):29-32. Dept of Neurobiol, Shanghai Med Univ, PRC. Effects of EAP on total power of EEG at different periods of global ischemia and reperfusion was studied using the gerbil model of acute global ischemia and reperfusion. EAP (7 Hz, 5-6 mA, for 30 min) was used at GV16 and GV08. Recording was made before ischemia and 0 min, 15 min, 30 min, 60 min, 120 min and 240 min after reperfusion respectively. Results: 1. In the control group, after 10 min of ischemia, the amplitude of EEG was severely inhibited, even flat, and the total power of EEG was significantly decreased to 1.4+1.3%. After reperfusion, recovery of total power was very slow. The peak level of recovery occurred at 120 min after reperfusion was 27.4+11.3%. 2. In comparison with the control group, EAP remarkably improved the recovery of EEG after ischemia and reperfusion. The recovery of total power was 71.5+16.5% (p <.01), and 75.3+18.4% (p <.01) at 120 min and 240 min after reperfusion respectively. EAP reduced the EEG inhibition during global ischemia and improved the recovery after reperfusion.

Ying_SX; Cheng JS (1994) Effects of EAP on C-FOS expression in gerbil hippocampus during transient global ischemia. AETRIJ Oct-Dec 19(4):207-213. Dept of Neurobiol, Shanghai Med Univ, PRC. Using experimental acute global ischemia in gerbils, we studied the effects of EAP on C-FOS expression and the histological changes in various regions of the hippocampus. EAP (7 Hz, 6 mA for 30 min) was given at GV16 + GV08. EAP substantially potentiated the induction of C-FOS protein-like immunoreactivity (CFPLI) in neurons of various hippocampal regions after transient global ischemia, especially in the CA1 subfield. It also prevented delayed degeneration after ischemia in most of the CA1 cells. EAP protected hippocampal neurons after cerebral ischemia and C-FOS may be involved in this process.