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At facilities where the number of cases of cardiopulmonary bypass(CPB) is less than 100 per year, which accounts for 60％ of the cardiac surgery facilities in Japan, it is difficult to acquire and maintain the operation technique of CPB by the open circuit. Therefore, a valve-type semi-closed extracorporeal circulation (VACC) system was devised. In the VACC, which is a closed circuit like ECMO (extracorporealmembrane oxygenation), the volume control reservoir(VR)is connected to the venous circuit via a check valve as a safety valve. The safety valve opens and closes depending on the pressure gradient between the VR which is under negative pressure and the venous circuit. As a result, the VACC can be switched between an open circuit and a closed circuit. For the purpose of improving safety in the case of air entering the venous circuit, which is the weakness of the closed circuit, water experiments to simulate an accidental venous decannulation were conducted. In the VACC, like the open circuit, when one of the two venous cannulas was decannulated, an air lock occurred. That is a phenomenon in which venous drainage and air movement are stagnant due to being obstructed by the siphon effect of a mass of air in the venous circuit. The safety valve was open when an air lock occurred, and it was easy for it to occur when the negative pressure was weaker. If a venous cannula is decannulated, the negative pressure in the venous circuit will be augmented, and then the pressure in the venous circuit will be limited to the pressure in the VR. Therefore, the suction power of a mass of air is reduced, and air movement is stagnant. As a result, an air lock occurs. When using a closed circuit, venous decannulation causes a large amount of air entering. On the other hand, the VACC can control air behavior in the venous circuit by adjusting the pressure in the VR; for example, by opening the VR to atmospheric pressure. [ABSTRACT FROM AUTHOR]

Since superior vena cava syndrome (SVCs) causes ntracranial hypertension and edema of the upper respiratory tract close attention should be paid to brain circulatory dysfunction and obstruction of the upper airway. A male patient with SVCs and complete obstruction of the bilateral internal jugular veins was scheduled for abdominoperineal resection of the rectum under general anesthesia To evaluate the brain circuation, we monitored the external jugular venous pressure and regional saturation of oxygen (rSO) by INVOS® in the cerebral frontal cortex. If the external ugular venous pressure would rise above 20 mmHg, we planned to change the horizontal supine position to a head up position and then remove blood from the external jugular vein. Fortunately, since the external jugular venous pressure was maintained within 20 mmHg, and since no great decreases in rSO2 occurred during surgery, we did not change the patient's position or remove blood from the patient. The surgical procedure was completed uneventfully, and pharyngoarngeal edema was not seen. He did not show any neurological deficits after surgery. From experience of khis patient, we concluded that monitoring of external cigular venous pressure and rSO2 is useful for anesthetic management in patints with SVCs.

We present 3 patients with transient global amnesia (TGA). Patient 1 was a 67-year-old man who had developed TGA 5 years ago. He showed sudden onset amnesia immediately after he quarreled with his wife loudly during driving. Three-Tesla (3T) diffusion-weighted magnetic resonance imaging (DWI) taken 18 hours after onset revealed a small hyperintense signal area in the right CA1 subfield of the hippocampus. Patient 2 was a 66-year-old woman who showed sudden onset amnesia immediately after she walked for about 20 minutes holding a heavy luggage with her arms. 3T DWI taken 64 hours after onset revealed a small hyperintense signal area in the left CA1 subfield of the hippocampus. Patient 3 was a 68-year-old woman who showed sudden onset amnesia immediately after she hurriedly cleaned up her house with a cleaner. 3T DWI taken 48 hours after onset revealed small hyperintense signal areas in the left CA1 subfield and the right subiculum proper of the hippocampus. She developed TGA recurrence 6 months after the first episode of TGA. All these 3 patients had no cardiovascular diseases. Their amnesia resolved within 5-6 hours. Magnetic resonance venography (MRV) revealed hypoplasia of the left transverse sinus in Patient 1 and Patient 3, and aplasia of the left transverse sinus in Patient 2. Ultrasound studies revealed a retrograde flow component of internal jugular vein during Valsalva maneuver in Patient 2. We speculate that an increased venous pressure might have precipitated cerebral venous ischemia in the hippocampus, which is most vulnerable to ischemic insults.

A 64-year-old man was admitted with hemoptysis. A chest X-ray showed a well-defined round nodule at the right tracheobronchial angle. Enhanced computed tomography revealed the superior vena cava to be completely occluded while the azygos vein was also observed to have formed an aneurysm. Bronchoscopy showed the submucosal bronchial vessels at the right second carina to be markedly dilated, and thus considered them to be the likely cause of hemoptysis. Based on the above findings, we considered the following events as the most likely to have taken place: The superior vena cava was completely occluded due to the long-term placement of a pacemaker. The blood flow of head and upper limbs could not sufficiently return to the heart, but instead flowed into the azygos vein via the collateral circulation. This resulted in both the formation of the azygos vein aneurysm and an elevated venous pressure of the bronchial vein. Due to this pressure elevation, the bronchial vein and small vessels had both ruptured, thereby inducing the onset of hemoptysis.

Background: After induction of spinal anesthesia, thoracic epidural pressure and left saphenous venous pressure were monitored and recorded during supine hypotensive syndrome in 8 pregnant patients who underwent elective cesarean section., Methods: A 22 G venous catheter was inserted into the left saphena, and an epidural catheter for 18 G needles was positioned 5 cm cephalad in the epidural space through a Tuohy needle at the T 11-12 intervertebral space. Each catheter was connected to a pressure transducer, and recording was started in a supine position immediately after induction of spinal anesthesia with 0.5% isobaric bupivacaine at the L 3-4 intervertebral space., Results: In all patients, epidural pressure and peripheral venous pressure synchronously increased as soon as they began to recover from hypotension and tachycardia regardless of uterine displacement to the left., Conclusions: The synchronous increase in both pressures was late after the hypotension probably because sympathetic block with spinal anesthesia inhibited vasoconstriction of the lower extremity, a factor to compensate for supine hypotensive syndrome. Only collateral flow via epidural venous plexus emptying into azygos system could not compensate for decreased venous return to the right atrium from obstructed inferior vena cava, and differences in the degree of compression of the inferior vena cava by gravid uterus would affect the recovery from supine hypotension.

A 26-years-old man with a giant mediastinum tumor was scheduled for reconstruction of the superior vena cave and tumor resection. Anesthetic management for reconstruction of the superior vena cava was performed by monitoring of peripheral venous pressure. A bypass between the inominate vein and right auricula was made by using an artificial vessel before clamping the superior vena cava. When the superior vena cava was clamped, peripheral venous pressure increased suddenly to 42 mmHg. Immediately after the venesection from the peripheral vessel, it was possible to control peripheral venous pressure at about 20 mmHg. Blood was re-transfused from the femoral vein to the patient. Cerebral neurological symptom due to the increasing venous pressure was not detected. In conclusion, monitoring peripheral venous pressure during reconstruction of the superior vena cava in a patient with a mediastinum tumor may be a useful technique.

It has been reported that the high flow and pressure perfusion produced the brain damage during selective cerebral perfusion. This time we studied the mechanism of this brain damage with mock circulation. We made the mock circulation system of brain with the hard shell reservoir as cranium, and with the triple soft bags as brain tissue, involving into reservoir. We designed the control group that intracranial pressure (ICP) was 0 mmHg at pump off, and the increasing intracranial pressure (IICP) group that ICP was 10 mmHg at pump off. We measured the flow-pressure relationship in the control and IICP group, and then stenosis in outflow. In results, the flow and pressure in both the inflow and outflow side increased significantly (p < 0.001) in control groups, as pump flow increased. The changes of the flow and pressure in IICP group showed a same tendency to the control group. Moreover, both the inflow volume into bag and the outflow volume from bag decreased as pump flow increased stepwisely. The pressure in both inflow and outflow side increased significantly and the volume of the inflow side in IICP group showed a tendency to decrease, compared with the control. The stenosis in the outflow side produced the significant increase in the pressure of both inflow and outflow side, and intracranium, with the same pump flow as the control without stenosis. In conclusion, the high flow perfusion produced the increase of the several pressure in intracranial and extracranial vessels. Moreover, the high flow perfusion produced the decrease of the intracranial blood volume cerebral blood flow. The high flow perfusion does not necessarily contribute to the cerebral tissue perfusion. The stenosis at the side of venous return produced relative high perfusion. This result suggests that the venous return should be taken care of during the selective cerebral perfusion.

The middle ear is a cavity surrounded by solid bones, lined with mucosa, which has a gas-filled lumen. Cavernous organs such as the ear should have their own ventilation system under atmospheric pressure. The mechanism of ventilation in the middle ear has not been sufficiently clarified. Ventilation performed in the middle ear may be classified into two types: 1) passive ventilation via the Eustachian tube, required in cases of abnormal pressure and 2) unique physiological active ventilation of the middle ear performed under atmospheric pressure and not involving the Eustachian tube. The purpose of the present study is to prove the existence of this active ventilation under atmospheric pressure. The subjects were 50 normal ears and elevation of middle ear pressure in the lateral position (determined by positional tympanometry) was studied. The change in the peak level, on tympanometry, was used as an index. The results were continuously recorded every 12 seconds. The following results were obtained. 1. Middle ear pressure was elevated by changing from the sitting to the lateral position. Venous pressure was regarded as a causative factor in this pressure elevation. 2. The elevated middle ear pressure in the lateral position suggested gas production from mastoid cells of the middle ear. The observation that the middle ear pressure was stabilized with the increase in pressure, up to a level of 85-90 mm H2O, indicated the existence of gas leakage from the Eustachian tube and a mechanism for controlling gas production from the mastoid cells of the middle ear.

Cuff-occluded rate of rise of peripheral venous pressure (CORRP) was evaluated for perioperative monitoring. We investigated the CORRP in 6 patients undergoing open laparotomy. These patients were given general anesthesia, and monitoring lines were inserted. Heart rate, blood pressure (BP), right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), pulmonary artery pressure (PAP), cardiac output (CO) and CORRP were monitored. CORRP is defined as the average rate (in millimeters of mercury per minute) of rise of peripheral venous pressure after proximal occlusion of that vein by a tourniquet (select pressure: 50 mmHg). In the actual measurement of CORRP, only the first 90% of the curve after occlusion of the tourniquet is used. CORRP correlated with RAP (r = 0.69 +/- 0.10), and PCWP (r = 0.79 +/- 0.07). On the other hand, there was no significant correlation between CORRP and BP, or PAP and CO. Snyder et al. described that CORRP seems to be an excellent indicator of acute volume change in the hyper- and hypovolemic canine model. We conclude that in these laparotomy patients, CORRP appears to be a sensitive and minimally invasive method of assessing volume status.

Pathophysiological mechanism of hemorrhagic infarction and brain edema following obliteration of venous outflow tract has been poorly understood. We analyzed a superacute change of the blood-brain barrier in a rat experimental model of venous hypertension produced by an embolic occlusion of superior sagittal sinus (SSS). In all thirty-seven animals received retrograde embolization, marked increments of SSS pressure were noted immediately after embolic occlusion of the sinus. Severity and geographical patterns of the disruption of blood-brain barrier were then analyzed photomicrographically, visualized by the autofluorescence of the exuded Evans blue with Hematoxylin-eosin stain. Relationship between the degree of SSS pressure increment and the severity of the blood-brain barrier destruction was studied. In ten out of the seventeen animals (59%), analyzed five minutes after embolization, exudation of the dye was demonstrated. The degree of SSS pressure increment in the animals with dye exudation was higher than in the animals without them. In five out of the nine animals (56%), analyzed fifteen minutes after embolization, exudation of the dye was also demonstrated. The degree of SSS pressure increments in the animals with dye exudation was statistically higher than those in the non-exuded ones. Especially, all the animals with SSS pressure higher than 75 mmHg were associated with severe exudation of the dye. The exudation of the dye was more prominent in the white matter than in the cortical gray matter. Following pathological analysis have revealed that exudation of the dye was most prominent around the capillary and the venule in the white matter. Microvacuolation around these vessels was also noted.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the appropriate treatment for patients with varix cruris, we performed three different methods of phlebography including direct phlebography, and compared their findings by each phlebography. Conventional ascending phlebography was taken routinely and initially in all limbs (n = 120). "Direct phlebography" developed by us was then indicated, when the visualization of the deep vein system was unclear by conventional ascending phlebography. This method was useful for the clear opacification of the deep vein system, and also was able to visualize the deep femoral vein clearly. After the precise diagnosis of varix cruris, descending phlebography under the Valsalva maneuver at supine position was carried out for the evaluation of the deep vein insufficiency. According to these phlebographic findings, conventional stripping with or without sub- or suprafascial ligation of communicating vein was indicated to saphenous typed varix cruris. The valvuloplasty to the highest valve in superficial femoral vein was carefully added in eight limbs which showed the significant reflux by added in eight limbs which showed the significant reflux by the descending phlebography. This valvuloplasty was remarkably contributed to the immediate healing of the stasis ulcer without recurrence. And compression sclerotherapy was selected to some patients with branch typed varix cruris.

Postoperative changes in peripheral venous functions were determined by Ga-In strain gauge plethysmography in 28 surgical patients, and central venous functions and urine catecholamine levels were also measured. The results were as follows: 1. The maximum venous outflow (MVO) and arterial blood inflow volume (AF) of the healthy arms tended to increase with age, but showed no sex or right-to-left difference. 2. MVO, AF and venous distensibility were decreased postoperatively, and the decreases were greater in the patients with major surgery than in those with minor surgery. 3. MVO in the patients with high urine levels of adrenaline and noradrenaline showed a greater decrease than those in normal subjects, and the majority of these patients were found to have had major surgery. There was a negative correlation between the urine noradrenaline level and MVO. 4. The decrease in peripheral venous functions preceded the decrease in central venous functions. 5. The postoperative decrease in peripheral venous functions was considered to be the result of active vasoconstriction due to hypersecretion of catecholamines caused by surgical stress and increase in the extravascular pressure. 6. Measurement of venous functions of the arm may be a good parameter for detecting circulatory disturbances due to surgical stress.

Two patients with orthostatic purpura were reported. Case 1: A 47-year-old man was admitted to our institution because of multiple purpuric eruptions over the legs after the long periods of sitting or standing. Bleeding time was 4.0 min. Platelet aggregation induced by ADP was disaggregated and no aggregation was observed when induced by collagen and epinephrine. He was diagnosed as having release abnormality of the platelets caused by glutathione administered for treatment of liver damage for several years. Purpura, however, appeared even though platelet function became normal after discontinuing glutathione. Purpura proved to be induced by the long periods of sitting or standing. Case 2: A 37-year-old woman was admitted to our hospital because of purpuric eruptions over the legs for three years. Bleeding time was 2.0 min. Platelet aggregation induced by ADP, epinephrine, collagen and ristocetin was normal. Purpura was caused by long periods of standing without movement. Wearing elastic pantyhose showed reduced appearance of the purpura. Biopsy specimens from both patients revealed no abnormal findings. Both patients had no abnormal results in coagulation studies. Purpura seemed to be caused by the increased capillary pressure after the prolonged periods of standing. No case report concerning orthostatic purpura or mechanical purpura has been published.

The percentage of splenic blood in portal venous flow (SV%) was measured in 96 patients by using scintiphotosplenoportography and angiography. The patients were divided into two groups: Group 1, without collateral pathways from the splenic vein; Group 2, with collateral pathways from the splenic vein. SV% was significantly lower in patients without liver diseases or in patients of Group 1 with liver cirrhosis (LC). SV% was significantly higher in patients with idiopathic portal hypertension (IPH). A significant correlation was observed between SV% and splenic volume or ICGR15. No significant correlation of SV% was found with etiology of LC in patients of Group 1, esophagogastric varices, Child's criteria, portal venous pressure, cholinesterase, hepaplastin test or prothrombin time. Hence, the local hyperdynamic state of the splenic region was detected in patients with CH, LC and IPH.

Renal cell carcinoma with extended tumor thrombi densely adherent to the vena caval wall sometimes requires vena caval resection. If the tumor is on the right side and the collateral veins of the left renal vein are abundant, vena caval reconstruction may not be required. We recently performed radical nephrectomy and vena caval resection on 2 right renal cell carcinoma patients. To decide the necessity of vena caval reconstruction, left renal vein pressure was measured before and after clamping of the vena cava. In case 1, because the pressure was elevated from 21 cmH2O, to 61 cmH2O, total replacement with Gore-Tex graft was performed. In case 2, because the pressure change was from 22 cmH2O to 23 cmH2O, reconstruction was not performed. The most important test to decide the necessity of vena caval reconstruction is thought to be the change of renal venous pressure before and after clamping of the vena cava.

In 17 compensated liver cirrhosis and 8 chronic hepatitis cases (no histories of cardiac or pulmonary disease), wedged hepatic venous pressure (WHVP), hemodynamics, and pulmonary function were measured and their clinical significance and interrelations evaluated. Both diseases were comparatively analyzed. WHVP was determined by wedging a catheter from the right femoral vein into the right hepatic vein. Hemodynamics was measured with a Swan-Ganz catheter. Spirography, flow-volume curve, closing-volume curve and pulmonary diffusion capacity were measured and aortic blood gas analyzed to assess pulmonary function. Esophageal endoscopy was used to diagnose the presence or absence of esophageal varices. The results showed that the group of liver cirrhosis patients featured elevated WHVP and a hyperhemodynamic pattern and a positive correlation between WHVP on the one hand and cardiac index and right left ventricle stroke work indexes on the other; there was a negative correlation between WHVP and the systemic vascular resistance and pulmonary vascular resistance indexes. The results showed an increase in oxygen consumption in the group of patients with esophageal varices. In all chronic hepatitis cases, findings were normal. Pulmonary function was characterized by abnormal %VC, PaO2, and pulmonary diffusion capacity in both groups along with abnormal PaCO2 in the liver cirrhosis group; no significant differences were noted between the two groups. These results indicate that liver cirrhosis elevates intarahepatic pressure, affecting systemic hemodynamics and resulting in a circulatory distribution disorder, leading to right and left ventricle overload and a decline in potential cardiac function. The results also indicated that mild pulmonary function disorder can occur as early in a state of chronic hepatitis.

In a prospective, randomized controlled trial, 43 patients with cirrhosis and variceal hemorrhage were allocated after control of the bleeding to treat by elective sclerotherapy alone (n = 23) or by oral propranolol after elective sclerotherapy (n = 20). The dose of oral propranolol was based on a reduction of the resting pulse rate by 25%. The end points of the study were rebleeding or death. Both treatment groups were comparable with respect to origin and severity of liver disease, size of esophageal varices and portal pressure at entry. The mean follow up was 27 +/- 19 months for all patients. Patients treated sclerotherapy alone had more rebleeding (n = 11) did than those in the sclerotherapy plus propranolol (n = 3). The cumulative percentages of patients free of rebleeding 1 and 2 years after inclusion were 77 and 66% in sclerotherapy alone, and 100 and 85% in sclerotherapy plus propranolol; the difference between the two groups was significant. No statistically significant effect on mortality was seen. These data support that oral propranolol after sclerotherapy reduces the risk of recurrent bleeding in cirrhotics treated elective sclerotherapy.

Though the retrograde perfusion via the coronary sinus is a useful way of myocardial protection for more complicated cardiac surgery, coronary venous injury and inadequate preservation of the right ventricle were considered to be disadvantageous. In order to deal effectively with these problems we made a 3-way balloon catheter (Retro-Higami type 12 Fr) and evaluated the importance of monitoring the perfusion pressure in the coronary sinus in 214 patients. The mean perfusion pressure during retrograde cardioplegia infused by a pump was 29.4 +/- 9.1 mmHg, and had significant relation to the left ventricular mass weight (LVMW) which was calculated by UCG method. High perfusion pressure above 40 mmHg, which could have induced coronary venous injury, was noticed in 24 patients, but proper countermeasures could avoid venous injury completely. In 16 of those the high perfusion pressure was due to inadequate position of a tip of the catheter, and in other 8 it was due to relatively high flow rate of cardioplegic solution to LVMW. Twenty-eight patients showed low perfusion pressures below 20 mmHg, due mainly to the leakage from the orifice of the coronary sinus. The coronary sinus pressure during continuous gravity retroperfusion which was 9.2 +/- 2.6 mmHg seemed to bring optimal delivery of cardioplegic solution to the myocardium. On the basis of the results obtained from this clinical study we conclude that the monitoring of coronary sinus pressure during retroperfusion is useful not only to avoid coronary venous injury but to maintain adequate perfusion.

Few reports have appeared in regard to cerebral perfusion pressure (CPP) accompanying fluctuations in intracranial pressure (ICP), arterial pressure (BP) and central venous pressure (CVP) as well as autoregulation of cerebral circulation in neonates and infants. Therefore, we report here on interesting findings we obtained from monitoring ICP, BP, and CVP during operations in 30 neonates or infants with congenital heart disease as our subjects. i) ICP fluctuates depending on arterial pressure and venous pressure, but changes in the latter display a clearer effect. ii) On inducing anesthesia the amplitude of ICP pulsating waves became gradually larger, but following intubation intracranial pressure was somewhat reduced and became stable. iii) Following thoracotomy CVP rose and at the same time intracranial pressure also increased somewhat. Before thoracotomy ICP pulsating waves resembled arterial pressure wave forms, but after thoracotomy they resembled central venous pressure wave forms. iv) In cases with two-peak ICP pulsating waves, when we conducted a study by blocking venous return from the internal carotid vein during the operation by the Queckenstedt method, ICP rose by increasing its amplitude, but the pulsating wave forms lost their venous component, and changed into a single peak consisting of an arterial component. v) In order to observe the relationship between changes in arterial pressure and ICP, when we looked at changes in ICP accompanying partial blockage of the descending aorta (DAo), simultaneously with the partial blocking of the DAo both AP and CVP rose, and ICP also rose accordingly. Also, when arterial blockage was relaxed, BP, CVP, and ICP immediately recovered completely to the status quo prior to the blocking procedure. This finding indicates that by blocking of the DAo, intracranial arterial and venous blood volume abruptly rapidly increase and since CVP also rises, therefore ICP rises to maintain a balance with these. As a result, this brings about the effect of normally maintaining the cerebral perfusion volume. vi) If we look at changes in ICP brought about by partial blocking of the ascending aorta, blockage of the artery brought about a further reduction in BP, and in this case since the arterial blood flow into the cranium also fell off markedly, we found that ICP also was reduced. The above results suggest that in the normal brains of neonates and infants even when under various conditions various fluctuations in corporeal circulation develop, cerebral perfusion volume adjusts itself in response to this, and thus autoregulation of cerebral blood flow is able to act in an adequate way.

A 43-year-old male was admitted for subcutaneous mass of rt. inguinal lesion. Saccular dilatation of vein is a rare phenomenon and usually termed "venous aneurysm". Venous aneurysm has been reported in the following vein: face, neck, extremities, superior vena cava region, portal vein region and by-pass grafting vein. This is the 1st report of a venous aneurysm found in V. saphena accessories in Japan. The true etiology is unknown, but underlying causes which produce damage to the venous wall (trauma, inflammation, congenital weakness, and localized degenerative change) have been mentioned as possible causes. Rarely, thrombosed venous aneurysm may cause pulmonary emboli. Definitive diagnosis is established by venography. Venous aneurysm often increases or reduces in size according to the change of venous pressure by proximal vein compression postural change and Valsalva maneuver. In general, surgical resection of the aneurysm is the treatment of choice.

The effect of disturbance of cerebral venous drainage on acute ischemic cerebral edema and cerebral circulation were studied by measuring local cerebral blood flow (LCBF) and local changes in brain water content using a middle cerebral artery (MCA) occlusion model. Rats were anesthetized with halothane and the stem of the left MCA was occluded. Disturbance of cerebral venous drainage was induced by bilateral occlusion of the external jugular veins, i.e., the right external jugular vein was cannulated and the left one was occluded by a clip. LCBF was measured by the 14C-iodoantipyrine (14C-IAP) autoradiographic method at 2 hours after MCA occlusion. Local changes in brain water content were studied 2 hours after MCA occlusion by measuring the specific gravity of cerebral tissue in the gradient column with bromobenzene and kerosene. The control rats which underwent the same anesthesia and surgical procedure including the MCA occlusion and cannulation into the right external jugular veins, but which did not undergo occlusion of the left external jugular veins, were prepared and studied at the same time after MCA occlusion. In the rats with bilateral occlusion of the external jugular veins, the external jugular venous pressure was evaluated up to about 8 mmHg (100 mmH2O) (control: 1.3 mmHg). At 2 hours after MCA occlusion, LCBF in the ischemic core was decreased. The ischemic area was more extensive in the rats with bilateral occlusion of the external jugular veins compared with the controls. Furthermore, specific gravity of the brain was decreased in the entire left MCA territory in the rats with bilateral occlusion of the external jugular veins.(ABSTRACT TRUNCATED AT 250 WORDS)

To estimate the pumping function of the left-sided heart in patients with "latent" left-sided heart failure due to heart disease which primarily affected the left-side of the heart (former NYHA class I and II), we measured (i) the increase of peripheral venous pressure in response to supine mild leg exercise (delta VP), and (ii) the increase of plasma noradrenaline (NA) concentration due to phentolamine (PH) injection (delta NAPH). We divided the patients into well-functioning left-sided heart group (delta CI/delta PAW greater than 0.180 L.min-1.M-2.mmHg-1) and poorly-functioning left-sided heart group (delta CI/delta PAW less than or equal to 0.180 L.min-1.M-2.mmHg-1) on the basis of a ratio (delta CI/delta PAW), relating the increase in cardiac index (delta CI) in response to exercise to the concomitant increase in mean pulmonary artery wedge pressure (delta PAW). This diving line (delta CI/delta PAW = 0.180 L.min-1.M-2.mmHg-1) correlated with delta VP (diving line: delta VP = 35 mmH2O) and with delta NAPH (diving line: delta NAPH = 0.353 ng/ml). Our results suggest that delta VP and delta NAPH reflected the pumping function of the left-sided heart with considerable accuracy.

Unlabelled: There are many problems about the cause, pathophysiology and treatment of acute brain swelling under intracranial hypertension frequently encountered in the neurosurgical clinics. Generally, rapid increase of the cerebral vasoparesis caused by unknown etiology is thought to be the main cause of acute brain swelling under intracranial hypertension. Moreover, disturbance of the cerebral venous circulatory system is discussed recently by many authors. But, research from the point of systemic respiration and hemodynamics is necessary for resolving these problems. This experiment was designed to study the effects of respiration and hemodynamics on the cerebral vasoparesis., Method: Using 22 adult dogs, acute intracranial hypertension was produced by epidural balloon inflation sustained at the level of 300 - 400 mmH2O. Simultaneously with measurement of intracranial pressure at the epidural space, superior sagittal sinus pressure, respirogram, systemic blood pressure (femoral artery), central venous pressure, common carotid blood flow, EKG and bipolar lead EEG were monitored continuously. The experimental group was divided by the respiratory loading into 5 groups as follows: control (6 cases), 10% CO2 hypercapnia (4 cases), 10% O2 hypoxia (4 cases), stenosis of airway (5 cases), 100% O2-controled respiration (3 cases)., Results and Conclusions: 1) Cerebral vasoparesis under acute intracranial hypertension took place earlier and showed more rapid progression in groups of stenosis of airway, hypercapnia and hypoxia than control group of spontaneous respiration in room air. No occurrence of cerebral vasoparesis was found out in a group of 100% O2 controlled respiration. It is proved that increased airway resistance or asphyxia, hypercapnia and hypoxia have strictly reference to the occurrence and progression of cerebral vasoparesis and for the prevention of cerebral vasoparesis, correct 100% O2 cont rolled respiration is effective. 2) From the hemodynamic change, the progression of rapid increase of cerebral blood volume with increase of blood volume in the superior sagitta sinus during cerebral vasoparesis under intracranial hypertension is presumed. It is suggested from the superior sagittal sinus pressure in various experimental groups that the site, reactivity and disturbed degree of the cerebral venous system are changed by the difference of respiratory or ventrilatory state and the cerebral venous circulatory disturbance has also reference to the occurrence of acute brain swelling. 3) During cerebral vasopareris under acute intracranial hypertension, remarkable supression of respiration, increased central venous pressure and increased common carotid blood flow were observed. It is concluded that the reaction of systemic hemodynamics following respiratory change effects on cerebral circulation markedly and they are being important factors to occurrence of acute brain swelling.

A new experimental model of the hemorrhagic infarction was devised to study the pathophysiology of the hemorrhagic infarction of the venous origin. To make a model of the hemorrhagic infarction by sinus occlusion, mixture of alpha-cyanoacrylate monomer and pantopaque was injected through a catheter introduced into the superior sagittal sinus in 15 dogs, using embolization technique. These dogs were divided into three groups according to the volume of the mixture injected into the sinus. In control groups (3 dogs), no mixture was injected. For partial sinus occlusion (5 dogs), 0.5-1.0 ml of mixture was injected into the sinus and 1.0-1.5 ml of mixture, for complete sinus occlusion (7 dogs). Changes of intracranial pressure (ICP), superior sagittal sinus pressure (SSSP), tissue pressure (TP) rCBF and histological changes were evaluated before and after sinus occlusion. The following results were obtained. (1) In control groups, ICP, SSSP and TP were 9 +/- 2.2 mmHg, 4 +/- 2.5 mmHg and 4-5 mmHg respectively, but in partial and complete sinus occlusion, SSSP and TP were higher than ICP. ICP, SSSP & TP were 32 +/- 5.4 mmHg, 35 +/- 6.5 mmHg and 37-42 mg, in partial sinus occlusion and 62 +/- 5.9 mmHg, 65 +/- 6.0 mmHg, 65-72 mmHg in complete sinus occlusion. (2) R-CBF in partial sinus occlusion showed no change even after sinus occlusion, but in complete sinus occlusion, decreased to 20% of that of the control group due to marked venous congestion.(ABSTRACT TRUNCATED AT 250 WORDS)

With an increasing number of patients with advanced liver cirrhosis, the discrepancy between the preoperative examination and results of surgery for bleeding varices is widening. To correct this discrepancy, additional prognostic examinations to Child's criteria and routine hepatic laboratory tests were studied in our 246 cirrhotic patients with esophageal varices. These included wedged hepatic vein pressure, clearance and maximal removal rate of indocyanine green, and hepaplastin test. We performed the endoscope assisted terminal esophagoproximal gastrectomy with the EEA stapler gun with devascularization and splenectomy. No operative death and complications developed when the results of following 4 preoperative examinations were: wedged hepatic vein pressure below 400 mm of saline, peripheral disappearance rate (K) of indocyanine green above 0.04 min-1, maximal removal rate (Rmax) of the dye above 0.3mg/kg/min and hepaplastin test more than 40%. It is necessary for these indicators to be satisfied simultaneously prior to performing this surgery. In addition, these values should be changed a little in their critical limits when these cirrhotic patients also had hepatoma and were candidates for hepatectomy.

The transvenous electrophrenic respiration (EPR) is one of the effective and relatively simple method for artificial respiration. Twenty seven mongrel dogs were subjected to the experiment which were subdevided into 4 groups. Stimulation is 44 times in group 1, 22 times in group 2 and 3. Ventilation is carried out by Harverd Respirator in group 4. The normal arterial pressure, the normal minute ventilatory volume and the normal arterial blood gases were unchanged for a 5 hour period of experiment in group 2. However, the frequent stimulation such as 44 times/min. in group 1 yielded the hypotension, the decreased ventilatory volume and brought the congestion of the portal venous area and rendered the subjects to death. The systemic pressure remained in slightly lowered levels in group 2, 3 and 4 at the end of a 24 hour of experiment. The ventilatory volume decreased one third of initial values in group 2 and 3 at the end of a 24 hour of experiment. The pulmonary arterial pressure decreased in group 3 significantly, whereas it increased in positive pressure respiration in group 4. Intermittent clinical application of EPR was performed in three patients. The arterial pressure, minute ventilatory volume, arterial gases and central venous pressure were maintained normal. The following conclusions were obtained: 1) EPR is more physiologic than positive pressure respiration in ventilatory and circulatory aspects. 2) Undesiable conditions of stimulation cause complications such as neural fatigue, portal hypertension, etc. 3) Intermittent clinical application of EPR has been quite successful in supporting the ventilation of the patients.

Hemodynamic changes of portal and hepatic circulation in dogs with chronic congestive liver (CCL) have been studied with reference to cardio-pulmonary (C-P) bypass. The CCL dogs were provided by means of cut of the chordae of tricuspid valve followed by breeding for 4 to 41 months. Five of CCL dogs and 10 of control dogs were served for C-P bypass for 90 minutes. The measurements of portal venous pressure (PVP), wedged hepatic venous pressure (WHVP) and hepatic tissue blood flow (HBF) by hydrogen gas clearance method were made before and during C-P bypass. Results were as follows. 1. HBF of CCL dogs after laparotomy decreased significantly (p less than 0.001) in comparison of control dogs (31.7 +/- 14.4 vs. 62.7 +/- 23.3 ml/min/100g). 2. During the C-P bypass, the rates of rise of PVP and WHVP in CCL dogs revealed a lesser prominent than those of control dogs. 3. No reduction of the HBF was seen during the C-P bypass in CCL dogs. These results lead the conclusion that the portal and hepatic circulation of CCL dogs poorly adapted to an unphysiological condition of C-P bypass. It is considered, however, that CCL itself is not a state of absolute contraindication for C-P bypass in open cardiac surgery.

The esophageal variceal pressure was determined by endoscopic pneumatic pressure sensor method in patients with liver cirrhosis, complicating esophageal varices. The variceal pressure by this method was significantly correlated with percutaneous transhepatic portal venous pressure. The variceal pressure was related with endoscopic findings of varices, especially of red-color sign, form and location. The variceal pressure below 200 mmH2O showed negligible risk of variceal bleeding, and the pressure over 350 mmH2O was associated with high risk of variceal bleeding. These results indicate that esophageal variceal pressure by this method may provide useful informations in natural history of esophageal varices.

A case with the Budd-Chiari syndrome due to the right hepatic occlusion who was successfully operated by using the internal shunt tube of the inferior vena cava was reported. The patients was 33 year old male. Midsternal incision and right subcostal oblique incision were made and the internal shunt tube was inserted through the right auricle to the inferior vena cava. The hepatic vein was approached through the longitudinal suprahepatic caval venotomy. Then membranous obstruction in the right hepatic vein ostia was resected. Mesenteric venous pressure dropped immediately from 360mm H2O to 160mm H2O by direct manometry. All the blood bled from the right hepatic vein was transfused through the internal shunt tube to the right atrium. The patient tolerated the procedure and his postoperative course was free from the complication. The resected membrane was congenital anomaly and an operative liver biopsy was demonstrated the evidence of congestive liver with fibrosis.

There are two types of internal spermatic veins (ISV) by radiographic examinations. In type 1, ISV is dilated with some collateral venous branches. On the other hand, ISV of type 2 is narrowed with increased collateral venous branches or abnormalities such as the circumaortic renal are seen. In these groups, pressure of renal vein and ISV were measured. As a result, renal vein pressure was about the same in type 1 as in the controls at 9.5 +/- 2.3 cmH2O but was higher in type 2 at 17.0 +/- 2.8 cmH2O. As for ISV, it was also about the same in type 2 as in the controls at 13.9 +/- 6.8 cmH2O but was markedly higher in type 2 at 33.3 +/- 3.9 cmH2O. When selective renal venography was performed, a contrast medium back-flow was seen in 9 out of 11 type 1 varicocele patients, but it was not seen in any of the cases with the nutcracker phenomenon. These results suggested that type 1 may be caused by the structural and functional disorders in the valve between the renal vein and ISV. In contrast, pathogenesis of type 2 varicocele may be due to an abnormality of the ISV in the embryo.

Using liver cirrhosis rats induced by intraperitoneal administration of 4% thioacetamide (TAA) consecutively for 10 weeks, the authors made a study on the activities of blood coagulation and fibrinolysis in the onset of acute ulcer after hepatectomy. The results were as follows: 1. On the 3rd day after hepatectomy increase in the portal blood pressure, approximate 30% decrease in gastric wall blood flow and increase in fibrinolysis in blood and gastric mucosa were observed. While no bleeding was recognized, edema and hyperemia were noticeable. 2. On the 3rd postoperative day when the maximum increase of fibrinolysis in blood and gastric mucosa was observed water immersion restraint stress was loade. Two hours after loading, fibrinolysis in blood and tissue increased further, and in accordance with it, bleeding and erosion were seen to a high degree in gastric mucosa. On the other hand, in the EACA group, in which anti-fibrinolytic agent, epsilon-amino carpic acid was administered, the increase was moderate in the fibrinolysis in blood and mucosa after loading the stress. Though bleeding and development of erosion were not completely controlled, values of fibriolytic activity of the tissue in the EACA group were lower than those of control group.

Although many authors suggested vascular compression of venous system under increased intracranial pressure, the exact site and mechanism of the compression are still obscure. By the previous reports obtained in mongrel dogs, we clarified that a vascular stenosis took place 1-2 mm lateral to the junction between the lateral lacuna and the superior sagittal sinus as the intracranial pressure (ICP) was elevated. The present study was designed to reinvestigate the internal pressure of the intracranial venous pathways using crab-eating monkeys under gradually increasing ICP. (1) METHODS: Using crab-eating monkeys, pressure of the cortical veins and the superior sagittal sinus was measured by cannulating small calibred (0.4 - 0.5 mm in outer diameter) polyethylene tube. The ICP was elevated by inflating rubber balloon placed in the epidural space. Pressure of the above mentioned vessels, systemic blood pressure and ICP were measured with a standard pressure transducer. Pressure gradient between the lateral lacuna and the superior sagittal sinus was measured by moving to and fro the tip of small calibred tube which was inserted into the lacuna under operation microscope. (2) RESULTS: The pressure of the cortical vein was constantly 50 - 250 mmH2O (4-18 mmHg) higher than the ICP in monkeys, regardless of the level of ICP (Fig. 1, 2 & 3). Pressure of the superior sagittal sinus was quite stable at the low level untill the ICP was elevated up to 500mmH2O (36 mmHg) and more or less increased thereafter (Fig. 1 & 2). The pressure in the parasagittal venous pathways presented abrupt alterations between the lacuna and the superior sagittal sinus in monkeys (Fig. 6). (3) CONCLUSIONS: It was concluded that a gradual stenosis of parasagittal venous pathways took place 1-2 mm lateral to the junction between the lateral lacuna and the superior sagittal sinus in monkeys when the ICP was gradually elevated. This result suggests that also in humans a gradual stenosis occurs in a similar fasion as the ICP is elevated. The results of the experiment obtained in monkeys were almost the same as those previously obtained in dogs.