Biomedical subjects

S Hoka

Publications and source records attributed to S Hoka.

66 records · Page 4Linked to original sources

PubMed1988

Decreased hindquarters venous distensibility during high salt intake in stroke-prone spontaneously hypertensive rats.

This study was done to examine whether high salt intake decreases venous distensibility in stroke-prone spontaneously hypertensive rats (SHR-sp). Ten weeks old male SHR-sp and normotensive Wistar-Kyoto rats (WKY) were fed either high (8%) or pressure-volume curves were obtained by infusing Krebs-Henseleit solution retrograde into the inferior vena cava at a rate of 12 or 2.1 ml/min. After 3 weeks of dietary treatment, high salt intake shifted the venous pressure-volume curves at maximal venodilatation caused by nitroprusside toward the pressure axis in SHR-sp but not in WKY. The venous pressure-volume curve during interruption of infusion was also shifted toward the pressure axis in SHR-sp on high salt diet as compared with that in SHR-sp on normal salt diet. Water content and thickness of the smooth muscle layer of the venous wall were not different between the two groups of SHR-sp. These results suggest that high salt intake for 3 weeks decreased hindquarters venous distensibility at maximal venodilatation in SHR-sp but not in WKY. The salt-induced decrease in venous distensibility in SHR-sp might be related to changes in interstitial space compliance or the adventitia since water content or thickness of the smooth muscle layer of the venous wall was not altered.

Animals↗

PubMed1987

Venodilator effects of adenosine triphosphate and sodium nitroprusside; comparisons during controlled hypotension.

Adenosine triphosphate as well as sodium nitroprusside has been used for hypotensive anesthesia. The purpose of this study was to examine the possibility that two hypotensive drugs may exert different effects on venous capacitance during controlled hypotension. In rats anesthetized with ketamine, mean arterial pressure was lowered to 50 mmHg by intravenous infusion of adenosine triphosphate or sodium nitroprusside. Venous capacitance was assessed before and during induced hypotension by measuring the mean circulatory filling pressure (MCFP). MCFP was measured after briefly arresting the circulation by inflating an indwelling balloon in the right atrium. MCFP was lower during adenosine triphosphate-induced as well as sodium nitroprusside-induced hypotension as compared with the respective value at control (P < 0.01 for adenosine triphosphate and sodium nitroprusside). However, the decrease in MCFP by adenosine triphosphate (0.8 +/- 0.1 mmHg) was less (P < 0.01) than that by sodium nitroprusside (2.3 +/- 0.3 mmHg). These results suggest that at a comparable level of arterial hypotension venodilator effect of adenosine triphosphate was less than that of sodium nitroprusside. Less venodilatation during adenosine triphosphate-induced hypotension may contribute to the maintenance of cardiac output during hypotensive anesthesia.

Journal Article↗

PubMed1987

Alteration of blood flow distribution and vascular capacitance during induced hypotension in deafferented dogs.

The effects of three hypotensive agents, sodium nitroprusside (SNP), nitroglycerin (NTG), and adenosine triphosphate (ATP), on blood flow distribution and vascular capacitance were examined in dogs anesthetized with sodium pentobarbital. To eliminate the modification by the baroreflex, carotid sinus was denervated and aortic and cardiopulmonary vagal fibers were sectioned. Total systemic circulation was divided into two parallel compartments, splanchnic (SP) and extra-splanchnic (ESP) vascular beds. Alteration of vascular capacitance was assessed by a change in systemic blood volume with constant cardiac output and constant venous pressure using a total heart-lung bypass. SNP- and ATP-induced hypotension caused blood flow redistribution from the SP to ESP beds, and this redistribution is greater (P less than 0.01) with ATP than that with SNP. In contrast, NTG-induced hypotension did not significantly cause redistribution. Systemic blood volume was increased during NTG- (10.4 +/- 2.2 ml/kg), and SNP-induced (4.8 +/- 1.1 ml/kg) hypotension. The increase by NTG was significantly greater (P less than 0.05) than that by SNP. In contrast, ATP-induced hypotension did not significantly change systemic blood volume. Since redistribution can result in a passive change in vascular capacitance, the differences in capacitance among SNP, NTG, and ATP can be explained in part by differences in redistribution of blood flow. Redistribution of blood flow from SP to ESP beds can increase venous return due to increasing the slope of the venous return curve. The results suggest that redistribution should be taken into consideration in evaluating the hemodynamic changes during induced hypotension.

Adenosine Triphosphate↗

PubMed1987

Halothane inhibits calcium accumulation following myocardial ischemia and calcium paradox in guinea pig hearts.

This study was performed to test the hypothesis that halothane inhibits calcium accumulation associated with myocardial ischemia and calcium paradox. Using a Langendorff preparation in isolated guinea pig hearts, tissue 45Ca was measured after 40 and 60 min of loading with 45Ca, followed by 20 min of washout period. Myocardial ischemia was produced by a 30-min occlusion of the left anterior descending coronary artery (LAD). LAD occlusion caused an increase in 45Ca content in the anterior left ventricular muscle (ischemic area) of 215% compared to that of the posterior left ventricular muscle (normal myocardium). The increase in 45Ca content in the ischemic area was significantly less (P less than 0.05) in the presence of halothane (1%) compared to the non-halothane group. Halothane did not significantly alter 45Ca content in the non-ischemic myocardium. Myocardial injury associated with calcium paradox, which was produced by a 10-min perfusion of the heart with calcium-free Krebs solution followed by normal calcium repletion, caused a significant increase (P less than 0.05) in the 45Ca content compared to control. Addition of halothane (1%) significantly depressed (P less than 0.05) the increase in 45Ca content caused by calcium paradox. It is suggested that halothane might inhibit calcium accumulation associated with myocardial ischemia and calcium paradox under certain experimental situations. The inhibitory effect of halothane on calcium accumulation may be beneficial for the ischemic heart during halothane anesthesia.

Anesthesia↗

PubMed1985

The effects of ketamine on venous capacitance in rats.

The purpose of this study was to examine the effects of ketamine and pentobarbital on venous capacitance in rats. Venous capacitance was assessed by measuring the mean circulatory filling pressure (MCFP) at three levels of blood volume in conscious rats as well as during anesthesia with ketamine (125 mg/kg, ip) or pentobarbital (50 mg/kg, ip). MCFP was measured during brief periods of circulatory arrest produced by inflating an indwelling balloon in the right atrium. MCFP was maintained during ketamine anesthesia at a level similar to that measured in conscious animals, while it was decreased (P less than 0.01) during pentobarbital anesthesia both at normal blood volume and following hemorrhage. These results suggest that ketamine did not alter but pentobarbital increased venous capacitance. The slope of the regression line relating MCFP and blood volume was not altered by ketamine but was increased (P less than 0.05) by pentobarbital, which suggests that ketamine did not alter but pentobarbital decreased total vascular compliance. These results suggest that ketamine maintains but pentobarbital decreases venous tone.

Animals↗

PubMed1985

Digitalis-induced augmentation of cardiopulmonary baroreflex control of forearm vascular resistance.

We sought to determine whether digitalis augments cardiopulmonary baroreflex control of forearm vascular resistance in normal young men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP) at 10 and 20 mm Hg, which decreased central venous pressure but did not alter blood pressure or heart rate. Decreases in forearm blood flow and increases in forearm vascular resistance with LBNP were greater after administration of lanatoside C (Cedilanid) than before, and the slope of the regression line relating changes in central venous pressure and those in forearm vascular resistance was steeper after lanatoside C. Vasoconstrictor responses to the cold pressor test did not differ before and after lanatoside C, which suggested that augmented responses to LBNP after the drug were not caused by a generalized change in reflex control. These results suggest that lanatoside C augments the tonic inhibitory influence of cardiopulmonary baroreceptors in normal men.

Adult↗

PubMed1984

Venous responses to salt loading in hypertensive subjects.

It has been previously suggested that salt loading produces structural changes of the arteries in hypertensive patients who respond to salt loading with a greater rise of blood pressure. This study examined the possibility that salt loading alters venous distensibility in hypertensive patients. Twenty-one patients with essential hypertension were placed on a low-sodium diet (70 meq) for 7 days and then were placed on a high-sodium diet (345 meq) for 7 days. Patients were arbitrarily divided into two groups based on the response of their blood pressure to salt loading: (1) those whose mean blood pressure increased by more than 10% while on the high-salt diet as compared with those on the low-salt diet (salt-responsive patients, n = 8) and (2) those whose mean blood pressure did not increase by more than 10% (salt-nonresponsive patients, n = 13). The venous pressure-volume relationship was determined in the forearm with a water-filled plethysmograph when patients were on the low- and high-salt diet. Venous pressure-volume curves were not different between salt-responsive and salt-nonresponsive patients while on the low-salt diet. High-salt intake shifted the curve toward the pressure axis for salt-responsive patients (p less than .05) but not for salt-nonresponsive patients. Phentolamine, 1 mg administered intravenously for 5 min, did not significantly alter venous pressure-volume curves for either group while on the low- or high-salt diet. These results suggest that salt loading decreased venous distensibility in salt-responsive patients, which resulted from nonadrenergic mechanisms: structural changes of the veins could perhaps be included as one of these mechanisms.

Adult↗

PubMed1984

Altered control of hindlimb vascular resistance by vagal afferents in spontaneously hypertensive rats. Difference in the early and late stage of hypertension.

The aim of this study was to examine whether control of vascular resistance by vagal afferents is altered in the early as well as late stage of hypertension. We examined the effects of vagotomy on hindlimb vascular resistance as well as on arterial baroreflex control of hindlimb vascular resistance in spontaneously hypertensive rats and Wistar-Kyoto rats, 12 and 35 weeks old. Vagotomy in rats with the intact arterial baroreceptors increased hindlimb vascular resistance in all four groups. Hindlimb vascular responses to graded sympathetic nerve stimulation were closely linear up to 6 Hz in all groups, and the slope of the response was approximately 1.4 times steeper in spontaneously hypertensive than in Wistar-Kyoto rats, in both the young and old groups. The increase in hindlimb vascular resistance after vagotomy normalized by the slope of the response to sympathetic nerve stimulation was greater in young spontaneously hypertensive rats than in young Wistar-Kyoto rats, but was less in old spontaneously hypertensive rats than in old Wistar-Kyoto rats. Vagotomy increased the gain of arterial baroreflex control of hindlimb vascular resistance in young spontaneously hypertensive rats, and in two groups of Wistar-Kyoto rats, but not in old spontaneously hypertensive rats. The percent increase in the gain of arterial baroreflex control of hindlimb vascular resistance after vagotomy tended to be greater in young spontaneously hypertensive than in young Wistar-Kyoto rats, but was less in old spontaneously hypertensive than in old Wistar-Kyoto rats. Central venous pressure and left ventricular end-diastolic pressure were higher in spontaneously hypertensive than in Wistar-Kyoto rats in both young and old groups. Left atrial distensibility assessed by obtaining the atrial pressure-volume relationship was comparable between young spontaneously hypertensive and young Wistar-Kyoto rats, but was less in old spontaneously hypertensive than in old Wistar-Kyoto rats. These results indicate that vagal afferents exert tonic inhibition on control of hindlimb vascular resistance in spontaneously hypertensive as well as in Wistar-Kyoto rats, and that tonic inhibitory influence of vagal afferents on control of hindlimb vascular resistance is altered in spontaneously hypertensive rats, augmented in young, but attenuated in old, spontaneously hypertensive rats, compared with that in age-matched Wistar-Kyoto rats. It is considered that altered control of vascular resistance by vagal afferents in spontaneously hypertensive rats may result from changes in vagal afferent activity.

Animals↗

PubMed1982

Limited maximal vasodilator capacity of forearm resistance vessels in normotensive young men with a familial predisposition to hypertension.

The study was performed to determine whether there is a structural vascular abnormality in normotensive subjects with hypertensive relatives. We examined maximal vasodilator capacity of forearm resistance vessels in 23 normotensive young men (mean blood pressure 94 +/- 0.4 mm Hg, mean +/- SE) with hypertensive relatives (age 24 +/- 0.1 years) and in 17 normotensive subjects (mean blood pressure 85 +/- 0.4 mm Hg) with no family history of hypertension (age 24 +/- 0.1 years). Maximal vasodilator capacity was examined by measuring minimal vascular resistance during peak reactive hyperemia after release from 10 minutes of arterial occlusion. Minimal forearm vascular resistance after release from 10 minutes of arterial occlusion was 25% higher (P less than 0.02) in subjects with hypertensive relatives (2.0 +/- 0.02 units) than that in subjects with no family history (1.5 +/- 0.01) units. We confirmed the previous findings that increasing metabolic vasodilator stimulus by performing intermittent handgrip exercise during 10 minutes of arterial occlusion did not augment peak dilation. This suggests that 10 minutes of arterial occlusion produced maximal vasodilation. Forearm vascular responses to ice on the forehead was greater in subjects with hypertensive relatives than those in subjects with no family history. These results suggest that there may be a structural abnormality in the forearm resistance vessels in normotensive subjects with family history of hypertension.

Adult↗

PubMedDate not supplied

Effect of epidural epinephrine infusion with bupivacaine on labor pain and mother-fetus outcome in humans.

BACKGROUND AND OBJECTIVES: Epinephrine is used with local anesthetics to prolong the duration of epidural analgesia and decrease the peak plasma concentrations of local anesthetics. In the practice of obstetric anesthesia, the utero-placental and fetal effects of epinephrine are controversial issues. We designed a prospective, randomized, and double-blind study to examine the effects of epinephrine infusion on the quality of analgesia and uterine or umbilical blood flows with Doppler ultrasound, as well as the duration of the first or the second stage of labor, and fetal outcome. METHODS: Twenty-eight parturients received continuous epidural bupivacaine 0.25% (4 mL/h) combined either with epinephrine (20 microg/h) (n = 13) or without epinephrine (n = 15) for analgesia during labor. If patients requested additional analgesia, an additional bolus of 1% or 1.5% lidocaine (6 to 10 mL) was administered. RESULTS: The total amount of additional lidocaine was greater in the plain bupivacaine group (130 [0, 280] mg; median [25th, 75th percentile] with P < .05) than in the epinephrine group (0 [0, 60] mg). Epinephrine infusion did not alter the resistance of the uterine and umbilical arteries as measured by resistance index. The duration of the first or second stages of labor did not significantly differ in the 2 groups. Epinephrine infusion did not change the fetal heart rate or the blood gas data in the umbilical artery. CONCLUSIONS: A low-dose epidural infusion of epinephrine decreased anesthetic requirements.

Adult↗

PubMedDate not supplied

Neurotoxicity of intrathecally administered tetracaine commences at the posterior roots near entry into the spinal cord.

BACKGROUND AND OBJECTIVES: Neurotoxicity of intrathecally administered local anesthetics is generating increased interest. This study was designed to examine the histopathologic effects of intrathecally administered tetracaine. METHODS: Sixty Wistar rats randomly received either 20%, 10%, 5%, 3%, 1%, 0.5%, or 0% tetracaine dissolved in 10% glucose solution or no solution via a chronically implanted intrathecal catheter. The spinal cord at L1, posterior and anterior roots and cauda equina were excised 5 days later, sectioned, processed, and prepared for light and electron microscopic examinations. RESULTS: Rats treated with tetracaine at 10% or 20% developed lesions in the posterior white matter and posterior roots. Rats injected with 3% or 5% tetracaine developed lesions, which began in the posterior roots close to the spinal cord and extended to the posterior white matter. The lesions were characterized by axonal degeneration. Injections of < or =1% of tetracaine did not cause any pathological changes. CONCLUSIONS: Our results suggest that the initial target of intrathecal tetracaine neurotoxicity may be the posterior roots at their entry into the spinal cord, where the axons are devoid of myelin sheath and thus representing a sensitive area for neurotoxic change.

Anesthetics, Local↗

PubMedDate not supplied

Modified application of intra-aortic balloon pump after repair of thoracic dissecting aneurysm.

We describe a patient who could not be weaned from cardiopulmonary bypass without mechanical circulatory assistance because of severe cardiac failure after surgical repair of a dissecting aneurysm of the descending aorta. Placement of an intra-aortic balloon in a conduit attached to the proximal aorta enabled the patient to recover from perioperative cardiac failure after all other measures had failed.

Adult↗